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1
Noh, Mi, Hee-Seong Jang, Jinu Kim, and Babu Padanilam. "Renal Sympathetic Nerve-Derived Signaling in Acute and Chronic Kidney Diseases." International Journal of Molecular Sciences 21, no. 5 (February 28, 2020): 1647. http://dx.doi.org/10.3390/ijms21051647.
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The kidney is innervated by afferent sensory and efferent sympathetic nerve fibers. Norepinephrine (NE) is the primary neurotransmitter for post-ganglionic sympathetic adrenergic nerves, and its signaling, regulated through adrenergic receptors (AR), modulates renal function and pathophysiology under disease conditions. Renal sympathetic overactivity and increased NE level are commonly seen in chronic kidney disease (CKD) and are critical factors in the progression of renal disease. Blockade of sympathetic nerve-derived signaling by renal denervation or AR blockade in clinical and experimental studies demonstrates that renal nerves and its downstream signaling contribute to progression of acute kidney injury (AKI) to CKD and fibrogenesis. This review summarizes our current knowledge of the role of renal sympathetic nerve and adrenergic receptors in AKI, AKI to CKD transition and CKDand provides new insights into the therapeutic potential of intervening in its signaling pathways.
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Kenney, Michael J., Dale E. Claassen, Richard J. Fels, and Cristina S. Saindon. "Cold stress alters characteristics of sympathetic nerve discharge bursts." Journal of Applied Physiology 87, no. 2 (August 1, 1999): 732–42. http://dx.doi.org/10.1152/jappl.1999.87.2.732.
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Frequency-domain analyses were used to determine the effect of cold stress on the relationships between the discharge bursts of sympathetic nerve pairs, sympathetic and aortic depressor nerve pairs, and sympathetic and phrenic nerve pairs in chloralose-anesthetized, baroreceptor-innervated rats. Sympathetic nerve discharge (SND) was recorded from the renal, lumbar, splanchnic, and adrenal nerves during decreases in core body temperature from 38 to 30°C. The following observations were made. 1) Hypothermia produced nonuniform changes in the level of activity in regionally selective sympathetic nerves. Specifically, cold stress increased lumbar and decreased renal SND but did not significantly change the level of activity in splanchnic and adrenal nerves. 2) The cardiac-related pattern of renal, lumbar, and splanchnic SND bursts was transformed to a low-frequency (0–2 Hz) pattern during cooling, despite the presence of pulse-synchronous activity in arterial baroreceptor afferents. 3) Peak coherence values relating the discharges between sympathetic nerve pairs decreased at the cardiac frequency but were unchanged at low frequencies (0–2 Hz), indicating that the sources of low-frequency SND bursts remain prominently coupled during progressive reductions in core body temperature. 4) Coherence of discharge bursts in phrenic and renal sympathetic nerve pairs in the 0- to 2-Hz frequency band increased during mild hypothermia (36°C) but decreased during deep hypothermia (30°C). We conclude that hypothermia profoundly alters the organization of neural circuits involved in regulation of sympathetic nerve outflow to selected regional circulations.
3
Taylor, R. F., and L. P. Schramm. "Spinally mediated inhibition of abdominal and lumbar sympathetic activities." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 254, no. 4 (April 1, 1988): R655—R658. http://dx.doi.org/10.1152/ajpregu.1988.254.4.r655.
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Renal, splenic, and lumbar sympathetic nerve activities were recorded in the paralyzed, anesthetized, artificially ventilated, and spinally transected rat. Electrical stimulation of the dorsolateral funiculus caudal to the spinal transection was used to generate stimulus-response curves for changes in sympathetic activity in each of the three sympathetic nerves using five stimulus frequencies. In all rats, spinal stimulation inhibited sympathetic activity in renal and splenogastric nerves by approximately 50%. In grouped data, threshold frequency for inhibition of renal and splenogastric sympathetic nerve activity was 5 Hz, and inhibitions were maximal (50-60%) at 10 Hz. In contrast, activity in the lumbar sympathetic chain was inhibited in only two of five rats, and grouped data did not exhibit any statistically significant inhibitions. We conclude that lumbar sympathetic activity which remains after spinal transection can be inhibited only marginally by spinal stimulation, which substantially reduces renal and splenogastric sympathetic activity.
4
Taylor, R. B., and L. C. Weaver. "Dorsal root afferent influences on tonic firing of renal and mesenteric sympathetic nerves in rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 264, no. 6 (June 1, 1993): R1193—R1199. http://dx.doi.org/10.1152/ajpregu.1993.264.6.r1193.
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After spinal cord transection in cats and rats, the activity of many sympathetic nerves is not entirely lost, and firing of other nerves continues unabated or is increased. This study was done to evaluate the importance of dorsal root afferent discharge on the generation of tonic sympathetic activity in renal and mesenteric postganglionic nerves in spinal rats and in rats with intact neuraxes. Sympathetic discharge was recorded in anesthetized rats, and peripheral afferent influences were eliminated by dorsal rhizotomy from T4 to L2. Activity of renal and mesenteric nerves was well maintained after high cervical and thoracic (T4) cord transections. Rhizotomy had no effect on sympathetic discharge in rats with intact neuraxes but decreased renal nerve activity significantly (-25%) in spinal rats. Because rhizotomy decreased mesenteric discharge in only three of six spinal rats, mean mesenteric nerve discharge was not decreased significantly. The decreased renal nerve discharge after dorsal rhizotomy could not be attributed to input from any specific spinal segment, and ipsilateral input was no greater than contralateral input. After rhizotomy, both renal and mesenteric nerves had substantial excitatory drive from the transected, deafferented spinal cord. These findings demonstrate that dorsal root afferent influences on spinal neurons can contribute to the generation of tonic discharge in some sympathetic nerves in spinal animals.
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Sripairojthikoon, W., and J. M. Wyss. "Cells of origin of the sympathetic renal innervation in rat." American Journal of Physiology-Renal Physiology 252, no. 6 (June 1, 1987): F957—F963. http://dx.doi.org/10.1152/ajprenal.1987.252.6.f957.
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Physiological studies are rapidly elucidating the function of the renal nerves; however, the anatomical location of the postganglionic cell bodies that supply the rat kidney has not been fully clarified. The origin of the sympathetic projection to the rat kidney was investigated in the present study by use of the fluorescent dye retrograde transport technique. Application of the dye to the renal nerves resulted in the fluorescent labeling of sympathetic cell bodies in paravertebral [thoracic (T) segment 6 through lumbar (L) segment 4] and prevertebral (renal, greater splanchnic, and celiac) ganglia and along the greater splanchnic nerve. Sympathetic neurons in all of these locations were round to fusiform in shape, 16-40 micron in diameter. They were dispersed uniformly throughout the paravertebral ganglia and splanchnic nerve, but in the celiac and greater splanchnic ganglia, cells projecting to the kidney were clustered near the origin of the renal nerve. In contrast to the cat, in which greater than 50% of the renal sympathetic innervation arises from the prevertebral ganglia, in the rat the majority (greater than 70%) of labeled renal sympathetic neurons were in the paravertebral ganglia, especially T12-L1. The distribution of renal sympathetic neurons in the paravertebral ganglia closely approximates the rostrocaudal distribution of renal afferent cell bodies in the dorsal root ganglia.
6
Kannan, H., Y. Hayashida, and H. Yamashita. "Increase in sympathetic outflow by paraventricular nucleus stimulation in awake rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 256, no. 6 (June 1, 1989): R1325—R1330. http://dx.doi.org/10.1152/ajpregu.1989.256.6.r1325.
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Our previous studies demonstrated that stimulation of the hypothalamic paraventricular nucleus (PVN) in anesthetized rats evoked a depressor response accompanied with a decrease in sympathetic outflow (H. Kannan, A. Niijima, and H. Yamashita, J. Auton. Nerv. Syst. 19: 83-86, 1987; H. Yamashita, H. Kannan, M. Kasai, and T. Osaka, J. Auton. Nerv. Syst. 19: 229-234, 1987). Because anesthesia may alter cardiovascular responses, we examined in conscious rats the effects of PVN stimulation on arterial pressure, heart rate, and renal sympathetic nerve activity. Electrical stimulation through chronically implanted electrodes evoked increases in arterial pressure and renal sympathetic nerve activity with a slight decrease in heart rate. The magnitude of responses was dependent on the frequency and the intensity of the stimulus. Latency of the excitatory response of the renal sympathetic nerve activity was approximately 70 ms. Microinjection of L-glutamate (0.5 M, 200 nl) into the PVN area also elicited increases in blood pressure and renal sympathetic nerve activity. These results suggest that activation of PVN neurons in conscious rats produces pressor responses due to an increase in the sympathetic outflow. These findings contrast with those obtained previously in anesthetized rats.
7
DiBona, G. F., and U. C. Kopp. "Neural control of renal function." Physiological Reviews 77, no. 1 (January 1, 1997): 75–197. http://dx.doi.org/10.1152/physrev.1997.77.1.75.
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The renal nerves are the communication link between the central nervous system and the kidney. In response to multiple peripheral and central inputs, efferent renal sympathetic nerve activity is altered so as to convey information to the major structural and functional components of the kidney, the vessels, glomeruli, and tubules, each of which is innervated. At the level of each of these individual components, information transfer occurs via interaction of the neurotransmitter released at the sympathetic nerve terminal-neuroeffector junction with specific postjunctional receptors coupled to defined intracellular signaling and effector systems. In response to normal physiological stimuli, changes in efferent renal sympathetic nerve activity contribute importantly to homeostatic regulation of renal blood flow, glomerular filtration rate, renal tubular epithelial cell solute and water transport, and hormonal release. Afferent input from sensory receptors located in the kidney participates in this reflex control system via renorenal reflexes that enable total renal function to be self-regulated and balanced between the two kidneys. In pathophysiological conditions, abnormal regulation of efferent renal sympathetic nerve activity contributes significantly to the associated abnormalities of renal function which, in turn, are of importance in the pathogenesis of the disease.
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Kopp, Ulla C. "Role of renal sensory nerves in physiological and pathophysiological conditions." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 308, no. 2 (January 15, 2015): R79—R95. http://dx.doi.org/10.1152/ajpregu.00351.2014.
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Whether activation of afferent renal nerves contributes to the regulation of arterial pressure and sodium balance has been long overlooked. In normotensive rats, activating renal mechanosensory nerves decrease efferent renal sympathetic nerve activity (ERSNA) and increase urinary sodium excretion, an inhibitory renorenal reflex. There is an interaction between efferent and afferent renal nerves, whereby increases in ERSNA increase afferent renal nerve activity (ARNA), leading to decreases in ERSNA by activation of the renorenal reflexes to maintain low ERSNA to minimize sodium retention. High-sodium diet enhances the responsiveness of the renal sensory nerves, while low dietary sodium reduces the responsiveness of the renal sensory nerves, thus producing physiologically appropriate responses to maintain sodium balance. Increased renal ANG II reduces the responsiveness of the renal sensory nerves in physiological and pathophysiological conditions, including hypertension, congestive heart failure, and ischemia-induced acute renal failure. Impairment of inhibitory renorenal reflexes in these pathological states would contribute to the hypertension and sodium retention. When the inhibitory renorenal reflexes are suppressed, excitatory reflexes may prevail. Renal denervation reduces arterial pressure in experimental hypertension and in treatment-resistant hypertensive patients. The fall in arterial pressure is associated with a fall in muscle sympathetic nerve activity, suggesting that increased ARNA contributes to increased arterial pressure in these patients. Although removal of both renal sympathetic and afferent renal sensory nerves most likely contributes to the arterial pressure reduction initially, additional mechanisms may be involved in long-term arterial pressure reduction since sympathetic and sensory nerves reinnervate renal tissue in a similar time-dependent fashion following renal denervation.
9
Bandali, Karim S., and Uwe Ackermann. "Are prostaglandins involved in atrial natriuretic peptide mechanisms of cardiovascular control?" Canadian Journal of Physiology and Pharmacology 77, no. 3 (March 1, 1999): 211–15. http://dx.doi.org/10.1139/y99-004.
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Atrial natriuretic peptide (ANP) can excite cardiac nerve endings and invoke a decrease in arterial blood pressure and a reduction in renal sympathetic nerve activity. Our laboratory has previously demonstrated that this renal depressor reflex was invoked by systemic injection of ANP and not by the direct application of ANP to the epicardium, a major locus for vagal afferents. We now examine whether inhibition of prostaglandin synthesis impairs reflex responses that are normally associated with ANP injections. Renal sympathetic nerve activity, arterial blood pressure, and heart rate were recorded in anesthetized rats. Indomethacin was used to inhibit prostaglandin synthesis through the cyclooxygenase pathway. The ANP-mediated decrease in arterial blood pressure and renal sympathetic nerve activity, observed when prostaglandin synthesis was inhibited, did not differ significantly from the decreases observed in these parameters when prostaglandin synthesis was not inhibited. Heart rate remained unchanged. Our results suggest that the sympatho-inhibitory effects of ANP do not require prostaglandins as intermediary compounds.Key words: sympathetic nervous system, renal nerves, prostaglandins.
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MacNeil, B. J., A. H. Jansen, A. H. Greenberg, and D. M. Nance. "Effect of acute adrenalectomy on sympathetic responses to peripheral lipopolysaccharide or central PGE2." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, no. 5 (May 1, 2000): R1321—R1328. http://dx.doi.org/10.1152/ajpregu.2000.278.5.r1321.
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The impact of plasma corticosterone levels on the sympathetic nervous system (SNS) response to intravenous lipopolysaccharide (LPS) or intracerebroventricular injections of PG was studied in anesthetized (urethan-chloralose) male Sprague-Dawley rats. For this, electrophysiological recordings of splenic and renal nerves were completed in control or adrenalectomized (ADX) rats. LPS (10 μg iv) similarly increased splenic and renal nerve activity in control rats with a shorter onset latency for the splenic nerve. Acute ADX enhanced the response of both nerves to LPS ( P < 0.005) and reduced the onset latency of the renal nerve ( P < 0.05). PGE2 (2 μg icv) rapidly increased the activity of both nerves but preferentially (magnitude and onset latency) stimulated the renal nerve ( P < 0.05). The magnitude of the splenic nerve response to PGE2 was unaffected by ADX. Unexpectedly, PGE2 was less effective at stimulating renal nerve activity in ADX animals relative to intact controls ( P < 0.05). Pretreatment of ADX rats with a CRF antagonist {[d-Phe12, Nle21,38, Cα-MeLeu37]CRF-(12—41)} reversed this effect such that the renal nerve responded to central PGE2 to a greater extent than the splenic nerve ( P< 0.05), as was the case in non-ADX rats. These data indicate that enhanced sensitivity of central sympathetic pathways does not account for the enhanced SNS responses to LPS in ADX rats. Also, a CRF-related process appears to diminish renal sympathetic outflow in ADX rats.
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MacNeil, B. J., A. H. Jansen, A. H. Greenberg, and D. M. Nance. "Activation and selectivity of splenic sympathetic nerve electrical activity response to bacterial endotoxin." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 270, no. 1 (January 1, 1996): R264—R270. http://dx.doi.org/10.1152/ajpregu.1996.270.1.r264.
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Regulatory interactions and neuroanatomic pathways have been described between the sympathetic nervous system and the immune system. It is not clear whether these pathways are activated during immune responses and if target specificity provides selective regulation of immune organs. The present study examined whether systemic injection of endotoxin [lipopolysaccharide (LPS)] induces sympathetic outflow to an immune organ (spleen). Sympathetic nerve activity was recorded from either the splenic or renal nerve of adult male rats after intravenous injections of LPS. Splenic nerve activity increased in a dose-dependent manner up to 175% of control after injection of LPS, with an onset time of 17.1-23.5 min. In contrast, renal nerve recordings showed a significantly slower onset time of 37.1-52.6 min at similar doses. In addition, splenic nerve recordings of 8/8 rats responded to 10 micrograms of LPS, whereas only 4/11 positive renal nerve responses were observed at this dose. The magnitude of the responses of both splenic and renal nerves were comparable. These data suggest that the splenic nerve responds to and is more sensitive to LPS-stimulated sympathetic activation in terms of latency and frequency of responses. Thus sympathetic outflow can be directed to an immune organ in response to a stimulus known to activate the immune system.
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Weaver, L. C., S. Genovesi, A. Stella, and A. Zanchetti. "Neural, hemodynamic, and renal responses to stimulation of intestinal receptors." American Journal of Physiology-Heart and Circulatory Physiology 253, no. 5 (November 1, 1987): H1167—H1176. http://dx.doi.org/10.1152/ajpheart.1987.253.5.h1167.
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Stimulation of visceral receptors with bradykinin has been shown to cause reflex increases in sympathetic nerve activity and systemic arterial pressure. In this investigation, serosal receptors of the intestine were stimulated by bradykinin in anesthetized cats to 1) compare mesenteric and renal sympathetic responses, 2) compare hemodynamic responses in mesenteric and renal beds, and 3) determine changes in renal function. This stimulation in intact animals caused pressor responses, significantly greater excitation of mesenteric than renal nerves, significantly greater mesenteric than renal vasoconstriction, diuresis, natriuresis, and, in denervated kidneys, increases in fractional sodium excretion. In vagotomized, sinoaortic-denervated cats, stimulation of intestinal receptors caused excitation of mesenteric nerve activity greater than renal for only 30 s. This sympathetic reflex response led to pressor responses, equal mesenteric and renal vasoconstriction, diuresis, natriuresis, and increased fractional excretion of sodium only in denervated kidneys. When abdominal perfusion pressure was held constant with an aortic snare in these same animals, the sympathetic reflexes initially caused greater mesenteric than renal vasoconstriction and antidiuresis and antinatriuresis only in innervated kidneys. These findings demonstrate that the intensity of hemodynamic and renal responses to stimulation of visceral receptors correlates well with the magnitude of sympathetic nerve responses.
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Yardley, C. P., R. D. Stein, and L. C. Weaver. "Tonic influences from the rostral medulla affect sympathetic nerves differentially." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 256, no. 2 (February 1, 1989): R323—R331. http://dx.doi.org/10.1152/ajpregu.1989.256.2.r323.
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Tonically active neurons in the rostral ventrolateral medulla (RVLM) that project to the autonomic regions of the spinal cord are essential for maintenance of arterial blood pressure at normal levels. Microinjection of glycine into the RVLM in anesthetized cats to inhibit the tonic discharge of these neurons caused variable initial responses in renal and mesenteric nerve discharge and arterial blood pressure. These initial responses were consistently followed by more prolonged decreases in renal and mesenteric nerve discharge and decreases in arterial blood pressure. The tonic influences of neurons in the RVLM were found to be distributed unequally to sympathetic nerves because activity of renal nerves was decreased significantly more than that of mesenteric nerves. The variable nerve and cardiovascular responses during the first 1-3 min after glycine injection were not solely due to loading or unloading of baroreceptors because similar initial responses were seen in vagotomized and sinoaortic denervated cats. Additionally, when muscimol was microinjected into the same sites, only consistent and prolonged decreases in nerve discharge and blood pressure occurred. The inhibitory actions of muscimol on RVLM neurons caused significantly greater decreases in renal than mesenteric nerve activity. Together, these findings demonstrate that the tonic discharge of neurons in the RVLM has unequal influences on renal and mesenteric nerves.
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Koganezawa, Tadachika, and Naohito Terui. "Differential responsiveness of RVLM sympathetic premotor neurons to hypoxia in rabbits." American Journal of Physiology-Heart and Circulatory Physiology 292, no. 1 (January 2007): H408—H414. http://dx.doi.org/10.1152/ajpheart.00881.2006.
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To determine whether differential sympathetic nerve responses to hypoxia are explained by opposing effects of hypoxia upon sympathetic premotor neurons in the rostral ventrolateral medulla (RVLM), the cardiac sympathetic nerve and the renal sympathetic nerve were recorded in anesthetized and vagotomized rabbits. Renal sympathetic nerve was activated by the injection of sodium cyanide solution close to the bifurcation of the common carotid artery and/or by inhalation of hypoxic gas (3% oxygen-97% nitrogen). On the other hand, cardiac sympathetic nerve was inhibited by these stimuli. Barosensitive (inhibited by the stimulation of baroreceptor afferents) reticulospinal (antidromically activated by the stimulation of the spinal cord) neurons in the RVLM were divided into three groups according to their responses to hypoxic stimulation: neurons (Type I, n = 25), the activity of which was inhibited by the injection of sodium cyanide solution close to the bifurcation of the common carotid artery and/or by inhalation of hypoxic gas, neurons (Type II, n = 99), the activity of which was facilitated by the same stimulation, and neurons (Type III, n = 11), the activity of which was not changed. These data indicated that the differential responses of cardiac and renal sympathetic nerves might be due to opposing effects of hypoxia on individual RVLM neurons.
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Kenney, M. J., C. C. Barney, T. Hirai, and C. V. Gisolfi. "Sympathetic nerve responses to hyperthermia in the anesthetized rat." Journal of Applied Physiology 78, no. 3 (March 1, 1995): 881–89. http://dx.doi.org/10.1152/jappl.1995.78.3.881.
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The aim of the present study was to characterize the sympathetic nerve responses to hyperthermia in chloralose-anesthetized rats. Discharges were recorded from the renal, lumbar, and splanchnic sympathetic nerves. Mean arterial pressure, heart rate, and sympathetic nerve discharge (SND) were recorded continuously during progressive increases in core body temperature (Tc) from 38.0 to 41.0 degrees C. The following observations were made: 1) significant increases in renal, lumbar, and splanchnic SND were observed during hyperthermia; 2) autospectral analysis of renal and lumbar SND revealed that the frequency distribution of SND can be altered during progressive increases in Tc; and 3) increases in splanchnic SND to acute heating were similar in baroreceptor-innervated and -denervated rats. We conclude that 1) hyperthermia is a potent stimulus to the sympathetic nervous system and increases the activity in three sympathetic nerves that innervate different regional arterial beds, 2) acute heating influences the neural circuits involved in generating SND as evidenced by changes in the basic pattern of renal and lumbar SND, and 3) the increase in splanchnic SND during hyperthermia is not opposed by the arterial and cardiopulmonary baroreceptors.
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DiBona, Gerald F., and Linda L. Sawin. "Effect of renal denervation on dynamic autoregulation of renal blood flow." American Journal of Physiology-Renal Physiology 286, no. 6 (June 2004): F1209—F1218. http://dx.doi.org/10.1152/ajprenal.00010.2004.
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Vasoconstrictor intensities of renal sympathetic nerve stimulation elevate the renal arterial pressure threshold for steady-state stepwise autoregulation of renal blood flow. This study examined the tonic effect of basal renal sympathetic nerve activity on dynamic autoregulation of renal blood flow in rats with normal (Sprague-Dawley and Wistar-Kyoto) and increased levels of renal sympathetic nerve activity (congestive heart failure and spontaneously hypertensive rats). Steady-state values of arterial pressure and renal blood flow before and after acute renal denervation were subjected to transfer function analysis. Renal denervation increased basal renal blood flow in congestive heart failure (+35 ± 3%) and spontaneously hypertensive rats (+21 ± 3%) but not in Sprague-Dawley and Wistar-Kyoto rats. Renal denervation significantly decreased transfer function gain (i.e., improved autoregulation of renal blood flow) and increased coherence only in spontaneously hypertensive rats. Thus vasoconstrictor intensities of renal sympathetic nerve activity impaired the dynamic autoregulatory adjustments of the renal vasculature to oscillations in arterial pressure. Renal denervation increased renal blood flow variability in spontaneously hypertensive rats and congestive heart failure rats. The contribution of vasoconstrictor intensities of basal renal sympathetic nerve activity to limiting renal blood flow variability may be important in the stabilization of glomerular filtration rate.
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Kunze, D. L. "Acute resetting of baroreceptor reflex in rabbits: a central component." American Journal of Physiology-Heart and Circulatory Physiology 250, no. 5 (May 1, 1986): H866—H870. http://dx.doi.org/10.1152/ajpheart.1986.250.5.h866.
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Electrical stimulation of the aortic nerve of the anesthetized rabbit was used to determine whether there is a central nervous system component to acute resetting of the baroreceptor reflex. After stimulation of the aortic nerve for 5 min at 10 Hz, a ramp test stimulus to the nerve produced a reflex arterial pressure response that was attenuated as compared with that produced by the same ramp prior to the five-min stimulation period. Renal sympathetic nerve activity was recorded simultaneously to determine whether a reduction in the magnitude of the reflex inhibition of sympathetic activity produced by the depressor nerve stimulation could account for the attenuated arterial pressure response. Renal activity during the test ramp was reduced to the same value both before and after the constant stimulus period and thus did not correlate with the attenuated pressure response. There was, however, prolonged inhibition of tonic sympathetic activity after the 5-min stimulus period such that during the test stimulus there was less sympathetic activity to inhibit. The results were similar when sympathetic activity was recorded from branches of the sciatic nerve and from thoracic postganglionic nerves. In these nerves the period of prolonged inhibition after aortic nerve stimulation was up to 5 min. The attenuated pressure response to baroreceptor nerve stimulation after a constant stimulus appears to reflect the reduced change in sympathetic activity rather than the value to which the sympathetic activity falls.
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Kopp, Ulla C., Michael Z. Cicha, Lori A. Smith, Jan Mulder, and Tomas Hökfelt. "Renal sympathetic nerve activity modulates afferent renal nerve activity by PGE2-dependent activation of α1- and α2-adrenoceptors on renal sensory nerve fibers." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 4 (October 2007): R1561—R1572. http://dx.doi.org/10.1152/ajpregu.00485.2007.
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Increasing efferent renal sympathetic nerve activity (ERSNA) increases afferent renal nerve activity (ARNA). To test whether the ERSNA-induced increases in ARNA involved norepinephrine activating α-adrenoceptors on the renal sensory nerves, we examined the effects of renal pelvic administration of the α1- and α2-adrenoceptor antagonists prazosin and rauwolscine on the ARNA responses to reflex increases in ERSNA (placing the rat's tail in 49°C water) and renal pelvic perfusion with norepinephrine in anesthetized rats. Hot tail increased ERSNA and ARNA, 6,930 ± 900 and 4,870 ± 670%·s (area under the curve ARNA vs. time). Renal pelvic perfusion with norepinephrine increased ARNA 1,870 ± 210%·s. Immunohistochemical studies showed that the sympathetic and sensory nerves were closely related in the pelvic wall. Renal pelvic perfusion with prazosin blocked and rauwolscine enhanced the ARNA responses to reflex increases in ERSNA and norepinephrine. Studies in a denervated renal pelvic wall preparation showed that norepinephrine increased substance P release, from 8 ± 1 to 16 ± 1 pg/min, and PGE2 release, from 77 ± 11 to 161 ± 23 pg/min, suggesting a role for PGE2 in the norepinephrine-induced activation of renal sensory nerves. Prazosin and indomethacin reduced and rauwolscine enhanced the norepinephrine-induced increases in substance P and PGE2. PGE2 enhanced the norepinephrine-induced activation of renal sensory nerves by stimulation of EP4 receptors. Interaction between ERSNA and ARNA is modulated by norepinephrine, which increases and decreases the activation of the renal sensory nerves by stimulating α1- and α2-adrenoceptors, respectively, on the renal pelvic sensory nerve fibers. Norepinephrine-induced activation of the sensory nerves is dependent on renal pelvic synthesis/release of PGE2.
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Kerman, I. A., and B. J. Yates. "Patterning of somatosympathetic reflexes." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 277, no. 3 (September 1, 1999): R716—R724. http://dx.doi.org/10.1152/ajpregu.1999.277.3.r716.
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In a previous study, we reported that vestibular nerve stimulation in the cat elicits a specific pattern of sympathetic nerve activation, such that responses are particularly large in the renal nerve. This patterning of vestibulosympathetic reflexes was the same in anesthetized and decerebrate preparations. In the present study, we report that inputs from skin and muscle also elicit a specific patterning of sympathetic outflow, which is distinct from that produced by vestibular stimulation. Renal, superior mesenteric, and lumbar colonic nerves respond most strongly to forelimb and hindlimb nerve stimulation (∼60% of maximal nerve activation), whereas external carotid and hypogastric nerves were least sensitive to these inputs (∼20% of maximal nerve activation). In contrast to vestibulosympathetic reflexes, the expression of responses to skin and muscle afferent activation differs in decerebrate and anesthetized animals. In baroreceptor-intact animals, somatosympathetic responses were strongly attenuated (to <20% of control in every nerve) by increasing blood pressure levels to >150 mmHg. These findings demonstrate that different types of somatic inputs elicit specific patterns of sympathetic nerve activation, presumably generated through distinct neural circuits.
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Neahring, J. C., S. Y. Jones, and G. F. DiBona. "Cardiopulmonary baroreflex function in nephrotic rats." Journal of the American Society of Nephrology 5, no. 12 (June 1995): 2082–86. http://dx.doi.org/10.1681/asn.v5122082.
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Efferent renal sympathetic nerve activity is increased in experimental nephrotic syndrome and exhibits attenuated cardiopulmonary baroreflex inhibition during volume expansion in anesthetized rats. Additional studies were performed in conscious rats to avoid the potentially confounding influences of anesthesia; these studies used another more specific standardized stimulus for cardiopulmonary baroreflex activation. Sprague Dawley rats were studied 3 to 4 wk after adriamycin injection (3.5 mg/kg iv); all rats developed proteinuria. In sinoaortic denervated rats (anesthetized), graded frequency stimulation of the central end of the cut right vagus nerve produced frequency-dependent decreases in mean arterial pressure, heart rate, and efferent renal sympathetic nerve activity. The decreases in mean arterial pressure and heart rate were similar in control and nephrotic rats, but efferent renal sympathetic nerve activity decreased significantly less in nephrotic than control rats over the entire frequency range (P < 0.02). In sinoaortic denervated rats (conscious), 10% body weight isotonic saline volume expansion decreased mean arterial pressure, heart rate, and efferent renal sympathetic nerve activity. The decreases in mean arterial pressure and heart rate were similar in control and nephrotic rats, but efferent renal sympathetic nerve activity decreased significantly less in nephrotic than control rats over the entire period of volume expansion (P < 0.04). In nephrotic syndrome, the cardiopulmonary baroreflex inhibition of efferent renal sympathetic nerve activity is decreased; the defect lies in the central portion of the reflex. This may contribute to the observed increase in efferent renal sympathetic nerve activity in nephrotic syndrome.
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Kenney, Michael J., Dale E. Claassen, Michelle R. Bishop, and Richard J. Fels. "Regulation of the sympathetic nerve discharge bursting pattern during heat stress." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 275, no. 6 (December 1, 1998): R1992—R2001. http://dx.doi.org/10.1152/ajpregu.1998.275.6.r1992.
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Frequency-domain analyses were used to determine the effect of heat stress on the relationships between the discharge bursts of sympathetic nerve pairs and sympathetic and phrenic nerve pairs in chloralose-anesthetized rats. Sympathetic nerve discharge (SND) was recorded from the renal, splanchnic, splenic, and lumbar nerves during increases in core body temperature (Tc) from 38 to 41.4 ± 0.3°C. The following observations were made: 1) hyperthermia transformed the cardiac-related bursting pattern of SND to a pattern that contained low-frequency, non-cardiac-related bursts, 2) the pattern transformation was uniform in regionally selective sympathetic nerves, 3) hyperthermia enhanced the frequency-domain coupling between SND and phrenic nerve bursts, and 4) low-frequency SND bursts recorded during hyperthermia contained significantly more activity than cardiac-related bursts. We conclude that acute heat stress profoundly affects the organization of neural circuits responsible for the frequency components in sympathetic nerve activity and that SND pattern transformation provides an important strategy for increasing the level of activity in sympathetic nerves during increased Tc.
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Tobey, J. C., and L. C. Weaver. "Pressoreceptor modulation of renal but not splenic sympathetic reflexes." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 252, no. 1 (January 1, 1987): R26—R33. http://dx.doi.org/10.1152/ajpregu.1987.252.1.r26.
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Influences of sinoaortic and vagally innervated vascular pressoreceptors on excitatory splenic and renal sympathetic responses to splenic receptor stimulation were investigated in anesthetized cats. These experiments demonstrated that these pressoreceptors have little apparent effect on the magnitude of splenic nerve responses to splenic receptor stimulation by capsaicin, bradykinin, or congestion. In contrast, activation of these pressoreceptors attenuated renal nerve responses to splenic receptor stimulation. Influences of sinoaortic and vagally innervated receptors on tonic sympathetic nerve activity also were evaluated. Stimulation of these receptors by small increases in arterial pressure (15–21 mmHg) caused equivalent inhibition of splenic and renal nerve activity; large increases (50–66 mmHg) caused significantly greater inhibition of renal than splenic nerve activity. These results illustrate that excitatory renal and splenic sympathetic responses to splenic receptor stimulation are not suppressed equally by pressoreceptor activation, vascular pressoreceptors can have greater inhibitory influences on tonic renal than splenic nerve activity, and vascular pressoreceptor influences on sympathetic reflexes are similar to those on tonic nerve activity.
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Dibona, G. F., S. Y. Jones, and L. L. Sawin. "Effect of endogenous angiotensin II on renal nerve activity and its cardiac baroreflex regulation." Journal of the American Society of Nephrology 9, no. 11 (November 1998): 1983–89. http://dx.doi.org/10.1681/asn.v9111983.
Full textAbstract:
The effects of physiologic alterations in endogenous angiotensin II activity on basal renal sympathetic nerve activity and its cardiac baroreflex regulation were studied. The effect of angiotensin II type 1 receptor blockade with intracerebroventricular losartan was examined in conscious rats consuming a low, normal, or high sodium diet that were instrumented for the simultaneous measurement of right atrial pressure and renal sympathetic nerve activity. The gain of cardiac baroreflex regulation of renal sympathetic nerve activity (% delta renal sympathetic nerve activity/mmHg mean right atrial pressure) was measured during isotonic saline volume loading. Intracerebroventricular losartan did not decrease arterial pressure but significantly decreased renal sympathetic nerve activity in low (-36+/-6%) and normal (-24+/-5%), but not in high (-2+/-3%) sodium diet rats. Compared with vehicle treatment, losartan treatment significantly increased cardiac baroreflex gain in low (-3.45+/-0.20 versus -2.89+/-0.17) and normal (-2.89+/-0.18 versus -2.54+/-0.14), but not in high (-2.27+/-0.15 versus -2.22+/-0.14) sodium diet rats. These results indicate that physiologic alterations in endogenous angiotensin II activity tonically influence basal levels of renal sympathetic nerve activity and its cardiac baroreflex regulation.
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Osborn, John W., Roman Tyshynsky, and Lucy Vulchanova. "Function of Renal Nerves in Kidney Physiology and Pathophysiology." Annual Review of Physiology 83, no. 1 (February 10, 2021): 429–50. http://dx.doi.org/10.1146/annurev-physiol-031620-091656.
Full textAbstract:
Renal sympathetic (efferent) nerves play an important role in the regulation of renal function, including glomerular filtration, sodium reabsorption, and renin release. The kidney is also innervated by sensory (afferent) nerves that relay information to the brain to modulate sympathetic outflow. Hypertension and other cardiometabolic diseases are linked to overactivity of renal sympathetic and sensory nerves, but our mechanistic understanding of these relationships is limited. Clinical trials of catheter-based renal nerve ablation to treat hypertension have yielded promising results. Therefore, a greater understanding of how renal nerves control the kidney under physiological and pathophysiological conditions is needed. In this review, we provide an overview of the current knowledge of the anatomy of efferent and afferent renal nerves and their functions in normal and pathophysiological conditions. We also suggest further avenues of research for development of novel therapies targeting the renal nerves.
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Pinkham, Maximilian I., Michael T. Loftus, Satya Amirapu, Sarah-Jane Guild, Gina Quill, William R. Woodward, Beth A. Habecker, and Carolyn J. Barrett. "Renal denervation in male rats with heart failure improves ventricular sympathetic nerve innervation and function." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 312, no. 3 (March 1, 2017): R368—R379. http://dx.doi.org/10.1152/ajpregu.00313.2016.
Full textAbstract:
Heart failure is characterized by the loss of sympathetic innervation to the ventricles, contributing to impaired cardiac function and arrhythmogenesis. We hypothesized that renal denervation (RDx) would reverse this loss. Male Wistar rats underwent myocardial infarction (MI) or sham surgery and progressed into heart failure for 4 wk before receiving bilateral RDx or sham RDx. After additional 3 wk, left ventricular (LV) function was assessed, and ventricular sympathetic nerve fiber density was determined via histology. Post-MI heart failure rats displayed significant reductions in ventricular sympathetic innervation and tissue norepinephrine content (nerve fiber density in the LV of MI+sham RDx hearts was 0.31 ± 0.05% vs. 1.00 ± 0.10% in sham MI+sham RDx group, P < 0.05), and RDx significantly increased ventricular sympathetic innervation (0.76 ± 0.14%, P < 0.05) and tissue norepinephrine content. MI was associated with an increase in fibrosis of the noninfarcted ventricular myocardium, which was attenuated by RDx. RDx improved LV ejection fraction and end-systolic and -diastolic areas when compared with pre-RDx levels. This is the first study to show an interaction between renal nerve activity and cardiac sympathetic nerve innervation in heart failure. Our findings show denervating the renal nerves improves cardiac sympathetic innervation and function in the post-MI failing heart.
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Pellegrino, Peter Ricci, Irving H. Zucker, Yiannis S. Chatzizisis, Han-Jun Wang, and Alicia M. Schiller. "Quantification of Renal Sympathetic Vasomotion as a Novel End Point for Renal Denervation." Hypertension 76, no. 4 (October 2020): 1247–55. http://dx.doi.org/10.1161/hypertensionaha.120.15325.
Full textAbstract:
Renal sympathetic denervation, a potentially revolutionary interventional treatment for hypertension, faces an existential problem due to the inability to confirm successful ablation of the targeted renal sympathetic nerves. Based on the observation that renal sympathetic nerve activity exerts rhythmic, baroreflex-driven, and vasoconstrictive control of the renal vasculature, we developed a novel technique for identifying rhythmic sympathetic vascular control using a time-varying, 2-component Windkessel model of the renal circulation. This technology was tested in 2 different animal models of renal denervation; 10 rabbits underwent chronic, surgical renal denervation, and 9 pigs underwent acute, functional renal denervation via intrathecal administration of ropivacaine. Both methods of renal denervation reduced negative admittance gain, negative phase shift renal vascular control at known sympathetic vasomotor frequencies, consistent with a reduction in vasoconstrictive, baroreflex-driven renal sympathetic vasomotion. Classic measures like mean renal blood flow and mean renal vascular resistance were not significantly affected in either model of renal denervation. Renal sympathetic vasomotion monitoring could provide intraprocedural feedback for interventionists performing renal denervation and serve more broadly as a platform technology for the evaluation and treatment of diseases affecting the sympathetic nervous system.
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Kenney, Michael J., Mark L. Weiss, Kaushik P. Patel, Yan Wang, and Richard J. Fels. "Paraventricular nucleus bicuculline alters frequency components of sympathetic nerve discharge bursts." American Journal of Physiology-Heart and Circulatory Physiology 281, no. 3 (September 1, 2001): H1233—H1241. http://dx.doi.org/10.1152/ajpheart.2001.281.3.h1233.
Full textAbstract:
Autospectral and coherence analyses were used to determine the effect of paraventricular nucleus (PVN) GABAA receptor antagonism [microinfusion or microinjections of bicuculline methiodide (BMI) 100 pmoles] on sympathetic nerve discharge (SND) frequency components (bursting pattern and relationships between discharges in regionally selective nerves) in α-chloralose-anesthetized rats. SND was recorded from the renal, splenic, and lumbar nerves. The following observations were made. First, PVN BMI microinjections, but not PVN saline or cortical BMI microinjections, transformed the cardiac-related SND bursting pattern in baroreceptor-innervated rats to one characterized by the presence of low-frequency bursts not synchronized to the cardiac cycle or phrenic nerve discharge bursts. Second, SND pattern changes were similar in the renal, splenic, and lumbar nerves, and peak coherence values relating low-frequency bursts in sympathetic nerve pairs (renal-splenic, renal-lumbar, and splenic-lumbar) were significantly increased from preinjection control after PVN BMI microinjection. Third, PVN BMI microinjections significantly increased the coupling between low-frequency SND bursts in baroreceptor-denervated rats. Finally, PVN BMI-induced changes in the SND bursting pattern were not observed after PVN pretreatment with muscimol (GABA agonist, 1 nmole). We conclude that PVN GABAA receptor antagonism profoundly alters the frequency components in sympathetic nerves.
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Gebber, G. L., S. Zhong, and S. M. Barman. "Synchronization of cardiac-related discharges of sympathetic nerves with inputs from widely separated spinal segments." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 268, no. 6 (June 1, 1995): R1472—R1483. http://dx.doi.org/10.1152/ajpregu.1995.268.6.r1472.
Full textAbstract:
We used phase spectral analysis to study the relationships between the cardiac-related discharges of pairs of postganglionic sympathetic nerves in urethan-anesthetized or decerebrate cats. Phase angle when converted to a time interval should equal the difference in conduction times from the brain to the nerves (i.e., transportation lag) if their cardiac-related discharges have a common central source. Transportation lag was estimated as the difference in the onset latencies of activation of the nerves by electrical stimulation of the medulla or cervical spinal cord. The phase angle for the cardiac-related discharges of two nerves was not always equivalent in time to the transportation lag. For example, in some cases the cardiac-related discharges of the renal nerve were coincident with or led those of the inferior cardiac nerve. In contrast, the electrically evoked responses of the renal nerve lagged those of the inferior cardiac nerve by > or = 32 ms. These observations are consistent with a model of multiple and dynamically coupled brain stem generators of the cardiac-related rhythm, each controlling a different sympathetic nerve or exerting nonuniform influences on different portions of the spinal sympathetic outflow.
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Undesser, K. P., J. Y. Pan, M. P. Lynn, and V. S. Bishop. "Baroreflex control of sympathetic nerve activity after elevations of pressure in conscious rabbits." American Journal of Physiology-Heart and Circulatory Physiology 248, no. 6 (June 1, 1985): H827—H834. http://dx.doi.org/10.1152/ajpheart.1985.248.6.h827.
Full textAbstract:
The purpose of this study was to assess the effect of rapid baroreceptor resetting on the baroreflex control of renal sympathetic nerve activity in conscious rabbits. Renal sympathetic nerve activity was recorded and used as an index of the efferent limb of the baroreflex. Heart rate and arterial pressure were also recorded. Arterial pressure was raised with either phenylephrine or angiotensin II to a level that eliminated renal sympathetic nerve activity and was maintained at this level for periods of time ranging from 1 to 60 min. On returning pressure to control levels, renal sympathetic nerve activity remained suppressed for up to 90 min, with the duration of the suppression dependent on the magnitude and duration of the pressure stimulus. During this period of suppressed nerve activity, baroreflex curves were generated. The curves produced at this time were also suppressed as compared with control baroreflex curves. With time, the suppressed baroreflex curves returned to control. Further studies were performed to show that the suppression of renal sympathetic nerve activity was mediated via the prolonged increase in baroreceptor afferent activity during the pressure stimulus and was not due to a central effect of phenylephrine. This study indicates that although baroreceptor afferent activity may reset rapidly, there does not appear to be an augmentation of renal sympathetic nerve activity as would be expected.
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Kerman, I. A., and B. J. Yates. "Regional and functional differences in the distribution of vestibulosympathetic reflexes." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 275, no. 3 (September 1, 1998): R824—R835. http://dx.doi.org/10.1152/ajpregu.1998.275.3.r824.
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Although considerable evidence suggests that the vestibular system regulates sympathetic outflow during movement and changes in posture, little is known about relative vestibular influences on activity of different sympathetic nerves and sympathetic efferents with different functions. In the present study, we demonstrated that electrical stimulation of the vestibular nerve in the cat elicited responses in sympathetic nerves innervating the head and abdominal viscera. This observation suggests that activity of sympathetic efferents innervating multiple body regions is affected by vestibular signals. These responses were attenuated by >80% when blood pressure was increased to >160 mmHg. Because raising blood pressure decreases the responsiveness of vasoconstrictor fibers, the simplest explanation for these data is that the vestibular system provides particularly strong inputs to components of the sympathetic nervous system that regulate peripheral vascular resistance. Furthermore, the relative magnitude of vestibulosympathetic reflexes was over four times larger in one sympathetic nerve composed mainly of vasoconstrictor efferents (renal nerve) than another nerve (external carotid nerve) containing similar types of fibers. Collectively, these data indicate that the vestibular system has selective influences on sympathetic outflow to particular tissues and body regions.
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DiBona, G. F., S. Y. Jones, and L. L. Sawin. "Effect of endogenous angiotensin II on renal nerve activity and its arterial baroreflex regulation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 271, no. 2 (August 1, 1996): R361—R367. http://dx.doi.org/10.1152/ajpregu.1996.271.2.r361.
Full textAbstract:
To determine the effects of physiological alterations in endogenous angiotensin II (ANG II) activity on basal renal sympathetic nerve activity and its arterial baroreflex regulation, the effect of ANG II receptor (AT1) blockade with losartan was examined in conscious rats consuming low, normal, or high sodium diet that were instrumented for the simultaneous measurement of arterial pressure and renal sympathetic nerve activity. Intravenous losartan decreased arterial pressure in low (-27 +/- 4 mmHg) and normal (-15 +/- 2 mmHg) but not in high sodium diet rats (-5 +/- 2 mmHg). When arterial pressure had been restored to the prelosartan value with methoxamine infusion, renal sympathetic nerve activity was decreased in low (-27 +/- 4%) and normal (-20 +/- 3%) but not in high sodium diet rats (-5 +/- 2%). Arterial baroreflex regulation of renal sympathetic nerve activity was shifted to a lower pressure (arterial pressure at midrange) in low (-8 +/- 2 mmHg) and normal (-7 +/- 2 mmHg) but not in high sodium diet rats (0 +/- 2 mmHg). Intracerebroventricular losartan did not significantly decrease arterial pressure but decreased renal sympathetic nerve activity in low (-28 +/- 5%) and normal (-20 +/- 4%) but not in high sodium diet rats (-2 +/- 2%). Arterial baroreflex regulation of renal sympathetic nerve activity was shifted to a lower pressure (arterial pressure at midrange) in low (-7 +/- 2 mmHg) and normal (-5 +/- 1 mmHg) but not in high sodium diet rats (0 +/- 2 mmHg). These results indicate that physiological alterations in endogenous ANG II activity tonically influence basal levels of renal sympathetic nerve activity and its arterial baroreflex regulation.
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Barrett, Carolyn J., Michael A. Navakatikyan, and Simon C. Malpas. "Long-term control of renal blood flow: what is the role of the renal nerves?" American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 280, no. 5 (May 1, 2001): R1534—R1545. http://dx.doi.org/10.1152/ajpregu.2001.280.5.r1534.
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We have developed a system for long-term continuous monitoring of cardiovascular parameters in rabbits living in their home cage to assess what role renal sympathetic nerve activity (RSNA) has in regulating renal blood flow (RBF) in daily life. Blood pressure, heart rate, locomotor activity, RSNA, and RBF were recorded continuously for 4 wk. Beginning 4–5 days after surgery a circadian rhythm, dependent on feeding time, was observed. When averaged over all days RBF to the innervated and denervated kidneys was not significantly different. However, control of RBF around these mean levels was dependent on the presence of the renal sympathetic nerves. In particular we observed episodic elevations in heart rate and other parameters associated with activity. In the denervated kidney, during these episodic elevations, the increase in renal resistance was closely related to the increase in arterial pressure. In the innervated kidney the renal resistance response was significantly more variable, indicating an interaction of the sympathetic nervous system. These results indicate that whereas overall levels of RSNA do not set the mean level of RBF the renal vasculature is sensitive to episodic increases in sympathetic nerve activity.
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Taylor, R. B., and L. C. Weaver. "Spinal stimulation to locate preganglionic neurons controlling the kidney, spleen, or intestine." American Journal of Physiology-Heart and Circulatory Physiology 263, no. 4 (October 1, 1992): H1026—H1033. http://dx.doi.org/10.1152/ajpheart.1992.263.4.h1026.
Full textAbstract:
The organization of sympathetic preganglionic neurons may be a substrate for selective control of sympathetic outflow to different vascular beds. This study was done to determine the spinal segments containing preganglionic neurons controlling discharge of renal, splenic, and mesenteric postganglionic nerves. In urethan-anesthetized rats, preganglionic neurons were stimulated by microinjecting D,L-homocysteic acid (3 nl, 0.17 M) into the lateral gray matter of the third thoracic (T3) to the fourth lumbar (L4) spinal segments. Responses from all three nerves could be elicited from segments T4-T13. The greatest increases in renal nerve discharge were evoked from segments T8-T12, the largest increase of 59 +/- 9% elicited from T10. Increases in splenic and mesenteric nerve discharge were smaller and were evoked more uniformly from T4-L3. The largest increases in discharge of splenic and mesenteric nerves were 19 +/- 5% (from T5) and 26 +/- 4% (from T10), respectively. The widely overlapping spinal cord segments controlling these three organs suggest that location of the preganglionic neurons in different spinal segments is not part of the mechanism for selective sympathetic control. However, the larger renal nerve responses demonstrate that sympathetic output to these organs can be differentiated at the level of the spinal cord.
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Komnenov, Dragana, Peter Levanovich, and Noreen Rossi. "Hypertension Associated with Fructose and High Salt: Renal and Sympathetic Mechanisms." Nutrients 11, no. 3 (March 7, 2019): 569. http://dx.doi.org/10.3390/nu11030569.
Full textAbstract:
Hypertension is a leading cause of cardiovascular and chronic renal disease. Despite multiple important strides that have been made in our understanding of the etiology of hypertension, the mechanisms remain complex due to multiple factors, including the environment, heredity and diet. This review focuses on dietary contributions, providing evidence for the involvement of elevated fructose and salt consumption that parallels the increased incidence of hypertension worldwide. High fructose loads potentiate salt reabsorption by the kidney, leading to elevation in blood pressure. Several transporters, such as NHE3 and PAT1 are modulated in this milieu and play a crucial role in salt-sensitivity. High fructose ingestion also modulates the renin-angiotensin-aldosterone system. Recent attention has been shifted towards the contribution of the sympathetic nervous system, as clinical trials demonstrated significant reductions in blood pressure following renal sympathetic nerve ablation. New preclinical data demonstrates the activation of the renal sympathetic nerves in fructose-induced salt-sensitive hypertension, and reductions of blood pressure after renal nerve ablation. This review further demonstrates the interplay between sodium handling by the kidney, the renin-angiotensin-aldosterone system, and activation of the renal sympathetic nerves as important mechanisms in fructose and salt-induced hypertension.
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Ditting, Tilmann, Peter Linz, Wolfgang Freisinger, Sonja Heinlein, Peter W. Reeh, Christian Fiedler, Kirsten Siegel, Karie E. Scrogin, Winfried Neuhuber, and Roland Veelken. "Norepinephrine reduces ω-conotoxin-sensitive Ca2+ currents in renal afferent neurons in rats." American Journal of Physiology-Renal Physiology 302, no. 3 (February 1, 2012): F350—F357. http://dx.doi.org/10.1152/ajprenal.00681.2010.
Full textAbstract:
Sympathetic efferent and peptidergic afferent renal nerves likely influence hypertensive and inflammatory kidney disease. Our recent investigation with confocal microscopy revealed that in the kidney sympathetic nerve endings are colocalized with afferent nerve fibers (Ditting T, Tiegs G, Rodionova K, Reeh PW, Neuhuber W, Freisinger W, Veelken R. Am J Physiol Renal Physiol 297: F1427–F1434, 2009; Veelken R, Vogel EM, Hilgers K, Amman K, Hartner A, Sass G, Neuhuber W, Tiegs G. J Am Soc Nephrol 19: 1371–1378, 2008). However, it is not known whether renal afferent nerves are influenced by sympathetic nerve activity. We tested the hypothesis that norepinephrine (NE) influences voltage-gated Ca2+ channel currents in cultured renal dorsal root ganglion (DRG) neurons, i.e., the first-order neuron of the renal afferent pathway. DRG neurons (T11–L2) retrogradely labeled from the kidney and subsequently cultured, were investigated by whole-cell patch clamp. Voltage-gated calcium channels (VGCC) were investigated by voltage ramps (−100 to +80 mV, 300 ms, every 20 s). NE and appropriate adrenergic receptor antagonists were administered by microperfusion. NE (20 μM) reduced VGCC-mediated currents by 10.4 ± 3.0% ( P < 0.01). This reduction was abolished by the α-adrenoreceptor inhibitor phentolamine and the α2-adrenoceptor antagonist yohimbine. The β-adrenoreceptor antagonist propranolol and the α1-adrenoceptor antagonist prazosin had no effect. The inhibitory effect of NE was abolished when N-type currents were blocked by ω-conotoxin GVIA, but was unaffected by other specific Ca2+ channel inhibitors (ω-agatoxin IVA; nimodipine). Confocal microscopy revealed sympathetic innervation of DRGs and confirmed colocalization of afferent and efferent fibers within in the kidney. Hence NE released from intrarenal sympathetic nerve endings, or sympathetic fibers within the DRGs, or even circulating catecholamines, may influence the activity of peptidergic afferent nerve fibers through N-type Ca2+ channels via an α2-adrenoceptor-dependent mechanism. However, the exact site and the functional role of this interaction remains to be elucidated.
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DiBona, GF. "Role of Renal Nerves in Edema Formation." Physiology 9, no. 4 (August 1, 1994): 183–88. http://dx.doi.org/10.1152/physiologyonline.1994.9.4.183.
Full textAbstract:
Once viewed as physiologically insignificant by no less an authority than Homer Smith, the renal nerves have emerged as a physiologically important regulator of renal tubular sodium reabsorption. Increased renal sympathetic nerve activity contributes significantly to the renal sodium retention in edema-forming states.
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DiBona, G. F., L. L. Sawin, and S. Y. Jones. "Differentiated sympathetic neural control of the kidney." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 271, no. 1 (July 1, 1996): R84—R90. http://dx.doi.org/10.1152/ajpregu.1996.271.1.r84.
Full textAbstract:
Anatomic and neurophysiological methods were used to identify functionally specific subgroups of renal sympathetic nerve fibers. The distribution of diameters of the predominating unmyelinated fibers showed a major mode at 1.1 microns and a minor mode at 1.6 microns. The conduction velocity was 2.10 +/- 0.10 m/s, consistent with unmyelinated C fibers. Analysis of strength-duration relationships during renal nerve stimulation showed that both rheobase and chronaxie values for renal blood flow were greater than those for urinary flow rate and were independent of stimulation frequency. This difference suggests a higher stimulation threshold (smaller diameter) for those renal nerve fibers involved in the renal blood flow response (renal vasoconstriction) compared with those for the urinary flow rate response (antidiuresis) to renal nerve stimulation. Single renal units that responded to preganglionic splanchnic nerve stimulation were studied. Those with spontaneous activity (88%) responded to stimulation of arterial baroreceptors, arterial and central chemoreceptors, and peripheral thermoreceptors, whereas those that lacked spontaneous activity (12%) responded only to stimulation of peripheral thermoreceptors (known to produce renal vasoconstriction). A minority population of single renal units has been identified that, although renal vasoconstrictor, does not exhibit other characteristic features of vasoconstrictor neurons (i.e., responsiveness to stimulation of arterial baroreceptors and arterial and central chemoreceptors). These findings suggest the existence of functionally specific subgroups of renal nerve fibers.
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Ma, Rong, Irving H. Zucker, and Wei Wang. "Central gain of the cardiac sympathetic afferent reflex in dogs with heart failure." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 6 (December 1, 1997): H2664—H2671. http://dx.doi.org/10.1152/ajpheart.1997.273.6.h2664.
Full textAbstract:
Previous studies from our laboratory have shown that the cardiac sympathetic afferent reflex is enhanced in dogs with experimental heart failure. The aim of the present study was to determine if the central gain of the cardiac sympathetic afferent reflex was also enhanced in dogs with heart failure. Fifteen dogs with pacing-induced heart failure were used in this study. Seventeen sham-operated dogs served as control. At the time of the acute experiment the dogs were anesthetized with α-chloralose. Arterial blood pressure, heart rate, and renal sympathetic nerve activity were recorded. After sinoaortic denervation and cervical vagotomy, a thoracotomy was performed in the second intercostal space. The left stellate ganglion was identified, and the left cardiac sympathetic nerves were cut. The central end of the left cardiac sympathetic nerves was placed on bipolar stimulating electrodes. The renal sympathetic nerve activity responses to electrical stimulation (30 Hz, 1 ms with varying voltages from 1 to 10 V; or 10 V, 1 ms with varying frequencies from 1 to 30 Hz) of the afferent cardiac sympathetic nerves were compared between sham and heart failure groups. Reflex renal sympathetic nerve activity responses to stimulation of the cardiac sympathetic nerves were significantly greater in the heart failure group compared with that in the sham group (21.4 ± 3.2 vs. 9.8 ± 2.9% at 10 V, 30 Hz and 27.7 ± 4.5 vs. 9.9 ± 3.4% at 30 Hz, 10 V, heart failure vs. sham group, respectively; for both relationships, P < 0.05). This enhanced central gain of the cardiac sympathetic afferent reflex in the heart failure group was significantly attenuated after intravenous and cerebroventricular injection of the angiotensin II receptor antagonist losartan (5 mg/kg iv and 0.125 mg/kg in 0.1 ml icv). These data suggest that the central gain of the cardiac sympathetic afferent reflex is enhanced in dogs with heart failure and central angiotensin II plays an important role in this enhanced response.
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Krassioukov, A. V., and L. C. Weaver. "Connections between the pontine reticular formation and rostral ventrolateral medulla." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 4 (October 1, 1993): H1386—H1392. http://dx.doi.org/10.1152/ajpheart.1993.265.4.h1386.
Full textAbstract:
Pontine reticular formation (PRF) neurons provide tonic excitatory drive to sympathetic nerves and are involved in cardiovascular control [K. Hayes and L. C. Weaver. Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H1567-H1575, 1992]. However, connections between the PRF and the well-known vasomotor region in the rostral ventrolateral medulla (RVLM) are unknown. In propofol (Diprivan)- anesthetized rats we investigated arterial pressure, heart rate, and renal nerve responses to microinjection of glycine (1.0 M, 60 nl) into the PRF before and after injection of the synaptic blocking agent cobalt chloride (4.0 mM, 200 nl) into the RVLM. Glycine injections into the PRF caused decreases in arterial pressure, heart rate, and discharge of renal sympathetic nerves. Synaptic blockade of the RVLM almost eliminated cardiovascular and sympathetic responses to glycine injections into the PRF and blocked somatosympathetic reflexes in the renal nerve. Cobalt injections into the RVLM had very small effects on basal renal nerve firing, arterial pressure, or heart rate. These results suggest that the neurons within the RVLM relay influences from the PRF to sympathetic preganglionic neurons. Because injections of the excitatory amino acid antagonist, kynurenate, into the RVLM also interrupted responses to blockade of the PRF and blocked somatosympathetic reflexes, glutamate is a likely neurotransmitter from the PRF to the RVLM and for somatosympathetic reflexes.
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DiBona, G. F., L. L. Sawin, and S. Y. Jones. "Characteristics of renal sympathetic nerve activity in sodium-retaining disorders." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 271, no. 1 (July 1, 1996): R295—R302. http://dx.doi.org/10.1152/ajpregu.1996.271.1.r295.
Full textAbstract:
Characteristics of renal sympathetic nerve activity in conscious rats with established congestive heart failure, cirrhosis, or nephrotic syndrome were analyzed using three methods: mean integrated voltage over time, power spectrum analysis, and sympathetic peak detection analysis. Compared with control rats, all three disease models had increased mean integrated voltage. On power spectrum analysis, all three disease models had increased relative power at the heart rate frequency, indicating that it was related to renal sympathetic nerve discharge coupled to the cardiac cycle. Congestive heart failure and nephrotic syndrome rats showed increased relative power in the low-frequency range, whereas cirrhotic and nephrotic syndrome rats showed decreased relative power in the high-frequency range. On sympathetic peak detection analysis, the frequency of sympathetic peaks was greater in the three disease models compared with the control rats. In cirrhotic rats, the distribution of sympathetic peak heights was shifted toward an increased number of peaks of lesser height. It is concluded that basal renal sympathetic nerve activity is chronically increased in these disease models. This is manifest as increased power coupled to the cardiac cycle, which may reflect the disease-specific defects in arterial and cardiac baroreflex control. In cirrhosis, there is possible selective activation of a subgroup of renal sympathetic nerve fibers.
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Chen, X. L., M. M. Knuepfer, and T. C. Westfall. "Hemodynamic and sympathetic effects of spinal administration of neuropeptide Y in rats." American Journal of Physiology-Heart and Circulatory Physiology 259, no. 6 (December 1, 1990): H1674—H1680. http://dx.doi.org/10.1152/ajpheart.1990.259.6.h1674.
Full textAbstract:
Intrathecal administration of 4 nmol/kg neuropeptide Y in Dial-urethane-anesthetized rats elicited decreases in arterial pressure, renal sympathetic nerve activity, and a slight decrease in heart rate. The depressor response was associated with a sustained hindquarters and mesenteric vasodilation resulting in a decrease in total peripheral resistance. Intrathecal NPY also resulted in a decrease in renal sympathetic nerve activity. There was a positive correlation between the percent changes in arterial pressure and renal sympathetic nerve activity. With the use of renal nerve activity and heart rate as indexes, NPY resulted in a decrease in baroreflex sensitivity. The depressor effect of intrathecal NPY did not appear to be due to spinal vasoconstriction and ischemia, since spinal microvascular resistance was decreased slightly. We conclude that the intrathecal administration of NPY produces an inhibition of sympathetic nerve activity, resulting in a decrease in total peripheral resistance and arterial pressure.
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Ramchandra, Rohit, Carolyn J. Barrett, Sarah-Jane Guild, Fiona McBryde, and Simon C. Malpas. "Role of renal sympathetic nerve activity in hypertension induced by chronic nitric oxide inhibition." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 292, no. 4 (April 2007): R1479—R1485. http://dx.doi.org/10.1152/ajpregu.00435.2006.
Full textAbstract:
Nitric oxide levels are diminished in hypertensive patients, suggesting nitric oxide might have an important role to play in the development of hypertension. Chronic blockade of nitric oxide leads to hypertension that is sustained throughout the period of the blockade in baroreceptor-intact animals. It has been suggested that the sympathetic nervous system is involved in the chronic increase in blood pressure; however, the evidence is inconclusive. We measured renal sympathetic nerve activity and blood pressure via telemetry in rabbits over 7 days of nitric oxide blockade. Nitric oxide blockade via Nω-nitro-l-arginine methyl ester (l-NAME) in the drinking water (50 mg·kg−1·day−1) for 7 days caused a significant increase in arterial pressure (7 ± 1 mmHg above control levels; P < 0.05). While the increase in blood pressure was associated with a decrease in heart rate (from 233 ± 6 beats/min before the l-NAME to 202 ± 6 beats/min on day 7), there was no change in renal sympathetic nerve activity (94 ± 4 %baseline levels on day 2 and 96 ± 5 %baseline levels on day 7 of l-NAME; baseline nerve activity levels were normalized to the maximum 2 s of nerve activity evoked by nasopharyngeal stimulation). The lack of change in renal sympathetic nerve activity during the l-NAME-induced hypertension indicates that the renal nerves do not mediate the increase in blood pressure in conscious rabbits.
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Helwig, Bryan G., Sujatha Parimi, Chanran K. Ganta, Richard Cober, Richard J. Fels, and Michael J. Kenney. "Aging alters regulation of visceral sympathetic nerve responses to acute hypothermia." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, no. 3 (September 2006): R573—R579. http://dx.doi.org/10.1152/ajpregu.00903.2005.
Full textAbstract:
Hypothermia produced by acute cooling prominently alters sympathetic nerve outflow. Skin sympathoexcitatory responses to skin cooling are attenuated in aged compared with young subjects, suggesting that advancing age influences sympathetic nerve responsiveness to hypothermia. However, regulation of skin sympathetic nerve discharge (SND) is only one component of the complex sympathetic nerve response profile to hypothermia. Whether aging alters the responsiveness of sympathetic nerves innervating other targets during acute cooling is not known. In the present study, using multifiber recordings of splenic, renal, and adrenal sympathetic nerve activity, we tested the hypothesis that hypothermia-induced changes in visceral SND would be attenuated in middle-aged and aged compared with young Fischer 344 (F344) rats. Colonic temperature (Tc) was progressively reduced from 38°C to 31°C in young (3 to 6 mo), middle-aged (12 mo), and aged (24 mo) baroreceptor-innervated and sinoaortic-denervated (SAD), urethane-chloralose anesthetized, F344 rats. The following observations were made. 1) Progressive hypothermia significantly ( P < 0.05) reduced splenic, renal, and adrenal SND in young baroreceptor-innervated F344 rats. 2) Reductions in splenic, renal, and adrenal SND to progressive hypothermia were less consistently observed and, when observed, were generally attenuated in baroreceptor-innervated middle-aged and aged compared with young F344 rats. 3) Differences in splenic, renal, and adrenal SND responses to reduced Tc were observed in SAD young, middle-aged, and aged F344 rats, suggesting that age-associated attenuations in SND responses to acute cooling are not the result of age-dependent modifications in arterial baroreflex regulation of SND. These findings demonstrate that advancing chronological age alters the regulation of visceral SND responses to progressive hypothermia, modifications that may contribute to the inability of aged individuals to adequately respond to acute bouts of hypothermia.
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Cohen, M. D., J. Finberg, M. Dibner-Dunlap, S. N. Yuih, and M. D. Thames. "Effects of desipramine hydrochloride on peripheral sympathetic nerve activity." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 258, no. 4 (April 1, 1990): R876—R882. http://dx.doi.org/10.1152/ajpregu.1990.258.4.r876.
Full textAbstract:
Tricyclic antidepressants cause orthostatic hypotension and have antiarrhythmic effects that may be partially due to effects on the sympathetic nervous system. We studied the influence of intravenous desipramine hydrochloride on renal (n = 12) and lumbar (n = 5) nerve traffic and mean arterial pressure in alpha-chloralose-anesthetized rabbits with sinoaortic and vagal denervation. Desipramine administration resulted in dose-dependent inhibition of renal and lumbar nerve activity that was markedly reduced or abolished by yohimbine (0.5 mg/kg iv), an alpha 2-blocker that enters the brain rapidly. In contrast, administration of phentolamine (0.75 mg/kg iv), an alpha 1- and alpha 2-blocker with limited access to the brain, failed to alter the responses to desipramine. Because renal nerves are postganglionic and lumbar nerves are preganglionic, desipramine does not act via a ganglionic mechanism. Our results are best explained by an effect of desipramine on the sympathetic nervous system mediated via central alpha 2-receptors. This sympathoinhibitory effect of desipramine may contribute to its postural hypotensive effect and to its efficacy as an antiarrhythmic agent.
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Sata, Yusuke, and Markus P. Schlaich. "The Potential Role of Catheter-Based Renal Sympathetic Denervation in Chronic and End-Stage Kidney Disease." Journal of Cardiovascular Pharmacology and Therapeutics 21, no. 4 (January 6, 2016): 344–52. http://dx.doi.org/10.1177/1074248415624156.
Full textAbstract:
Sympathetic activation is a hallmark of chronic and end-stage renal disease and adversely affects cardiovascular prognosis. Hypertension is present in the vast majority of these patients and plays a key role in the progressive deterioration of renal function and the high rate of cardiovascular events in this patient cohort. Augmentation of renin release, tubular sodium reabsorption, and renal vascular resistance are direct consequences of efferent renal sympathetic nerve stimulation and the major components of neural regulation of renal function. Renal afferent nerve activity directly influences sympathetic outflow to the kidneys and other highly innervated organs involved in blood pressure control via hypothalamic integration. Renal denervation of the kidney has been shown to reduce blood pressure in many experimental models of hypertension. Targeting the renal nerves directly may therefore be specifically useful in patients with chronic and end-stage renal disease. In this review, we will discuss the potential role of catheter-based renal denervation in patients with impaired kidney function and also reflect on the potential impact on other cardiovascular conditions commonly associated with chronic kidney disease such as heart failure and arrhythmias.
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DiBona, G. F., and L. L. Sawin. "Increased renal nerve activity in cardiac failure: arterial vs. cardiac baroreflex impairment." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 268, no. 1 (January 1, 1995): R112—R116. http://dx.doi.org/10.1152/ajpregu.1995.268.1.r112.
Full textAbstract:
Cardiac failure is characterized by increased renal sympathetic nerve activity that is associated with an impairment of both arterial and cardiac baroreceptor reflex function. These reflex dysfunctions are in the afferent limb at the level of the peripheral baroreceptors. This study sought to define the relative quantitative magnitude of the defects in arterial and cardiac baroreceptor function in cardiac failure. Renal sympathetic nerve activity was measured in anesthetized normal control rats and rats with cardiac failure (left coronary ligation) during sequential random order sinoaortic denervation and vagotomy to interrupt afferent input from the arterial and cardiac baroreceptors, respectively. Increases in renal sympathetic nerve activity after individual or combined sinoaortic denervation and vagotomy were less (P < 0.05 for both) in cardiac failure than in normal control rats in both order sequences (42 +/- 5 vs. 87 +/- 8%; 44 +/- 5 vs. 108 +/- 7%). In cardiac failure rats, vagotomy produced lesser increases (P < 0.05 for both) in renal sympathetic nerve activity than sinoaortic denervation in both order sequences (10 +/- 4 vs. 32 +/- 5%; 13 +/- 2 vs. 30 +/- 5%). The relative magnitude of impaired cardiac baroreceptor reflex function that is associated with the increased renal sympathetic nerve activity of cardiac failure is greater than that of impaired arterial baroreceptor reflex function.
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Dibona, Gerald F., Susan Y. Jones, and Linda L. Sawin. "Angiotensin receptor antagonist improves cardiac reflex control of renal sodium handling in heart failure." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 2 (February 1, 1998): H636—H641. http://dx.doi.org/10.1152/ajpheart.1998.274.2.h636.
Full textAbstract:
In rats with congestive heart failure, type 1 angiotensin II receptor antagonist treatment (losartan) decreases basal renal sympathetic nerve activity and improves arterial baroreflex regulation of renal sympathetic nerve activity. This investigation examined the effect of losartan on cardiac baroreflex regulation of renal sympathetic nerve activity and renal sodium handling in rats with congestive heart failure. Losartan treatment decreased arterial pressure from 120 ± 3 to 93 ± 5 mmHg and increased the afferent (from 0.95 ± 0.21 to 2.22 ± 0.42% Δafferent vagal nerve activity/mmHg mean right atrial pressure, P < 0.05) and overall gain (from −1.14 ± 0.19 to −4.20 ± 0.39% Δrenal sympathetic nerve activity/mmHg mean right atrial pressure, P < 0.05) of the cardiac baroreflex. During isotonic saline volume loading, urinary sodium excretion increased from 2.4 ± 0.8 to 10.5 ± 1.3 μeq/min in vehicle-treated rats (excretion of 52 ± 3% of the load) and from 3.0 ± 1.0 to 15.1 ± 1.8 μeq/min in losartan-treated rats (excretion of 65 ± 4% of the load, P < 0.05). When rats were changed from a low- to a high-sodium diet, cumulative sodium balance over 5 days was 7.8 ± 0.6 meq in vehicle-treated rats and 4.2 ± 0.4 meq in losartan-treated rats ( P < 0.05). In congestive heart failure, losartan treatment improved cardiac baroreflex regulation of renal sympathetic nerve activity, which was associated with improved ability to excrete acute and chronic sodium loads.
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Katona, P. G., K. Dembowsky, J. Czachurski, and H. Seller. "Chemoreceptor stimulation on sympathetic activity: dependence on respiratory phase." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 257, no. 5 (November 1, 1989): R1027—R1033. http://dx.doi.org/10.1152/ajpregu.1989.257.5.r1027.
Full textAbstract:
Experiments were performed on chloralose-anesthetized, vagotomized, paralyzed, and artificially ventilated cats breathing 100% O2. Peripheral chemoreceptors were stimulated by rapid injections of CO2-saturated NaHCO3 in different phases of the respiratory cycle. Responses of cardiac and renal sympathetic nerves were computed by digital integration. Spontaneous sympathetic activity was consistently modulated by respiration, the modulation being greater for cardiac than for renal nerves. Cardiac nerve responses to peripheral chemoreceptor stimulation depended on the respiratory phase for at least one experimental condition in four of seven animals: the responses were largest during late inspiration and smallest (or absent) during postinspiration and early expiration. Renal nerve responses depended on respiratory phase in only two of eight animals. An average end-tidal CO2 concentration increase from 4.6 +/- 0.8% (SD) to 6.7 +/- 0.9% enhanced the respiratory modulation of spontaneous activity but reduced the responses to peripheral chemoreceptor stimulation. The results indicate that the respiratory modulation of chemoreceptor-induced sympathetic responses was less prominent than the modulation of spontaneous activity. It is hypothesized that the phase dependence of the responses is caused by the spontaneously occurring expiratory diminution of sympathetic activity rather than by an inherent gating of the chemoreceptor reflex.
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Kenney, M. J., F. Blecha, R. J. Fels, and D. A. Morgan. "Altered frequency responses of sympathetic nerve discharge bursts after IL-1β and mild hypothermia." Journal of Applied Physiology 93, no. 1 (July 1, 2002): 280–88. http://dx.doi.org/10.1152/japplphysiol.01250.2001.
Full textAbstract:
Although interleukin-1β (IL-1β) administration produces nonuniform changes in the level of sympathetic nerve discharge (SND), the effect of IL-1β on the frequency-domain relationships between discharges in different sympathetic nerves is not known. Autospectral and coherence analyses were used to determine the effect of IL-1β and mild hypothermia (60 min after IL-1β, colonic temperature from 38°C to 36°C) on the relationships between renal-interscapular brown adipose tissue (IBAT) and splenic-lumbar sympathetic nerve discharges in chloralose-anesthetized rats. The following observations were made. 1) IL-1β did not alter renal-IBAT coherence values in the 0- to 2-Hz frequency band or at the cardiac frequency (CF). 2) Peak coherence values relating splenic-lumbar discharges at the CF were significantly increased after IL-1β and during hypothermia. 3) Hypothermia after IL-1β significantly reduced the coupling (0–2 Hz and CF) between renal-IBAT but not splenic-lumbar SND bursts. 4) Combining IL-1β and mild hypothermia had a greater effect on renal-IBAT SND coherence values than did mild hypothermia alone. These data demonstrate functional plasticity in sympathetic neural circuits and suggest complex relationships between immune products and SND regulation.
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Dibona, Gerald F., and Linda L. Sawin. "Functional significance of the pattern of renal sympathetic nerve activation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 277, no. 2 (August 1, 1999): R346—R353. http://dx.doi.org/10.1152/ajpregu.1999.277.2.r346.
Full textAbstract:
To assess the renal functional significance of the pattern of renal sympathetic nerve activation, computer-generated stimulus patterns (delivered at constant integrated voltage) were applied to the decentralized renal sympathetic nerve bundle and renal hemodynamic and excretory responses determined in anesthetized rats. When delivered at the same integrated voltage, stimulus patterns resembling those observed in in vivo multifiber recordings of renal sympathetic nerve activity (diamond-wave patterns) produced greater renal vasoconstrictor responses than conventional square-wave patterns. Within diamond-wave patterns, increasing integrated voltage by increasing amplitude produced twofold greater renal vasoconstrictor responses than by increasing duration. With similar integrated voltages that were subthreshold for renal vasoconstriction, neither diamond- nor square-wave pattern altered glomerular filtration rate, whereas diamond- but not square-wave pattern reversibly decreased urinary sodium excretion by 25 ± 3%. At the same number of pulses per second, intermittent stimulation produced faster and greater renal vasoconstriction than continuous stimulation. At the same number of pulses per second, increases in rest period during intermittent stimulation proportionally augmented the renal vasoconstrictor response compared with that observed with continuous stimulation; the maximum augmentation of 55% occurred at a rest period of 500 ms. These results indicate that the pattern of renal sympathetic nerve stimulation (activity) significantly influences the rapidity, magnitude, and selectivity of the renal vascular and tubular responses.