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1
Lai, Ching Jung, Ting Ruan, and Yu Ru Kou. "The involvement of hydroxyl radical and cyclooxygenase metabolites in the activation of lung vagal sensory receptors by circulatory endotoxin in rats." Journal of Applied Physiology 98, no. 2 (February 2005): 620–28. http://dx.doi.org/10.1152/japplphysiol.00539.2004.
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Circulatory endotoxin can stimulate vagal pulmonary C fibers and rapidly adapting receptors (RARs) in rats, but the underlying mechanisms are not clear. We investigated the involvement of hydroxyl radicals and cyclooxygenase metabolites in the stimulation of C fibers and RARs by circulatory endotoxin (50 mg/kg) in 112 anesthetized, paralyzed, and artificially ventilated rats. In rats pretreated with the vehicle, endotoxin stimulated C fibers and RARs and caused a slight increase in total lung resistance (Rl) and a decrease in dynamic lung compliance. In rats pretreated with dimethylthiourea (a hydroxyl radical scavenger) alone, indomethacin (a cyclooxygenase inhibitor) alone, or a combination of the two, C-fiber and RAR responses [C fiber: change (Δ) = −62, −79, and −85%; RAR: Δ = −80, −84, and −84%, respectively] were reduced, and the Rl response was prevented. The suppressive effects of a combination of dimethylthiourea and indomethacin on the C-fiber and RAR responses were not superior to indomethacin alone. In rats pretreated with isoproterenol (a bronchodilator), the C-fiber response was not significantly affected (Δ = −26%), the RAR response was reduced (Δ = −88%), and the Rl response was prevented. None of these pretreatments affected the dynamic lung compliance response. These results suggest that 1) both hydroxyl radicals and cyclooxygenase metabolites are involved in the endotoxin-induced stimulation of C fibers and RARs, and 2) the involvement of these two metabolites in the C-fiber stimulation may be due to their chemical effects, whereas that in the RAR stimulation may be due to their bronchoconstrictive effects.
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Tanaka, H., M. Yanase-Fujiwara, and K. Kanosue. "Effects of centrally and systemically administered indomethacin on body temperature in exercising rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 265, no. 1 (July 1, 1993): R230—R234. http://dx.doi.org/10.1152/ajpregu.1993.265.1.r230.
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Subcutaneous and intracerebroventricular (icv) injections of indomethacin were used to test whether prostaglandin synthesis is essential for the exercise-induced increase in a rat's body temperature. At an air temperature of 24 degrees C, male Wistar rats ran on a treadmill at 10-15 m/min 20 min after 300-micrograms icv injection or 60 min after 15-mg/kg sc injection of indomethacin or of control vehicle. The rectal temperature (Tre) of control rats in 17 control experiments increased by 1.0 degree C during exercise, whereas the Tre of the rats pretreated with intracerebroventricular indomethacin increased by only 0.4 degrees C. Threshold Tre for tail vasodilation was significantly lower in rats pretreated with indomethacin than the control rats (38.4 +/- 0.1 vs. 38.9 +/- 0.1 degrees C), but O2 uptake did not differ between indomethacin-pretreated and control rats. Subcutaneous injection of indomethacin did not affect the body temperature, tail vasomotor activity, or O2 uptake of exercising rats. Intracerebroventricular indomethacin did not affect Tre or tail vasomotor activity of rats resting at ambient temperatures of 24 and 28 degrees C. Present results suggest that prostaglandin synthesis is required for the vasoconstrictive effect of exercise on skin blood vessels and thus for the exercise-induced elevation of body temperature.
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Fu, Ziwei, Jiajia Hu, Li Zhou, Yanting Chen, Mokan Deng, Xiyang Liu, Jiahui Su, Aihua Lu, Xiaodong Fu та Tianxin Yang. "(Pro)renin receptor contributes to pregnancy-induced sodium-water retention in rats via activation of intrarenal RAAS and α-ENaC". American Journal of Physiology-Renal Physiology 316, № 3 (1 березня 2019): F530—F538. http://dx.doi.org/10.1152/ajprenal.00411.2018.
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The (pro)renin receptor (PRR) is a new component of the renin-angiotensin-aldosterone system (RAAS) and regulates renin activity. The objective of the present study was to test potential roles of the renal PRR and intrarenal RAAS in the physiological status of late pregnancy. Late pregnant Sprague-Dawley rats were studied 19–21 days after sperm was observed in vaginal smears. Experiments were performed using age-matched virgin rats and late pregnant rats treated with the specific PRR inhibitor PRO20 (700 μg·kg−1·day−1 sc for 14 days, 3 times/day for every 8 h) or vehicle. The indices of RAAS, including PRR, renin, angiotensin II, and aldosterone levels, were examined by immunoblotting, qRT-PCR, or ELISA. Further analyses of renal epithelial sodium channel (ENaC) expression, sodium-water retention, and plasma volume were performed. We first present evidence for the activation of intrarenal RAAS in late pregnant rats, including increases in urinary renin activity, active and total renin content, and prorenin content, angiotensin II and aldosterone excretion, in parallel with increased renal PRR expression and urinary soluble PRR excretion. Functional evidence demonstrated that PRR antagonism with PRO20 effectively suppressed the indices of intrarenal RAAS in late pregnant rats. In addition, our results revealed that renal α-ENaC expression, sodium-water retention, and plasma volume were elevated during late pregnancy, which were all attenuated by PRO20. In summary, the present study examined the renal mechanism of sodium-water retention and plasma volume expansion in late pregnant rats and identified a novel role of PRR in regulation of intrarenal RAAS and α-ENaC and thus sodium and fluid retention associated with pregnancy.
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Asarian, Lori, and Nori Geary. "Sex differences in the physiology of eating." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 305, no. 11 (December 1, 2013): R1215—R1267. http://dx.doi.org/10.1152/ajpregu.00446.2012.
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Hypothalamic-pituitary-gonadal (HPG) axis function fundamentally affects the physiology of eating. We review sex differences in the physiological and pathophysiological controls of amounts eaten in rats, mice, monkeys, and humans. These controls result from interactions among genetic effects, organizational effects of reproductive hormones (i.e., permanent early developmental effects), and activational effects of these hormones (i.e., effects dependent on hormone levels). Male-female sex differences in the physiology of eating involve both organizational and activational effects of androgens and estrogens. An activational effect of estrogens decreases eating 1) during the periovulatory period of the ovarian cycle in rats, mice, monkeys, and women and 2) tonically between puberty and reproductive senescence or ovariectomy in rats and monkeys, sometimes in mice, and possibly in women. Estrogens acting on estrogen receptor-α (ERα) in the caudal medial nucleus of the solitary tract appear to mediate these effects in rats. Androgens, prolactin, and other reproductive hormones also affect eating in rats. Sex differences in eating are mediated by alterations in orosensory capacity and hedonics, gastric mechanoreception, ghrelin, CCK, glucagon-like peptide-1 (GLP-1), glucagon, insulin, amylin, apolipoprotein A-IV, fatty-acid oxidation, and leptin. The control of eating by central neurochemical signaling via serotonin, MSH, neuropeptide Y, Agouti-related peptide (AgRP), melanin-concentrating hormone, and dopamine is modulated by HPG function. Finally, sex differences in the physiology of eating may contribute to human obesity, anorexia nervosa, and binge eating. The variety and physiological importance of what has been learned so far warrant intensifying basic, translational, and clinical research on sex differences in eating.
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Johansson, Maria E., Irene J. Andersson, Camilla Alexanderson, Ole Skøtt, Agneta Holmäng, and Göran Bergström. "Hyperinsulinemic rats are normotensive but sensitized to angiotensin II." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 294, no. 4 (April 2008): R1240—R1247. http://dx.doi.org/10.1152/ajpregu.00493.2007.
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The effect of insulin on blood pressure (BP) is debated, and an involvement of an activated renin-angiotensin aldosterone system (RAAS) has been suggested. We studied the effect of chronic insulin infusion on telemetry BP and assessed sympathetic activity and dependence of the RAAS. Female Sprague-Dawley rats received insulin (2 units/day, INS group, n = 12) or insulin combined with losartan (30 mg·kg−1·day−1, INS+LOS group, n = 10), the angiotensin II receptor antagonist, for 6 wk. Losartan-treated (LOS group, n = 10) and untreated rats served as controls ( n = 11). We used telemetry to measure BP and heart rate (HR), and acute ganglion blockade and air-jet stress to investigate possible control of BP by the sympathetic nervous system. In addition, we used myograph technique to study vascular function ex vivo. The INS and INS+LOS groups developed euglycemic hyperinsulinemia. Insulin did not affect BP but increased HR (27 beats/min on average). Ganglion blockade reduced mean arterial pressure (MAP) similarly in all groups. Air-jet stress did not increase sympathetic reactivity but rather revealed possible blunting of the stress response in hyperinsulinemia. Chronic losartan markedly reduced 24-h-MAP in the INS+LOS group (−38 ± 1 mmHg P < 0.001) compared with the LOS group (−18 ± 1 mmHg, P ≤ 0.05). While insulin did not affect vascular function per se, losartan improved endothelial function in the aorta of insulin-treated rats. Our results raise doubt regarding the role of hyperinsulinemia in hypertension. Moreover, we found no evidence that insulin affects sympathetic nervous system activity. However, chronic losartan treatment revealed an important interaction between insulin and RAAS in BP control.
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Carreño, Flávia Regina, Lisa L. Ji, and J. Thomas Cunningham. "Altered central TRPV4 expression and lipid raft association related to inappropriate vasopressin secretion in cirrhotic rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 2 (February 2009): R454—R466. http://dx.doi.org/10.1152/ajpregu.90460.2008.
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Inappropriate vasopressin (AVP) release causes dilutional hyponatremia in many pathophysiological states such as cirrhosis. The central molecular mechanisms that mediate inappropriate AVP release are unknown. We tested the hypothesis that changes in the expression or trafficking of TRPV4 in the central nervous system may contribute to inappropriate AVP release in the bile duct ligation (BDL) model of cirrhosis in the rat. Four weeks after surgery, BDL rats demonstrated significantly increased plasma vasopressin and plasma renin activity (PRA), hypervolemia, and decreased plasma osmolality. These effects were blocked by providing BDL rats with 2% saline to drink for 15 days. TRPV4 protein expression was significantly increased in brain punches from BDL rats containing the supraoptic nucleus (SON) of the hypothalamus (100% ± 11 to 157% ± 4.8), and this effect was blocked in BDL rats given saline. Immunohistochemistry demonstrated a significant increase in TRPV4-positive cells and the percentage of AVP neurons that also were TRPV4-positive in the SON of BDL rats. In the hypothalamus of BDL rats, TRPV4 lipid raft association increased compared with sham (from 100% ± 2.1 to 326.1% ± 16). This effect was significantly attenuated in BDL rats given 2% saline to drink (174% ± 11). In the brain stem, TRPV4 lipid raft association was reduced by BDL and inversely related to plasma AVP and PRA. We speculate that changes in TRPV4 expression and compartmentalization within lipid rafts could contribute to a feed-forward mechanism related to AVP release in cirrhosis.
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Friederich-Persson, Malou, and Patrik Persson. "Mitochondrial angiotensin II receptors regulate oxygen consumption in kidney mitochondria from healthy and type 1 diabetic rats." American Journal of Physiology-Renal Physiology 318, no. 3 (March 1, 2020): F683—F688. http://dx.doi.org/10.1152/ajprenal.00417.2019.
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Exaggerated activation of the renin-angiotensin-aldosterone system (RAAS) is a key feature in diseases such as hypertension, diabetes, and chronic kidney disease. Recently, an intracellular RAAS was demonstrated with angiotensin II (ANG II) type 1 (AT1) and type 2 (AT2) receptors expressed in nuclei and mitochondria. Diabetes is associated with both mitochondrial dysfunction and increased intracellular ANG II concentration in the kidney cortex. The present study investigated the role of ANG II signaling in kidney cortex mitochondria isolated from control and streptozotocin-induced diabetic rats. Mitochondrial oxygen consumption was evaluated after addition of ANG II alone or after preincubation with candesartan (AT1 receptor antagonist), PD-123319 (AT2 receptor antagonist), or the two in combination. ANG II binds to only mitochondrial AT2 receptors in control rats and both AT1 receptors and AT2 receptors in diabetic rats. ANG II decreased oxygen consumption in mitochondria from both control and diabetic rats. ANG II response was reversed to increased oxygen consumption by the nitric oxide synthase inhibitor N-nitro-l-arginine methyl ester. AT1 receptor inhibition did not affect the response to ANG II, whereas AT2 receptor inhibition abolished the response in mitochondria from control rats and reversed the response to increased oxygen consumption through superoxide-induced mitochondrial uncoupling in mitochondria from diabetic rats. ANG II decrease mitochondrial respiration via AT2 receptor-mediated nitric oxide release in both control and diabetic rats. AT1 receptors do not regulate mitochondria function in control rats, whereas ANG II via AT1 receptors increase mitochondria leak respiration in diabetic animals.
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Wakabayashi, Y., E. Yamada, T. Yoshida, and N. Takahashi. "Effect of intestinal resection and arginine-free diet on rat physiology." American Journal of Physiology-Gastrointestinal and Liver Physiology 269, no. 2 (August 1, 1995): G313—G318. http://dx.doi.org/10.1152/ajpgi.1995.269.2.g313.
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The small intestine has been presumed to release citrulline as a precursor for the endogenous arginine synthesis. We studied the effect of intestinal resection and arginine-free diet on rat physiology. We maintained rats with massively resected small intestine (R rats) and those with transected intestines (T rats) on either control or an arginine-free diet. After 4 wk, R rats fed deficient diet [R(-)] lost weight by a mean of 46 g, whereas R rats fed control diet [R(+)] and T rats fed control [T(+)] and deficient diet [T(-)] gained 30-96 g. Average nitrogen balance was 150, 60, 110, and -33 mg/day for T(+), T(-), R(+), and R(-), respectively. The concentrations of arginine in skeletal muscle were 654, 163, 230, and 84 nmol/g, respectively, and those in plasma were 133, 50, 103, and 54 microM, respectively. The concentrations of citrulline in R rats were halved compared with T rats irrespective of diet. We conclude that arginine is synthesized in a small intestine-dependent manner in the rat.
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Musch, T. I., A. Bruno, G. E. Bradford, A. Vayonis, and R. L. Moore. "Measurements of metabolic rate in rats: a comparison of techniques." Journal of Applied Physiology 65, no. 2 (August 1, 1988): 964–70. http://dx.doi.org/10.1152/jappl.1988.65.2.964.
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Two different open-circuit techniques of measuring metabolic rate were examined in rats at rest and during exercise. With one technique ambient air was drawn through a tightly fitting mask that was secured to the rat's head, whereas with the other technique the rat was placed into and ambient air was drawn through a Plexiglas box. Two series of experiments were performed. In series I, two groups were studied that consisted of rats that had received myocardial infarctions produced by coronary arterial ligations and rats that had received sham operations. In this series of experiments O2 uptake (VO2) and CO2 production (VCO2) were measured at rest, during four levels of submaximal exercise, and during maximal treadmill exercise in the same group of rats by use of both techniques in random order. VO2, VCO2, and the calculated respiratory exchange ratio (R) were similar at rest, during the highest level of submaximal exercise (20% grade, 37 m/min), and during maximal exercise; however, VO2 and VCO2 were significantly lower with the metabolic box technique compared with the mask technique during the three lowest work loads (5% grade, 19 m/min; 10% grade, 24 m/min; and 15% grade, 31 m/min). These differences appeared to be associated with a change in gait produced when the mask was worn. In series II, the arterial blood gas and acid-base responses to both submaximal and maximal exercise were measured using both techniques in a group of instrumented rats that had a catheter placed into the right carotid artery.(ABSTRACT TRUNCATED AT 250 WORDS)
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Miranda, Carlos A., Jae Wook Lee, Chung-Lin Chou, and Mark A. Knepper. "Tolvaptan as a tool in renal physiology." American Journal of Physiology-Renal Physiology 306, no. 3 (February 1, 2014): F359—F366. http://dx.doi.org/10.1152/ajprenal.00330.2013.
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For decades, the Brattleboro rat has been a useful model in kidney physiology. These animals manifest central diabetes insipidus (lack of circulating vasopressin) due to a mutation in the vasopressin-neurophysin gene. V2 receptor-mediated vasopressin actions in the kidney can be assessed in these animals by infusing the V2-selective vasopressin analog 1-desamino-8-d-arginine vasopressin (dDAVP). However, the major commercial supplier in the United States has ceased production, creating the need for another reliable experimental model of V2 receptor-mediated vasopressin action in rodents. We designed an in vivo protocol to investigate vasopressin responses in the rat kidney using osmotic minipumps loaded with tolvaptan, a nonpeptide competitive inhibitor of the vasopressin V2 receptor. Tolvaptan-infused rats had a mean urinary osmolality of <300 vs. >2,000 mosmol/kgH2O in vehicle-infused rats. The tolvaptan infusion produced large decreases in the renal abundance of aquaporin-2 (AQP2), aquaporin-3 (AQP3), the β-subunit of the epithelial sodium channel (β-ENaC), and γ-ENaC that were comparable to the differences seen in vehicle-infused vs. vasopressin-infused Brattleboro rats. Thus we conclude that tolvaptan infusion in rats provides an additional model (besides dDAVP-infusion in the Brattleboro rat) for the assessment of V2 receptor-mediated vasopressin actions in the kidney. We also provide ancillary in vitro data in rat inner-medullary-collecting-duct suspensions showing that tolvaptan can block vasopressin's effects on phosphorylation of the water channel AQP2 in vitro. Specifically, tolvaptan almost completely inhibited the ability of vasopressin to increase AQP2 phosphorylation at Ser256, Ser264, and Ser269, while strongly inhibiting a vasopressin-induced decrease in AQP2 phosphorylation at Ser261.
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Barney, Christopher C. "Restrained rats and the observer effect in physiology." Experimental Physiology 96, no. 12 (November 23, 2011): 1253–54. http://dx.doi.org/10.1113/expphysiol.2011.061267.
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Kanosue, K., Y. H. Zhang, M. Yanase-Fujiwara, and T. Hosono. "Hypothalamic network for thermoregulatory shivering." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 267, no. 1 (July 1, 1994): R275—R282. http://dx.doi.org/10.1152/ajpregu.1994.267.1.r275.
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Warming one side of a rat's preoptic area and anterior hypothalamus (POAH) suppresses shivering on both sides of the body, and the present study evaluated the extent to which signals mediating this suppression cross the midline within and below the POAH. Hind paw shivering during unilateral POAH thermal stimulation was measured for rats in which the POAH had been midsagittally transected and for rats in which one side of the hypothalamus had been coronally transected just caudal to the POAH. In midsagittally transected rats, unilateral warming on either side of the POAH suppressed shivering equally on both sides of the body. In unilaterally transected rats, POAH warming on the transected side did not affect shivering, but warming the intact side suppressed shivering equally on both sides of the body. When a unilateral transection of only the lateral part of the hypothalamus included the medial forebrain bundle, the effect was the same as that of a unilateral transection of the whole hypothalamus. These results indicate that no information controlling shivering is exchanged between the left and right POAH and that efferent signals from the POAH, descending through the medial forebrain bundle, cross the midline somewhere below the hypothalamus to innervate both sides of the body equally.
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Kanosue, K., M. Yanase-Fujiwara, and T. Hosono. "Hypothalamic network for thermoregulatory vasomotor control." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 267, no. 1 (July 1, 1994): R283—R288. http://dx.doi.org/10.1152/ajpregu.1994.267.1.r283.
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Warming one side of a rat's preoptic area and anterior hypothalamus (POAH) causes skin vasodilation on both sides of the body, and the present study evaluated the extent to which signals mediating this vasodilation cross the midline within and below the POAH. Hind paw vasomotion during unilateral POAH thermal or electrical stimulation was measured for rats in which the POAH had been midsagittally transected and for rats in which one side of the hypothalamus had been coronally transected just below the POAH. In midsagittally transected rats, unilateral POAH thermal or electrical stimulation produced bilateral paw vasodilation, but the ipsilateral dilation occurred at a hypothalamic temperature lower than that at which contralateral dilation occurred. In the unilaterally transected rats, unilateral POAH warming produced bilateral vasodilation and, regardless of which side of the POAH was warmed, the threshold stimulus temperature was always lower for vasodilation on the intact side. Unilateral transection of a part of the hypothalamus that included the medial forebrain bundle had the same effect as did unilateral transection of the whole hypothalamus. Information controlling thermoregulatory vasomotion thus crosses the midline both within and below the POAH. Although efferent signals descending through the medial forebrain bundle innervate skin blood vessels on both sides of the body, this innervation is stronger on the ipsilateral side.
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Whaley-Connell, Adam, Javad Habibi, Yongzhong Wei, Alex Gutweiler, Jessica Jellison, Charles E. Wiedmeyer, Carlos M. Ferrario, and James R. Sowers. "Mineralocorticoid receptor antagonism attenuates glomerular filtration barrier remodeling in the transgenic Ren2 rat." American Journal of Physiology-Renal Physiology 296, no. 5 (May 2009): F1013—F1022. http://dx.doi.org/10.1152/ajprenal.90646.2008.
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Recent evidence suggests that mineralocorticoid receptor (MR) antagonism has beneficial effects on tissue oxidative stress and insulin metabolic signaling as well as reducing proteinuria. However, the mechanisms by which MR antagonism corrects both renin-angiotensin-aldosterone system (RAAS) impairments in renal insulin metabolic signaling and filtration barrier/podocyte injury remain unknown. To explore this potential beneficial interactive effect of MR antagonism we used young transgenic (mRen2)27 (Ren2) rats with increased tissue RAAS activity and elevated serum aldosterone levels. Ren2 and age-matched Sprague-Dawley (SD) control rats (age 6–7 wk) were implanted with a low dose of the MR antagonist spironolactone (0.24 mg/day) or vehicle, both delivered over 21 days. Albuminuria, podocyte-specific proteins (synaptopodin, nephrin, and podocin), and ultrastructural analysis of the glomerular filtration barrier were measured in relation to RAAS activation of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, reactive oxygen species (ROS), and the redox-sensitive Rho kinase (ROK). Insulin metabolic signaling was determined via measurement of insulin receptor substrate-1 (IRS-1) phosphorylation, IRS-1 ubiquitin/proteasomal degradation, and phosphorylation of Akt. Ren2 rats exhibited albuminuria, loss of podocyte-specific proteins, and podocyte foot process effacement contemporaneous with reduced renal IRS-1 and protein kinase B/Akt phosphorylation compared with SD control rats (each P < 0.05). Ren2 kidneys also manifested increased NADPH oxidase/ROS/ROK in conjunction with enhanced renal tissue levels of angiotensin II (ANG II), ANG-(1-12), and angiotensin type 1 receptor. Low-dose spironolactone treatment reduced albuminuria and tissue RAAS activity and improved podocyte structural and protein integrity with improvements in IRS-1/Akt phosphorylation. Thus, in this model of RAAS activation, MR antagonism attenuates glomerular/podocyte remodeling and albuminuria, in part through reductions in redox-mediated impairment of insulin metabolic signaling.
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Holloszy, John O. "Mortality rate and longevity of food-restricted exercising male rats: a reevaluation." Journal of Applied Physiology 82, no. 2 (February 1, 1997): 399–403. http://dx.doi.org/10.1152/jappl.1997.82.2.399.
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Holloszy, John O. Mortality rate and longevity of food-restricted exercising male rats: a reevaluation. J. Appl. Physiol. 82(2): 399–403, 1997.—Food restriction increases the maximal longevity of rats. Male rats do not increase their food intake to compensate for the increase in energy expenditure in response to exercise. However, a decrease in the availability of energy for growth and cell proliferation that induces an increase in maximal longevity in sedentary rats only results in an improvement in average survival, with no extension of maximal life span, when caused by exercise. In a previous study (J. O. Holloszy and K. B. Schechtman. J. Appl. Physiol. 70: 1529–1535, 1991), to test the possibility that exercise prevents the extension of life span by food restriction, wheel running and food restriction were combined. The food-restricted runners showed the same increase in maximal life span as food-restricted sedentary rats but had an increased mortality rate during the first one-half of their mortality curve. The purpose of the present study was to determine the pathological cause of this increased early mortality. However, in contrast to our previous results, the food-restricted wheel-running rats in this study showed no increase in early mortality, and their survival curves were virtually identical to those of sedentary animals that were food restricted so as to keep their body weights the same as those of the runners. Thus it is possible that the rats in the previous study had a health problem that had no effect on longevity except when both food restriction and exercise were superimposed on it. Possibly of interest in this regard, the rats in this study did considerably more voluntary running than those in the previous study. It is concluded that 1) moderate caloric restriction combined with exercise does not normally increase the early mortality rate in male rats, 2) exercise does not interfere with the extension of maximal life span by food restriction, and 3) the beneficial effects of food restriction and exercise on survival are not additive or synergistic.
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Zachar, Rikke, Ammar Al-Mashhadi, Henrik Dimke, Per Svenningsen, Boye L. Jensen та Mattias Carlström. "Hydronephrosis is associated with elevated plasmin in urine in pediatric patients and rats and changes in NCC and γ-ENaC abundance in rat kidney". American Journal of Physiology-Renal Physiology 315, № 3 (1 вересня 2018): F547—F557. http://dx.doi.org/10.1152/ajprenal.00635.2017.
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Obstruction of urine flow at the level of the pelvo-ureteric junction (UPJO) and subsequent development of hydronephrosis is one of the most common congenital renal malformations. UPJO is associated with development of salt-sensitive hypertension, which is set by the obstructed kidney, and with a stimulated renin-angiotensin-aldosterone system (RAAS) in rodent models. This study aimed at investigating the hypothesis that 1) in pediatric patients with UPJO the RAAS is activated before surgical relief of the obstruction; 2) in rats with UPJO the RAAS activation is reflected by increased abundance of renal aldosterone-stimulated Na transporters; and 3) the injured UPJO kidney allows aberrant filtration of plasminogen, leading to proteolytic activation of the epithelial Na channel γ-subunit (γ-ENaC). Hydronephrosis resulting from UPJO in pediatric patients and rats was associated with increased urinary plasminogen-to-creatinine ratio. In pediatric patients, plasma renin, angiotensin II, urine and plasma aldosterone, and urine soluble prorenin receptor did not differ significantly before or after surgery, or compared with controls. Increased plasmin-to-plasminogen ratio was seen in UPJO rats. Intact γ-ENaC abundance was not changed in UPJO kidney, whereas low-molecular cleavage product abundance increased. The Na-Cl cotransporter displayed significantly lower abundance in the UPJO kidney compared with the nonobstructed contralateral kidney. The Na-K-ATPase α-subunit was unaltered. Treatment with an angiotensin-converting enzyme inhibitor (8 days, captopril) significantly lowered blood pressure in UPJO rats. It is concluded that the RAAS contributes to hypertension following partial obstruction of urine flow at the pelvo-ureteric junction with potential contribution from proteolytic activation of ENaC.
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Guerrero, Fr, and H. Burnet. "Effects of compression rate on rats carotid blood flow." Archives of Physiology and Biochemistry 103, no. 2 (January 1995): 196–201. http://dx.doi.org/10.3109/13813459508996133.
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Hidayat, Rachmat, and Patricia Wulandari. "Anatomy and Physiology of Animal Model Rats in Biomedical Research." Biomedical Journal of Indonesia 7, no. 2 (March 12, 2021): 265–69. http://dx.doi.org/10.32539/bji.v7i2.287.
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A distinguishing feature of rodents, including rats, is the absence of canines and thepresence of prominent incisors. Rats are monophydontic, meaning they grow one setof teeth in their lifetime. The enamel of the rodent incisor contains iron, which givesit its yellow-orange color. Rats are mammals and as such, possess many similaritieswith other mammals. Only the peculiarities of the rat’s anatomy are addressed. Malerats reach puberty at 40 - 60 days of age. Descent of the testes usually occursbetween days 30 - 60. Sperm counts vary by strain. The male rat has an os penis.Male rats have the following accessory sexual organs: ampulla, seminal vesicles,prostate, bulbourethral glands, coagulating glands, and preputial glands. Thecoagulating gland and prostatic and vesicular secretions are responsible for thecopulation plug, a firm plug deposited in the vagina of the female after copulation.(This plug, when found outside the female rat, is capsuleshaped and approximately5 mm long.) The male rat has no nipples. The adult male rat has a prominentscrotum and a longer anogenital distance than the female rat.
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Sokoloff, Greta, Robert F. Kirby, and Mark S. Blumberg. "Further evidence that BAT thermogenesis modulates cardiac rate in infant rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 274, no. 6 (June 1, 1998): R1712—R1717. http://dx.doi.org/10.1152/ajpregu.1998.274.6.r1712.
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Previous research in infant rats suggested that brown adipose tissue (BAT), by providing warm blood to the heart during moderate cold exposure, protects cardiac rate. This protective role for BAT thermogenesis was examined further in the present study. In experiment 1, 1-wk-old rats in a warm environment were pretreated with saline or chlorisondamine (a ganglionic blocker), and then BAT thermogenesis was stimulated by injection with the β3-agonist CL-316243. In experiment 2, pups were pretreated with chlorisondamine and injected with CL-316243, and after BAT thermogenesis was stimulated the interscapular region of the pups was cooled externally with a thermode. In both experiments, cardiac rate, oxygen consumption, and physiological temperatures were monitored. Activation of BAT thermogenesis substantially increased cardiac rate in saline- and chlorisondamine-treated pups, and focal cooling of the interscapular region was sufficient to lower cardiac rate. The results of these studies support the hypothesis that BAT thermogenesis contributes directly to the modulation of cardiac rate.
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Gall, Andrew J., Alyssa M. Goodwin, Ohanes S. Khacherian, and Laura B. Teal. "Superior Colliculus Lesions Lead to Disrupted Responses to Light in Diurnal Grass Rats (Arvicanthis niloticus)." Journal of Biological Rhythms 35, no. 1 (October 17, 2019): 45–57. http://dx.doi.org/10.1177/0748730419881920.
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The circadian system regulates daily rhythms of physiology and behavior. Although extraordinary advances have been made to elucidate the brain mechanisms underlying the circadian system in nocturnal species, less is known in diurnal species. Recent studies have shown that retinorecipient brain areas such as the intergeniculate leaflet (IGL) and olivary pretectal nucleus (OPT) are critical for the display of normal patterns of daily activity in diurnal grass rats ( Arvicanthis niloticus). Specifically, grass rats with IGL and OPT lesions respond to light in similar ways to intact nocturnal animals. Importantly, both the IGL and OPT project to one another in nocturnal species, and there is evidence that these 2 brain regions also project to the superior colliculus (SC). The SC receives direct retinal input, is involved in the triggering of rapid eye movement sleep in nocturnal rats, and is disproportionately large in the diurnal grass rat. The objective of the current study was to use diurnal grass rats to test the hypothesis that the SC is critical for the expression of diurnal behavior and physiology. We performed bilateral electrolytic lesions of the SC in female grass rats to examine behavioral patterns and acute responses to light. Most grass rats with SC lesions expressed significantly reduced activity in the presence of light. Exposing these grass rats to constant darkness reinstated activity levels during the subjective day, suggesting that light masks their ability to display a diurnal activity profile in 12:12 LD. Altogether, our data suggest that the SC is critical for maintaining normal responses to light in female grass rats.
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Monson, C. B., S. L. Patterson, J. M. Horowitz, and J. Oyama. "Thermoregulation in hypergravity-acclimated rats." Journal of Applied Physiology 67, no. 1 (July 1, 1989): 383–89. http://dx.doi.org/10.1152/jappl.1989.67.1.383.
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To determine the effect of hypergravity acclimation on thermoregulation, core temperature (Tc), tail temperature (Tt), and O2 consumption (VO2) were measured in control rats (raised at 1 G) and in rats acclimated to 2.1 G. When the animals were exposed to a low ambient temperature of 9 degrees C, concurrently with a hypergravic field of 2.1 G, Tc of rats raised at 1 G fell markedly by approximately 6 degrees C (to 30.8 +/- 0.6 degrees C) while that of the rats raised at 2.1 G remained relatively constant (falling only approximately 1 degree C to 36.4 +/- 0.3 degrees C). Thus prior acclimation to a 2.1-G field enabled rats to maintain Tc when cold exposed in a 2.1-G field. To maintain Tc, thermogenic mechanisms were successfully activated in the 2.1-G-acclimated rats as shown by measurements of VO2. In contrast, VO2 measurements showed that rats reared at 1 G and then cold exposed at 2.1 G did not activate thermogenic mechanisms sufficiently to prevent a fall in Tc. In other experiments, rats acclimated to either 1 or 2.1 G were found to lack the ability to maintain their Tc when exposed to a 5.8-G field or when exposed to prolonged cold exposure at 1 G. Results are interpreted as showing that when placed in a 2.1-G field, rats acclimated to 2.1 G can more closely maintain their Tc near 37 degrees C when cold exposed than can rats acclimated to 1 G. However, this enhanced regulatory ability of 2.1-G-acclimated rats over 1.0-G-acclimated rats is restricted to 2.1-G fields and is not observed in 1.0- and 5.8-G fields.
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Olver, T. Dylan, Matthew W. McDonald, Kenneth N. Grisé, Adwitia Dey, Matti D. Allen, Philip J. Medeiros, James C. Lacefield, et al. "Exercise training enhances insulin-stimulated nerve arterial vasodilation in rats with insulin-treated experimental diabetes." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 306, no. 12 (June 15, 2014): R941—R950. http://dx.doi.org/10.1152/ajpregu.00508.2013.
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Insulin stimulates nerve arterial vasodilation through a nitric oxide (NO) synthase (NOS) mechanism. Experimental diabetes reduces vasa nervorum NO reactivity. Studies investigating hyperglycemia and nerve arterial vasodilation typically omit insulin treatment and use sedentary rats resulting in severe hyperglycemia. We tested the hypotheses that 1) insulin-treated experimental diabetes and inactivity (DS rats) will attenuate insulin-mediated nerve arterial vasodilation, and 2) deficits in vasodilation in DS rats will be overcome by concurrent exercise training (DX rats; 75–85% V̇o2 max, 1 h/day, 5 days/wk, for 10 wk). The baseline index of vascular conductance values (VCi = nerve blood flow velocity/mean arterial blood pressure) were similar ( P ≥ 0.68), but peak VCi and the area under the curve (AUCi) for the VCi during a euglycemic hyperinsulinemic clamp (EHC; 10 mU·kg−1·min−1) were lower in DS rats versus control sedentary (CS) rats and DX rats ( P ≤ 0.01). Motor nerve conduction velocity (MNCV) was lower in DS rats versus CS rats and DX rats ( P ≤ 0.01). When compared with DS rats, DX rats expressed greater nerve endothelial NOS (eNOS) protein content ( P = 0.04). In a separate analysis, we examined the impact of diabetes in exercise-trained rats alone. When compared with exercise-trained control rats (CX), DX rats had a lower AUCi during the EHC, lower MNCV values, and lower sciatic nerve eNOS protein content ( P ≤ 0.03). Therefore, vasa nervorum and motor nerve function are impaired in DS rats. Such deficits in rats with diabetes can be overcome by concurrent exercise training. However, in exercise-trained rats (CX and DX groups), moderate hyperglycemia lowers vasa nervorum and nerve function.
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Cao, Xue, Zhijun Sun, Boya Zhang, Xueqi Li, and Hongyuan Xia. "The Effects of Ivabradine on Cardiac Function after Myocardial Infarction are Weaker in Diabetic Rats." Cellular Physiology and Biochemistry 39, no. 5 (2016): 2055–64. http://dx.doi.org/10.1159/000447901.
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Background/Aims: Plasma norepinephrine (NE) and brain natriuretic peptide (BNP, termed BNP-45 in rats) are considered as essential neurohormones indicating heart failure progression. The purposes of this study were to examine the effects of ivabradine (IBD) on cardiac function and plasma NE and BNP-45 after chronic ischemic heart failure (CHF) in non-diabetic rats and diabetic rats. We further determined if sympathetic NE uptake-1 (a major pathway to metabolize NE) mechanism is responsible for the role played by IBD. Methods: We ligated rat's coronary artery to induce CHF; and injected streptozotocin (STZ) to induce diabetic hyperglycemia. Echocardiography was employed to determine cardiac function. We used ELISA to examine plasma NE and BNP-45; and Western Blot analysis to examine the protein levels of NE uptake-1 in sympathetic nerves. Results: CHF increased the levels of NE and BNP-45 in non-STZ rats and STZ rats. Systemic injection of IBD significantly attenuated the augmented NE and BNP-45 and impaired left ventricular function induced by CHF in those rats. This effect appeared to be less in STZ rats. A liner relation was observed between the NE/BNP-45 levels and left ventricular function after administration of IBD. Also, IBD was observed to have a recovery effect on the downregulated NE uptake-1 evoked by CHF, but to a smaller degree in STZ rats. Conclusion: Our data revealed specific signaling mechanisms by which IBD improves the cardiac function as IBD alleviates impaired NE uptake-1and thereby decreases heightened NE and BNP-45 induced by CHF. Our data also demonstrated that the effects of IBD are weakened after diabetic hyperglycemia likely due to worsen NE uptake-1 pathway. Thus, targeting sympathetic NE uptake-1 signaling molecules has clinical implications for treatment and management of CHF in diabetes. Our data were also to shed light on strategies for application of this drug because NE and BNP play an important role in regulation of progression and prognosis of CHF, and in particular, because IBD affects NE uptake-1 pathway in hyperglycemic animals to a less degree.
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Stupka, Nicole, and Peter M. Tiidus. "Effects of ovariectomy and estrogen on ischemia-reperfusion injury in hindlimbs of female rats." Journal of Applied Physiology 91, no. 4 (October 1, 2001): 1828–35. http://dx.doi.org/10.1152/jappl.2001.91.4.1828.
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The effects of estrogen and ovariectomy on indexes of muscle damage after 2 h of complete hindlimb ischemia and 2 h of reperfusion were investigated in female Sprague-Dawley rats. The rats were assigned to one of three experimental groups: ovariectomized with a 17β-estradiol pellet implant (OE), ovariectomized with a placebo pellet implant (OP), or control with intact ovaries (R). It was hypothesized that following ischemia-reperfusion (I/R), muscle damage indexes [serum creatine kinase (CK) activity, calpain-like activity, inflammatory cell infiltration, and markers of lipid peroxidation (thiobarbituric-reactive substances)] would be lower in the OE and R rats compared with the OP rats due to the protective effects of estrogen. Serum CK activity following I/R was greater ( P < 0.01) in the R rats vs. OP rats and similar in the OP and OE rats. Calpain-like activity was greatest in the R rats ( P < 0.01) and similar in the OP and OE rats. Neutrophil infiltration was assessed using the myeloperoxidase (MPO) assay and immunohistochemical staining for CD43-positive (CD43+) cells. MPO activity was lower ( P < 0.05) in the OE rats compared with any other group and similar in the OP and R rats. The number of CD43+ cells was greater ( P < 0.01) in the OP rats compared with the OE and R rats and similar in the OE and R rats. The OE rats had lower ( P < 0.05) thiobarbituric-reactive substance content following I/R compared with the R and OP rats. Indexes of muscle damage were consistently attenuated in the OE rats but not in the R rats. A 10-fold difference in serum estrogen content may mediate this. Surprisingly, serum CK activity and muscle calpain-like activity were lower ( P< 0.05) in the OP rats compared with the R rats. Increases in serum insulin-like growth factor-1 content ( P < 0.05) due to ovariectomy were hypothesized to account for this finding. Thus both ovariectomy and estrogen supplementation have differential effects on indexes of I/R muscle damage.
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Tomohiro, A., S. Kimura, H. He, Y. Fujisawa, A. Nishiyama, K. Kiyomoto, Y. Aki, T. Tamaki, and Y. Abe. "Regional blood flow in Dahl-Iwai salt-sensitive rats and the effects of dietary L-arginine supplementation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 272, no. 4 (April 1, 1997): R1013—R1019. http://dx.doi.org/10.1152/ajpregu.1997.272.4.r1013.
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The purpose of the present study was to determine 1) whether different organs undergo similar increase in vascular resistance in Dahl-Iwai salt-sensitive (S) rats, and 2) the effects of chronic oral L-arginine supplementation on the regional hemodynamics in S rats. Male 6-wk-old S rats and salt-resistant (R) rats were maintained on an 8% NaCl chow for 4 wk. One group (S or R rats) was maintained on tap water and the other group (S/Arg or R/Arg rats) received tap water containing L-arginine at a concentration of 1.5%. Organ blood flow and cardiac output were measured with microspheres in the conscious condition. Mean blood pressure in S, S/Arg, R, and R/Arg rats was 159 +/- 5, 138 +/- 3, 111 +/- 4, and 112 +/- 4 mmHg, respectively. Urinary excretion of protein and albumin in S/Arg rats was significantly suppressed compared with S rats. Concerning regional hemodynamics, the flow rate of the kidney was lower in S rats than in R rats, but there were no differences between S and R rats in the flow rates of the brain, heart, lung, liver, spleen, intestine, skeletal muscle, and skin. Thus the renal blood flow was solely reduced in S rats on a high-salt diet. The flow rate of the kidney in S/Arg rats was maintained at a higher level compared with that of S rats. L-Arginine treatment tended to produce a recovery in the urinary excretion of guanosine 3',5'-cyclic monophosphate in S rats, but had no effect in R rats. Thus the supplementation of L-arginine prevented the increase in blood pressure in S rats on a high-salt diet and normalized the abnormality of renal hemodynamics accompanying salt-induced hypertension.
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Muzi-Filho, Humberto, Larissa B. Jannuzzi, Ana C. S. Bouzan, Sarana Alves-Barros, Danilo S. Alves-Bezerra, Amaury Pereira-Acácio, Bruna S. N. Ferreira, Debora Silva-Pereira, Gloria Costa-Sarmento, and Adalberto Vieyra. "Histone Deacetylase Activity and the Renin-Angiotensin-Aldosterone System: Key Elements in Cardiorenal Alterations Provoked by Chronic Malnutrition in Male Adult Rats." Cellular Physiology and Biochemistry 54, no. 6 (November 18, 2020): 1143–62. http://dx.doi.org/10.33594/000000306.
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BACKGROUND/AIMS: Chronic malnutrition (M) affects >1 billion people worldwide. Epidemiological data point to long-term renal and cardiovascular outcomes (e.g. arterial hypertension, cardiorenal syndromes). The renin-angiotensin-aldosterone system (RAAS) has been implicated in the physiopathology of these disturbances, but M-induced alterations in RAAS-modulated renal Na+ handling and their cardiovascular repercussions are not known. Moreover, altered tissue-specific histone deacetylases (HDAC) results in arterial hypertension and the use of sodium Valproate (Val; a HDAC inhibitor) reduces blood pressure. However, there are no reports regarding the renal and cardiovascular effects of HDAC inhibition in M, or on the signaling pathways involved. The central aim of our study has been to investigate whether alterations in the HDAC/RAAS axis underpin alterations in active Na+ transport in the kidney and heart, and affects blood pressure. METHODS: Male rats aged 28 days were given either a control (C) or a multideficient diet (Regional Basic Diet, RBD), which mimics alimentary habits from developing countries. Subgroups received Losartan (Los), a blocker of type 1 Angiotensin II receptors. When the rats reached 70 days, new subgroups received Val until they were 90 days of age. Homogenates and enriched plasma membrane fractions from renal cortex corticis and cardiomyocytes were obtained by differential centrifugation of the tissues. The activity of renal and cardiac deacetylases was assayed by measuring - after incubation with the membranes - the amount of deacetylated lysines in a substrate containing an acetylated lysine side chain. Protein kinases activities were measured following the incorporation of the γ-phosphoryl group of [γ-32P]ATP into Ser/Thr residues of histone type III-S. The activity of Na+-transporting ATPases (kidney and heart) was quantified by measuring the release of Pi from ATP that was sensitive to ouabain ((Na++K+)ATPase), or sensitive to furosemide (Na+-ATPase). Tail-cuff plethysmography was used to measure systolic blood pressure and heart rate. RESULTS: M provoked HDAC downregulation, which was reversed by Los and Val, either alone or in combination, with selective upregulation of protein kinases C and A (PKC, PKA) in renal cortex corticis, but not in left ventricle cardiomyocytes. The 2 kinases were strongly inhibited by Los and Val in both organs. Malnourished rats developed elevated systolic arterial pressure (SAP) and heart rate (HR) at 70 days of age; Los and Val restored the control SAP, but not HR. Functional and the above biochemical alterations were associated with the deregulation of renal and cardiac Na+-transporting ATPases. (Na++K+)ATPase activities were downregulated in M rats in both organs, and were further inhibited by the pharmacological treatments in the renal cortex corticis (C and M groups) and the left ventricle (only in C rats). No additional effect was found in cardiac (Na++K+)ATPase from M rats. Ouabain-resistant Na+-ATPase was upregulated in renal cortex corticis and downregulated in cardiomyocytes, returning to C values after administration of Los and Val. CONCLUSION: The HDAC/RAAS axis appears to be a key regulator of Na+-transporting ATPases in renal cortex corticis and cardiomyocytes via an appropriate balance of PKC and PKA activities. Modifications within the HDAC/RAAS axis provoked by chronic M - with repercussions in renal and cardiac Na+ transport - underpin alterations in bodily Na+ homeostasis that culminate with the onset of arterial hypertension and potential cardiorenal syndrome.
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Lambert, M. I., and T. D. Noakes. "Spontaneous running increases VO2max and running performance in rats." Journal of Applied Physiology 68, no. 1 (January 1, 1990): 400–403. http://dx.doi.org/10.1152/jappl.1990.68.1.400.
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The effect of spontaneous running activity on maximal O2 consumption (VO2max), running performance, and submaximal O2 consumption (VO2submax, running economy) was studied in rats to determine whether this exercise mode can produce significant training adaptations. Twenty male Long-Evans rats (300 +/- 20 g) were housed in spontaneous activity running wheels, and after 8 wk they were divided into high-, average-, and low-performing groups according to the average spontaneous running distance and tested for maximal running performance, VO2max, and VO2submax. The average-performing rats ran 52% longer than the control rats (P less than 0.01) and 19% longer than the low-performing rats (P less than 0.05). There was no difference in maximum running time to exhaustion between the average- and high-performing rats. The low-performing rats ran 28% longer than the control rats (P less than 0.05). The VO2max of the average-performing rats was 12% greater than in the control rats (P less than 0.01). There were no differences in VO2max between either low-performing and control rats or between average- and high-performing rats. Although the VO2submax was not different between low-, average-, and high-performing rats, in all three groups it was lower than in the control rats (P less than 0.01). Accordingly, we recommend that only those Long-Evans rats that, on average, spontaneously run greater than 11.6 km/wk for a minimum of 8 wk be considered to have undergone a training effect. Rats that perform poorly can be identified as early as 2 wk after the start of training.
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Brown, D. R., D. A. Morgan, J. D. Peuler, and P. Thoren. "24-hour blood pressure recordings in Dahl rats on high- and low-salt diets." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 257, no. 5 (November 1, 1989): R1225—R1231. http://dx.doi.org/10.1152/ajpregu.1989.257.5.r1225.
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The goal of this study was to determine if the baroreflex abnormality previously shown in Dahl-sensitive (DS) rats would increase blood pressure and heart rate (HR) variability. Mean arterial pressure (MAP) and HR were sampled every 2 s for 24 h from Dahl-resistant (DR) and DS rats on low- and high-salt diets (n = 12-13 in each group). MAP +/- SD was significantly elevated in the DS rats on high-salt diets (DSH); the SD of MAP in the DSH rats was also significantly higher compared with similar measurements in rats on high-salt diets (DRH) and DS rats on low-salt diets (DSL) when SD was divided by MAP. MAP was higher at night than during the day in the DSH rats. In contrast, HR and HR variability were not significantly different between the groups. The baroreflex control of HR, determined by means of graded injections of phenylephrine, was least in the DSH rats and increased, respectively, with DSL rats, DRH rats, and DR rats on low-salt diets. There was no significant correlation between the baroreflex control of HR and MAP or the SD of MAP in the DSH rats, suggesting that there is not a simple relationship between baroreflex gain and the overall behavior of MAP in DSH rats.
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Holloszy, J. O., and E. K. Smith. "Longevity of cold-exposed rats: a reevaluation of the "rate-of-living theory"." Journal of Applied Physiology 61, no. 5 (November 1, 1986): 1656–60. http://dx.doi.org/10.1152/jappl.1986.61.5.1656.
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It has been postulated that increased energy expenditure results in shortened survival. To test this “rate-of-living theory” we examined the effect of raising energy expenditure by means of cold exposure on the longevity of rats. Male 6-mo-old SPF Long-Evans rats were gradually accustomed to immersion in cool water (23 degrees C). After 3 mo they were standing in the cool water for 4 h/day, 5 days/wk. They were maintained on this program until age 32 mo. The cold exposure resulted in a 44% increase in food intake (P less than 0.001). Despite their greater food intake, the cold-exposed rats' body weights were significantly lower than those of control animals from age 11 to 32 mo. The average age at death of the cold-exposed rats was 968 +/- 141 days compared with 923 +/- 159 days for the controls. The cold exposure appeared to protect against neoplasia, particularly sarcomas; only 24% of the necropsied cold-exposed rats had malignancies compared with 57% for the controls. The results of this study provide no support for the concept that increased energy expenditure decreases longevity.
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Legendre, Ariadne, Emilia Papakonstantinou, Marie-Claude Roy, Denis Richard, and Ruth B. S. Harris. "Differences in response to corticotropin-releasing factor after short- and long-term consumption of a high-fat diet." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 3 (September 2007): R1076—R1085. http://dx.doi.org/10.1152/ajpregu.00592.2006.
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We previously reported an exaggerated endocrine and weight loss response to stress in rats fed a high-fat (HF) diet for 5 days. Others report blunted stress-induced anxiety in rats made obese on a HF diet. Experiments described here tested whether sensitivity to stress-related peptides was changed in obese and nonobese HF-fed rats. Third ventricle infusion of corticotropin-releasing factor (CRF) in rats made obese on HF diet (40% kcal fat) produced an exaggerated hypophagia, which is thought to be mediated by CRF2 receptors. Obese rats responded to a lower dose of CRF for a longer time than rats fed a low-fat (LF) diet (12% kcal fat). CRF-induced release of corticosterone, which is thought to be mediated by CRF1 receptors, was not exaggerated in obese HF-fed rats. In contrast, rats fed HF diet for 5 days showed the same food intake and corticosterone response to CRF as LF-fed rats. CRF mRNA expression in the paraventricular nucleus of the hypothalamus was stimulated by mild stress (ip saline injection and placement in a novel cage) in LF-fed rats but not in rats fed HF diet for 5 days because of a nonsignificant increase in expression in nonstressed HF-fed rats. In addition, nonstressed levels of urocortin (UCN) I mRNA expression in the Edinger-Westphal nucleus were significantly inhibited in HF-fed rats. These data suggest that rats that have become obese on a HF diet show a change in responsiveness to stress peptides, whereas the increased stress response in nonobese HF-fed rats may be associated with changes in basal CRF and UCN I mRNA expression.
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Fletcher, E. C., J. Lesske, R. Behm, C. C. Miller, H. Stauss, and T. Unger. "Carotid chemoreceptors, systemic blood pressure, and chronic episodic hypoxia mimicking sleep apnea." Journal of Applied Physiology 72, no. 5 (May 1, 1992): 1978–84. http://dx.doi.org/10.1152/jappl.1992.72.5.1978.
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We have described a rat model that responds to repetitive episodic hypoxia (12-s infusions of nitrogen into daytime sleeping chambers every 30 s, 7 h/day for 35 days) with an increase in diurnal systemic blood pressure. We hypothesized that afferent information from the peripheral chemoreceptors may be necessary to produce diurnal blood pressure elevation in this hypoxia model. Carotid body denervation (CBD) was accomplished by severing both carotid sinus nerves in two groups of male Wistar rats (250–375 g). Group 4 CBD rats were subjected to intermittent hypoxia for 35 days (3–5% nadir ambient O2) as described above, whereas group 5 CBD rats remained unhandled in their usual cages. Additional sham-operated controls included group 2 sham-“hypoxia” rats, which were housed in chambers identical to the hypoxia rats but supplied with compressed air instead of nitrogen, group 1 (not denervated) rats, which remained unhandled in their usual cages, and group 3 sham-operated rats, which were subjected to 35 days of intermittent hypoxia identical to group 4 CBD rats. Femoral arterial baseline and end-of-study blood pressures were measured in conscious rats. The group 3 rats exposed to episodic hypoxia displayed a 13-mmHg increase in mean blood pressure, whereas the other groups showed no significant change from baseline. Left ventricular hypertrophy was evident in all rats exposed to episodic hypoxia, but right ventricular hypertrophy was evident only in the group 4 rats. All CBD rats developed increased hematocrit and hemoglobin, while the group 3 rats (non-CBD, episodic hypoxia) did not. The baroreceptor reflex at baseline was not depressed in the CBD rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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Gupta, A. K., R. Clark, and K. A. Kirchner. "Verapamil prevents insulin antinatriuresis in euglycemic rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 262, no. 6 (June 1, 1992): R1145—R1148. http://dx.doi.org/10.1152/ajpregu.1992.262.6.r1145.
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To determine whether calcium entry is necessary for insulin antinatriuresis, urinary sodium excretion was determined before and during euglycemic insulin administration in rats receiving verapamil (10 micrograms.kg-1.min-1) or vehicle. In vehicle rats, insulin reduced sodium excretion from 2.7 +/- 0.5 to 0.98 +/- 0.2 mu eq/min (P less than 0.05) without altering arterial pressure or inulin clearance. Insulin did not reduce sodium excretion in rats receiving verapamil. Baseline mean arterial pressure was lower in verapamil rats than in vehicle rats. To exclude the possibility that lower baseline arterial pressures prevented insulin antinatriuresis, insulin's effect on sodium excretion was determined in rats receiving captopril at a dose that reduced arterial pressure to the level observed in verapamil rats, and in verapamil rats with angiotensin II levels fixed to maintain arterial pressure equivalent to vehicle rats. In captopril rats, insulin reduced (P less than 0.05) sodium excretion from 1.07 +/- 0.3 to 0.3 +/- 0.01 mu eq/min, even though arterial pressure was not different from that in verapamil rats. Insulin failed to reduce sodium excretion in verapamil rats receiving angiotensin II. Thus verapamil prevents insulin antinatriuresis by renal mechanisms related to inhibition of calcium entry. Additionally, insulin antinatriuresis is independent of angiotensin II.
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Pflueger, Axel C., Timothy S. Larson, Siegfried Hagl, and Franklyn G. Knox. "Role of nitric oxide in intrarenal hemodynamics in experimental diabetes mellitus in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 277, no. 3 (September 1, 1999): R725—R733. http://dx.doi.org/10.1152/ajpregu.1999.277.3.r725.
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The role of nitric oxide (NO) in the regulation of the intrarenal microcirculation in streptozotocin (STZ)-induced diabetes mellitus in rats is not clear. We examined renal cortical and papillary hemodynamics in STZ rats and determined the effects of systemic inhibition and stimulation of NO synthesis. Renal blood flow in cortical (QCC), and inner medullary ascending (QAV) and descending (QDV) vasa recta capillaries was measured by fluorescence videomicroscopy in STZ Munich-Wistar rats and nondiabetic control rats. Ten days after STZ injection (80 mg/kg ip), basal QCC and QDV were significantly greater in STZ rats ( n = 16) compared with control rats ( n = 15). Infusion of N G-monomethyl-l-arginine (l-NMMA, 15 mg/kg bolus, 500 μg ⋅ min−1 ⋅ kg−1iv) decreased QCC (−41%), QAV (−38%), and QDV (−37%) in control rats ( n = 6) and to a significantly greater magnitude than in STZ rats ( n = 7), QCC (−14%), QAV (−20%), and QDV (−25%). Coinfusion ofl-arginine (l-Arg, 1 mg ⋅ kg−1 ⋅ min−1iv) with l-NMMA increased QCC to a significantly greater extent ( P < 0.01) in control rats compared with STZ rats. In subsequent studies, infusion ofl-Arg alone increased QCC (+50%), QAV (+16%), and QDV (+11%) in control rats ( n = 5) but had no effect in STZ rats ( n = 5). These results show that the response of renal cortical and papillary capillary blood flow to both inhibition and stimulation of NO synthesis is attenuated in the early onset of STZ-diabetes mellitus rats compared with control rats.
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Sahebjami, H., and J. MacGee. "Effects of starvation on lung mechanics and biochemistry in young and old rats." Journal of Applied Physiology 58, no. 3 (March 1, 1985): 778–84. http://dx.doi.org/10.1152/jappl.1985.58.3.778.
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Two groups of rats (young and old) were food-deprived for 3 wk and were compared with age-matched fed groups. Final body weight and dry and wet weights of lungs were significantly reduced in both young and old starved rats. As determined by saline volume-pressure (VP) curves, lungs of young starved rats accepted significantly less volume at all pressure levels compared with lungs of young fed rats. When expressed as a percent of maximum lung volume, the VP curve in young starved rats was significantly shifted upward at low lung volumes. In the old rats, the VP curves were similar in fed and starved rats. Total lung content of protein, DNA, crude connective tissue, hydroxyproline, and elastin were significantly reduced in young starved compared with young fed rats, whereas in old starved rats only protein and DNA contents were lower than those in old fed animals. It appears that in rapidly growing young rats starvation leads to growth retardation, loss of connective tissue components, and possibly reduction in tissue elastic forces at low lung volumes, whereas starvation has no significant effects on lung mechanics and connective tissue in old rats.
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Bouitbir, Jamal, Anne-Laure Charles, Laurence Rasseneur, Stéphane Dufour, François Piquard, Bernard Geny, and Joffrey Zoll. "Atorvastatin treatment reduces exercise capacities in rats: involvement of mitochondrial impairments and oxidative stress." Journal of Applied Physiology 111, no. 5 (November 2011): 1477–83. http://dx.doi.org/10.1152/japplphysiol.00107.2011.
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Physical exercise exacerbates the cytotoxic effects of statins in skeletal muscle. Mitochondrial impairments may play an important role in the development of muscular symptoms following statin treatment. Our objective was to characterize mitochondrial function and reactive oxygen species (ROS) production in skeletal muscle after exhaustive exercise in atorvastatin-treated rats. The animals were divided into four groups: resting control (CONT; n = 8) and exercise rats (CONT+EXE; n = 8) as well as resting (ATO; n = 10) and exercise (ATO+EXE; n = 8) rats that were treated with atorvastatin (10 mg·kg−1·day−1for 2 wk). Exhaustive exercise showed that the distance that was covered by treated animals was reduced ( P < 0.05). Using dihydroethidium staining, we showed that the ROS level was increased by 60% in the plantaris muscle of ATO compared with CONT rats and was highly increased in ATO+EXE (226%) compared with that in CONT+EXE rats. The maximal mitochondrial respiration (Vmax) was decreased in ATO rats compared with that in CONT rats ( P < 0.01). In CONT+EXE rats, Vmaxsignificantly increased compared with those in CONT rats ( P < 0.05). Vmaxwas significantly lower in ATO+EXE rats (−39%) compared with that in CONT+EXE rats ( P < 0.001). The distance that was covered by rats significantly correlated with Vmax( r = 0.62, P < 0.01). The glycogen content was decreased in ATO, CONT+EXE, and ATO+EXE rats compared with that in CONT rats ( P < 0.05). GLUT-4 mRNA expression was higher after exhaustive exercise in CONT+EXE rats compared with the other groups ( P < 0.05). Our results show that exhaustive exercise exacerbated metabolic perturbations and ROS production in skeletal muscle, which may reduce the exercise capacity and promote the muscular symptoms in sedentary atorvastatin-treated animals.
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Madden, Christopher J., Sean D. Stocker, and Alan F. Sved. "Attenuation of homeostatic responses to hypotension and glucoprivation after destruction of catecholaminergic rostral ventrolateral medulla neurons." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 3 (September 2006): R751—R759. http://dx.doi.org/10.1152/ajpregu.00800.2005.
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This study determined the effect of destruction of rostral ventrolateral medulla (RVLM)-C1 cells on integrated sympathetic and hormonal responses to hypotension or glucoprivation. Injection of anti-dopamine β-hydroxylase-saporin into the RVLM resulted in 29–99% depletion of RVLM-C1 neurons and ∼60% reduction in the number of A5 neurons. As in our previous study in unanesthetized rats, resting mean arterial pressure (MAP) was reduced by ∼10 mmHg in rats with >80% depletion of RVLM-C1 cells compared with control rats, although resting heart rate (HR) did not differ significantly. In the present study, resting plasma levels of norepinephrine (NE) did not differ significantly between control rats and rats with >80% depletion of RVLM-C1 cells, although there was a tendency for RVLM-C1 lesioned rats to have lower levels. Also consistent with our previous study, hydralazine (HDZ)-evoked hypotension resulted in smaller increases in HR and plasma levels of NE in rats with >80% depletion of RVLM-C1 cells compared with control rats. Furthermore, the elevated plasma levels of posterior pituitary hormones vasopressin and oxytocin evoked by HDZ were blunted in RVLM-C1 lesioned rats compared with control rats, even though MAP fell to lower levels in the lesioned rats. Plasma renin activity, plasma osmolality, and plasma protein concentrations did not differ between control rats and rats with >80% depletion of RVLM-C1 neurons. In response to systemic administration of 2-deoxyglucose, the circulating level of epinephrine and the resulting hyperglycemia were attenuated in rats with >80% depletion of RVLM-C1 cells compared with control rats. These results demonstrate that RVLM-C1 cells, in addition to playing a role in acute cardiovascular reflexes, play an important role in integrated sympathetic and hormonal responses to homeostatic challenges such as hypotension and glucoprivation.
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Thomas, E. M., and S. M. Armstrong. "Effect of ovariectomy and estradiol on unity of female rat circadian rhythms." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 257, no. 5 (November 1, 1989): R1241—R1250. http://dx.doi.org/10.1152/ajpregu.1989.257.5.r1241.
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Sixteen rats were ovariectomized and given either a 1-cm implant of crystalline estradiol-17 beta (eight rats) or an empty implant (eight rats). A further six rats were sham ovariectomized and given empty implants, and eight rats were left unoperated. The rats were exposed to 70 days of constant dim light (LL) with a maximum illumination level of 20 lx, and circadian running and drinking rhythms were monitored. In LL, both the running and drinking activity rhythms of the ovariectomized, blank-implanted rats became markedly disrupted, whereas unoperated and sham-operated rats maintained unified rhythms. Estradiol-implanted rats developed fewer rhythm desynchronies, and the majority displayed a single band of free-running activity. Rather than being arrhythmic, the activity of the LL-exposed ovariectomized rats appeared to contain several free-running components. Thus these data are consistent with the concept of a multioscillatory basis to the circadian system and support a role for the ovary and its hormone estradiol in the maintenance of coherence between component oscillators.
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Tkacs, Nancy C., and Barry E. Levin. "Obesity-prone rats have preexisting defects in their counterregulatory response to insulin-induced hypoglycemia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 287, no. 5 (November 2004): R1110—R1115. http://dx.doi.org/10.1152/ajpregu.00312.2004.
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Rats that develop diet-induced obesity (DIO) on a 31% fat [high-energy (HE)] diet have defective sensing and responding to altered glucose levels compared with diet-resistant (DR) rats. Thus we postulated that they would also have defective counterregulatory responses (CRR) to insulin-induced hypoglycemia (IIH). Chow-fed selectively bred DIO and DR rats underwent three sequential 60-min bouts of IIH separated by 48 h. Glucose levels fell comparably, but DIO rats had 22–29% lower plasma epinephrine (Epi) levels during the first two bouts than DR rats. By the third trial, despite comparable Epi levels, DIO rats had lower 30-min glucose levels and rebounded less than DR rats 85 min after intravenous glucose. Although DIO rats gained more carcass and fat weight after 4 wk on an HE diet than DR rats, they were unaffected by prior IIH. Compared with controls, DR rats with prior IIH and HE diet had higher arcuate nucleus neuropeptide Y (50%) and proopiomelanocortin (POMC; 37%) mRNA and an inverse correlation ( r = 0.85; P = 0.004) between POMC expression and body weight gain on the HE diet. These data suggest that DIO rats have a preexisting defect in their CRR to IIH but that IIH does not affect the expression of their hypothalamic neuropeptides or weight gain as it does in DR rats.
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Saunders, P. R., N. P. Hanssen, and M. H. Perdue. "Cholinergic nerves mediate stress-induced intestinal transport abnormalities in Wistar-Kyoto rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 273, no. 2 (August 1, 1997): G486—G490. http://dx.doi.org/10.1152/ajpgi.1997.273.2.g486.
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We have previously reported that acute stress alters intestinal transport physiology in Wistar-Kyoto rats, a stress-susceptible strain. In this study, we tested the hypothesis that the abnormalities in these rats are due to cholinergic mechanisms. Atropine- or saline-treated rats were exposed to acute restraint stress, and, subsequently, electrophysiological parameters of excised jejunal segments were assessed in Ussing chambers. Compared with the parent Wistar rat strain, Wistar-Kyoto rats demonstrated significantly greater stress-induced changes in ion secretion and permeability. The activity of cholinesterase in intestinal mucosal homogenates was significantly less in Wistar-Kyoto than in Wistar rats. Atropine pretreatment of rats before stress corrected the epithelial pathophysiology. Our results suggest that stress stimulated the release of acetylcholine, resulting in altered epithelial function in these genetically predisposed rats.
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Yao, Xing-Hai, Li Chen, and B. L. Grégoire Nyomba. "Adult rats prenatally exposed to ethanol have increased gluconeogenesis and impaired insulin response of hepatic gluconeogenic genes." Journal of Applied Physiology 100, no. 2 (February 2006): 642–48. http://dx.doi.org/10.1152/japplphysiol.01115.2005.
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Rat offspring exposed to ethanol (EtOH rats) during pregnancy are insulin resistant, but it is unknown whether they have increased gluconeogenesis. To address this issue, we determined blood glucose and liver gluconeogenic genes, proteins, and enzyme activities before and after insulin administration in juvenile and adult EtOH rats and submitted adult EtOH rats to a pyruvate challenge. In juvenile rats, basal glucose; peroxisome proliferator-activated receptor-coactivator-1α protein and mRNA; and phospho enolpyruvate carboxykinase enzyme activity, protein, and mRNA were similar between groups. After insulin injection, these parameters failed to decrease in EtOH rats, but glucose decreased by 30% and gluconeogenic enzymes, proteins, and mRNAs decreased by 50–70% in control rats. In adult offspring, basal peroxisome proliferator-activated receptor-coactivator-1α protein and mRNA levels were 40–80% higher in EtOH rats than in controls. Similarly, basal phospho enolpyruvate carboxykinase activity, protein, and mRNA were ∼1.8-fold greater in EtOH rats than in controls. These parameters decreased by ∼50% after insulin injection in control rats, but they remained unchanged in EtOH rats. After insulin injection in the adult rats, glucose decreased by 60% in controls but did not decrease significantly in EtOH rats. A subset of adult EtOH rats had fasting hyperglycemia and an exaggerated glycemic response to pyruvate compared with controls. The data indicate that, after prenatal EtOH exposure, the expression of gluconeogenic genes is exaggerated in adult rat offspring and is insulin resistant in both juvenile and adult rats, explaining increased gluconeogenesis. These alterations persist through adulthood and may contribute to the pathogenesis of Type 2 diabetes after exposure to EtOH in utero.
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Teske, J. A., A. S. Levine, M. Kuskowski, J. A. Levine, and C. M. Kotz. "Elevated hypothalamic orexin signaling, sensitivity to orexin A, and spontaneous physical activity in obesity-resistant rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 4 (October 2006): R889—R899. http://dx.doi.org/10.1152/ajpregu.00536.2005.
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Selectively-bred obesity-resistant [diet resistant (DR)] rats weigh less than obesity-prone [diet-induced obese (DIO)] rats, despite comparable daily caloric intake, suggesting phenotypic energy expenditure differences. Human data suggest that obesity is maintained by reduced ambulatory or spontaneous physical activity (SPA). The neuropeptide orexin A robustly stimulates SPA. We hypothesized that DR rats have greater: 1) basal SPA, 2) orexin A-induced SPA, and 3) preproorexin, orexin 1 and 2 receptor (OX1R and OX2R) mRNA, compared with DIO rats. A group of age-matched out-bred Sprague-Dawley rats were used as additional controls for the behavioral studies. DIO, DR, and Sprague-Dawley rats with dorsal-rostral lateral hypothalamic (rLHa) cannulas were injected with orexin A (0, 31.25, 62.5, 125, 250, and 500 pmol/0.5 μl). SPA and food intake were measured for 2 h after injection. Preproorexin, OX1R and OX2R mRNA in the rLHa, and whole hypothalamus were measured by real-time RT-PCR. Orexin A significantly stimulated feeding in all rats. Orexin A-induced SPA was significantly greater in DR and Sprague-Dawley rats than in DIO rats. Two-mo-old DR rats had significantly greater rLHa OX1R and OX2R mRNA than DIO rats but comparable preproorexin levels. Eight-mo-old DR rats had elevated OX1R and OX2R mRNA compared with DIO rats, although this increase was significant for OX2R only at this age. Thus DR rats show elevated basal and orexin A-induced SPA associated with increased OX1R and OX2R gene expression, suggesting that differences in orexin A signaling through OX1R and OX2R may mediate DIO and DR phenotypes.
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Odenweller, C. M., C. T. Hsu, E. Sipe, J. P. Layshock, S. Varyani, R. L. Rosian, and S. E. DiCarlo. "Laboratory exercise using "virtual rats" to teach endocrine physiology." Advances in Physiology Education 273, no. 6 (December 1997): S24. http://dx.doi.org/10.1152/advances.1997.273.6.s24.
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Animal experimentation is limited in many curricula due to the expense, lack of adequate animal facilities and equipment, and limited experience of the teachers. There are also ethical concerns dealing with the comfort and safety of the animals. To overcome these obstacles, we developed a "dry laboratory" using "virtual rats." The "virtual rat" eliminates the obstacles inherent in animal experimentation, such as inadequate budgets, as well as avoiding important animal rights issues. Furthermore, no special materials are required for the completion of this exercise. Our goal in developing this dry laboratory was to create an experience that would provide students with an appreciation for the value of laboratory data collection and analysis. Students are exposed to the challenge of animal experimentation, experimental design, data collection, and analysis and interpretation without the issues surrounding the use of live animals.
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Sørensen, DB, K. Mortensen, T. Bertelsen, and K. Vognbjerg. "Enriching the metabolic cage: effects on rat physiology and behaviour." Animal Welfare 17, no. 4 (November 2008): 395–403. http://dx.doi.org/10.1017/s0962728600027901.
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AbstractMetabolic cages are used for housing rats and mice for up to five days for collection of urine and/or faeces. The small, barren area of the metabolic cage compromises animal welfare as the animals lack a solid floor, shelter, nest material and social contact. We constructed and tested a practically-applicable enrichment device designed to meet behavioural needs for environmental complexity. The influence of this device on the cage preferences and stress levels of the animals was evaluated. A box-shaped enrichment device was designed and implemented in existing metabolic cages. Male Tac:SD rats were housed for five days in an enriched metabolic cage (EMC; n = 12) or a standard metabolic cage (SMC; n = 12), and data were collected on bodyweight, food and water intake, urination and defaecation, as well as urinary corticosterone and creatinine. Moreover, open-field behaviour and cage preferences were assessed. Rats in both groups gained significantly less weight when housed in metabolic cages. Furthermore, SMC rats failed to increase their weight gain after being housed in the metabolic cage. Defaecation was significantly higher in the SMC than in the EMC and so was urinary creatinine. No group differences were found in open-field behaviour. However, in comparing activity before and after housing in the metabolic cage, only SMC animals exhibited significantly lower total activity. In a preference test, a preference for the tunnel connecting the cages in the preference test and a side preference for the left side were found. This side preference was eliminated when the EMC was placed on the right side, whereas the right side was significantly avoided when the EMC was placed on the left side. Based on these results, we conclude that, to some extent, the enrichment device improved the welfare of rats housed in EMC, compared to those in SMC.
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Margiocco, M. L., M. Borgarelli, T. I. Musch, D. M. Hirai, K. S. Hageman, R. J. Fels, A. A. Garcia, and M. J. Kenney. "Effects of combined aging and heart failure on visceral sympathetic nerve and cardiovascular responses to progressive hyperthermia in F344 rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 299, no. 6 (December 2010): R1555—R1563. http://dx.doi.org/10.1152/ajpregu.00434.2010.
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Sympathetic nerve discharge (SND) responses to hyperthermia are attenuated in aged rats without heart failure (HF) and in young HF (YHF) rats, demonstrating that individually aging and HF alter SND regulation. However, the combined effects of aging and HF on SND regulation to heat stress are unknown, despite the high prevalence of HF in aged individuals. We hypothesized that SND responses to heating would be additive when aging and HF are combined, demonstrated by marked reductions in SND and mean arterial pressure (MAP) responses to heating in aged HF (AHF) compared with aged sham HF (ASHAM) rats, and in AHF compared with YHF rats. Renal and splenic SND responses to hyperthermia (colonic temperature increased to 41.5°C) were determined in anesthetized YHF, young sham (YSHAM), AHF, and ASHAM Fischer rats. HF was induced by myocardial infarction and documented using echocardiographic, invasive, and postmortem measures. The severity of HF was similar in YHF and AHF rats. SND responses to heating were attenuated in YHF compared with YSHAM rats, demonstrating an effect of HF on SND regulation in young rats. In contrast, AHF and ASHAM rats demonstrated similar SND responses to heating, suggesting a prominent influence of age on SND regulation in AHF rats. Splenic SND and MAP responses to heating were similar in YHF, AHF, and ASHAM rats, indicating that the imposition of HF in young rats changes the regulatory status of these variables to one consistent with aged rats. These data suggest that the effect of HF on SND regulation to hyperthermia is age dependent.
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Pedersen, Michael, Christian T. Brandt, Gitte M. Knudsen, Christian Østergaard, Peter Skinhøj, Niels Frimodt-Møller, and Kirsten Møller. "Cerebral blood flow autoregulation in early experimental S. pneumoniae meningitis." Journal of Applied Physiology 102, no. 1 (January 2007): 72–78. http://dx.doi.org/10.1152/japplphysiol.00697.2006.
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We studied cerebral blood flow (CBF) autoregulation and intracranial pressure (ICP) during normo- and hyperventilation in a rat model of Streptococcus pneumoniae meningitis. Meningitis was induced by intracisternal injection of S. pneumoniae. Mean arterial blood pressure (MAP), ICP, cerebral perfusion pressure (CPP, defined as MAP − ICP), and laser-Doppler CBF were measured in anesthetized infected rats ( n = 30) and saline-inoculated controls ( n = 30). CPP was either incrementally reduced by controlled hemorrhage or increased by intravenous norepinephrine infusion. Twelve hours postinoculation, rats were studied solely during normocapnia, whereas rats studied after 24 h were exposed to either normocapnia or to acute hypocapnia. In infected rats compared with control rats, ICP was unchanged at 12 h but increased at 24 h postinoculation (not significant and P < 0.01, respectively); hypocapnia did not lower ICP compared with normocapnia. Twelve hours postinoculation, CBF autoregulation was lost in all infected rats but preserved in all control rats ( P < 0.01). Twenty-four hours after inoculation, 10% of infected rats had preserved CBF autoregulation during normocapnia compared with 80% of control rats ( P < 0.01). In contrast, 60% of the infected rats and 100% of the control rats showed an intact CBF autoregulation during hypocapnia ( P < 0.05 for the comparison of infected rats at normocapnia vs. hypocapnia). In conclusion, CBF autoregulation is lost both at 12 and at 24 h after intracisternal inoculation of S. pneumoniae in rats. Impairment of CBF autoregulation precedes the increase in ICP, and acute hypocapnia may restore autoregulation without changing the ICP.
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Harris, Ruth B. S., Emily W. Kelso, William P. Flatt, Harvey J. Grill, and Timothy J. Bartness. "Testosterone replacement does not normalize carcass composition in chronically decerebrate male rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 6 (June 2009): R1687—R1694. http://dx.doi.org/10.1152/ajpregu.00019.2009.
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Chronically decerebrate (CD) rats, in which the forebrain and its descending projections are completely neurally isolated from hindbrain and rostral projections, gain substantial amounts of body fat, lose lean tissue, and have low circulating testosterone concentrations. We tested whether testosterone replacement would normalize body composition of male CD rats. Five groups of rats were used: CD placebo, CD testosterone, control placebo, castrate placebo, and castrate testosterone. Testosterone replacement was initiated at the first stage of CD surgery in both CDs and castrate controls. The second stage of CD surgery occurred 8 days later, and the study ended 15 days later. Testosterone implants produced 10-fold normal circulating concentrations. Food intake was fixed for all rats by tube feeding. CD rats had substantially more body fat and less lean tissue than neurally intact rats. Testosterone replacement did not affect adiposity of CD rats but did increase carcass water content. Energy expenditure of CD rats was significantly lower than that of control placebo and castrated rats. Testosterone lowered respiratory equivalency ratio and ameliorated a fall in energy expenditure late in the intermeal interval in CD rats. Castration increased, and testosterone decreased luteinizing hormone (LH) and follicle stimulating hormone (FSH) in neurally intact controls. LH was undetectable, and FSH was equivalent to neurally intact controls in CD rats, and neither was affected by testosterone. Collectively, low testosterone did not explain obesity or decreased lean body mass of CD rats, although CD rats exhibited abnormal levels of circulating reproductive hormones and disrupted testosterone negative feedback.
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Levin, Barry E., and Ambrose A. Dunn-Meynell. "Sibutramine alters the central mechanisms regulating the defended body weight in diet-induced obese rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 6 (December 1, 2000): R2222—R2228. http://dx.doi.org/10.1152/ajpregu.2000.279.6.r2222.
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Chronic administration of sibutramine lowers body weight, presumably by altering brain monoamine metabolism. Here the effect of sibutramine on sympathoadrenal function (24-h urine norepinephrine and epinephrine levels) and arcuate nucleus (ARC) neuropeptide Y (NPY) and proopiomelanocortin (POMC) expression was assessed in diet-induced obese rats fed a low-fat diet. Chronic (10 wk) sibutramine [5 mg · kg−1 · day−1 ip; rats fed ad libitum and injected with sibutramine (AS)] lowered body weight by 15% but only transiently (3–4 wk) reduced intake compared with vehicle-treated controls [rats fed chow ad libitum and injected with vehicle daily (AV)]. Other rats food restricted (RS) to 90% of the weight of AS rats and then given sibutramine restored their body weights to the level of AS rats when allowed libitum food intake. After reequilibration, RS rats were again energy restricted to reduce their weight to 90% of AS rats, and additional vehicle-treated rats (RV) were restricted to keep their body weights at the level of AS rats for 3 wk more. Terminally, total adipose depot weights and leptin levels paralleled body weights (AV > AS = RV > RS), although AS rats had heavier abdominal and lighter peripheral depots than RV rats of comparable body weights. Sibutramine treatment increased sympathetic activity, attenuated the increased ARC NPY, and decreased POMC mRNA levels induced by energy restriction in RV rats. Thus sibutramine lowered the defended body weight in association with compensatory changes in those central pathways involved in energy homeostasis.
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Şentürk, Ümit Kemal, Filiz Gündüz, Oktay Kuru, Mehmet R. Aktekin, Dijle Kipmen, Özlem Yalçin, Melek Bor-Küçükatay, Akin Yeşilkaya, and Oğuz K. Başkurt. "Exercise-induced oxidative stress affects erythrocytes in sedentary rats but not exercise-trained rats." Journal of Applied Physiology 91, no. 5 (November 1, 2001): 1999–2004. http://dx.doi.org/10.1152/jappl.2001.91.5.1999.
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Oxidant stress is one of the factors proposed to be responsible for damaged erythrocytes observed during and after exercise. The impact of exertional oxidant stress after acute exhaustive treadmill running on erythrocyte damage was investigated in sedentary (Sed) and exercise-trained (ET) rats treated with or without antioxidant vitamins C and E. Exhaustive exercise led to statistically significant increments in the levels of thiobarbituric acid-reactive substance (TBARS) and H2O2-induced TBARS in Sed rats and resulted in functional and structural alterations in erythrocytes (plasma hemoglobin concentrations, methemoglobin levels, and rise in osmotic fragility of erythrocytes with decrease in erythrocyte deformability). Administration of antioxidant vitamin for 1 mo before exhaustive exercises prevented lipid peroxidation (TBARS, H2O2-induced TBARS) in Sed rats without any functional or structural alterations in erythrocytes. Parameters indicating erythrocyte lipid peroxidation and deterioration after exhaustive exercise in rats trained regularly with treadmill running for 1 mo were not different from those in Sed controls. Erythrocyte lipid peroxidation (TBARS) increased in exhausted-ET rats compared with ET controls; however, the plasma hemoglobin, methemoglobin levels, and erythrocyte osmotic fragility and deformability did not differ. Exhaustive exercise-induced lipid peroxidation in ET rats on antioxidant vitamin treatment was prevented, whereas functional and structural parameters of erythrocytes were not different from those of the ET controls. We conclude that exertional oxidant stress contributed to erythrocyte deterioration due to exercise in Sed but not in ET rats.
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Schlenker, Evelyn H. "Dextromethorphan affects ventilation differently in male and female rats." Journal of Applied Physiology 81, no. 5 (November 1, 1996): 1911–16. http://dx.doi.org/10.1152/jappl.1996.81.5.1911.
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Schlenker, Evelyn H. Dextromethorphan affects ventilation differently in male and female rats. J. Appl. Physiol. 81(5): 1911–1916, 1996.—Subcutaneous administration of aspartic acid results in a long-lasting but reversible depression of ventilation in male but not in female rats. Aspartic acid acts on N-methyl-d-aspartate receptors. The present study tested the hypothesis that a noncompetitive N-methyl-d-aspartate-receptor antagonist, dextromethorphan (Dex), would depress ventilation in female rats and stimulate it in male rats. Moreover, Dex administered prior to aspartic acid should prevent the aspartic acid-induced depression of ventilation in male rats. In female rats, Dex caused a 30% depression of ventilation relative to saline at 5 and 10 mg/kg ( P < 0.01) but not at the highest dose (20 mg/kg). In male rats, Dex had no effect on ventilation. At a dose of 20 mg/kg, Dex depressed oxygen consumption to 50% of the saline value at all time points in female rats ( P < 0.001) and in male rats 45 and 60 min after administration. The time points when Dex depressed ventilation and oxygen consumption were different in female rats, suggesting that the depression of ventilation was not the result of a depression in oxygen consumption. During a hypercapnic challenge (7% CO2), female rats treated with 5 and 10 mg/kg of Dex exhibited a smaller increase in ventilatory response relative to saline treatment. At a dose of 20 mg/kg, the hypercapnic responsiveness of male rats was markedly stimulated (85.8 ± 8.95 ml/min) relative to saline (50.6 ± 9.14 ml/min; P < 0.001). Finally, Dex administered before aspartic acid prevented the aspartic acid-induced depression of ventilation in male rats. Thus, in rats, Dex has gender-specific effects on ventilation and these effects are not associated with changes in oxygen consumption.
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Hofer, M. A. "Nutrient control of cardiac rate in infant rats: role of arterial baroreceptors." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 249, no. 4 (October 1, 1985): R443—R448. http://dx.doi.org/10.1152/ajpregu.1985.249.4.r443.
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A surgical procedure is described for the deafferentation of carotid sinus (CS) and aortic depressor (AD) baroreceptors in 2-wk suckling rats. Baroreflex testing in unanesthetized pups showed that cardiac rate responses to acute elevations of blood pressure were reduced to less than 9% of controls after combined denervation (CSAD), 28% after AD and 47% after CS denervation at 4 h. After 24 h of nutrient deprivation, resting cardiac rates of sham operated controls fell a mean of -148 beat/min, significantly more than CS, AD, or CSAD groups (P less than 0.01). Baroreflex test responses in individuals correlated significantly with their later responses to nutrient deprivation (r = 0.67, P less than 0.01). There were no significant differences in base-line cardiac rate, systolic blood pressure, or cardiac rate during 24 h intragastric milk infusion between deafferented and control pups. These experiments suggest that arterial baroreceptors are important in the cardiovascular adjustments after nutrient deprivation in suckling rats.