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1
Noureddine, Fatima Y., Raffaele Altara, Fan Fan, Andriy Yabluchanskiy, George W. Booz, and Fouad A. Zouein. "Impact of the Renin–Angiotensin System on the Endothelium in Vascular Dementia: Unresolved Issues and Future Perspectives." International Journal of Molecular Sciences 21, no. 12 (June 16, 2020): 4268. http://dx.doi.org/10.3390/ijms21124268.
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The effects of the renin–angiotensin system (RAS) surpass the renal and cardiovascular systems to encompass other body tissues and organs, including the brain. Angiotensin II (Ang II), the most potent mediator of RAS in the brain, contributes to vascular dementia via different mechanisms, including neuronal homeostasis disruption, vascular remodeling, and endothelial dysfunction caused by increased inflammation and oxidative stress. Other RAS components of emerging significance at the level of the blood–brain barrier include angiotensin-converting enzyme 2 (ACE2), Ang(1–7), and the AT2, Mas, and AT4 receptors. The various angiotensin hormones perform complex actions on brain endothelial cells and pericytes through specific receptors that have either detrimental or beneficial actions. Increasing evidence indicates that the ACE2/Ang(1–7)/Mas axis constitutes a protective arm of RAS on the blood–brain barrier. This review provides an update of studies assessing the different effects of angiotensins on cerebral endothelial cells. The involved signaling pathways are presented and help highlight the potential pharmacological targets for the management of cognitive and behavioral dysfunctions associated with vascular dementia.
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Bernardi, Stella, Barbara Toffoli, Federica Tonon, Morena Francica, Elena Campagnolo, Tommaso Ferretti, Sarah Comar, Fabiola Giudici, Elisabetta Stenner, and Bruno Fabris. "Sex Differences in Proatherogenic Cytokine Levels." International Journal of Molecular Sciences 21, no. 11 (May 29, 2020): 3861. http://dx.doi.org/10.3390/ijms21113861.
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Background: It has been shown that sex affects immunity, including cytokine production. Given that atherosclerosis is an inflammatory disease promoted by specific cytokines, such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α, we aimed at evaluating whether sex could affect the levels of these proatherogenic cytokines in a group of healthy adults. In this analysis, we also included other cytokines and peptides that have been implicated in atherosclerosis development and progression. Methods: A total of 104 healthy adults were recruited; we measured circulating levels of IL-1β, IL-6, TNF-α, angiotensins and angiotensin-converting enzyme-2 (ACE2), as well as osteoprotegerin and receptor activator of nuclear factor κB ligand (RANKL). Results: IL-1β, IL-6, and TNF-α were significantly higher in men as compared to women. They were all associated with testosterone and the testosterone/estradiol ratio. They remained significantly associated with sex (but not with hormones) after being tested for potential confounders. Conclusions: Sex seems to influence the levels of proatherogenic cytokines. This is consistent not only with sex differences in vulnerability to infections but also with the higher cardiovascular risk exhibited by the male gender as compared to the female gender. Nevertheless, this association is only partly explained by hormone levels.
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Pandey, K. N., and T. Inagami. "Regulation of renin angiotensins by gonadotropic hormones in cultured murine Leydig tumor cells. Release of angiotensin but not renin." Journal of Biological Chemistry 261, no. 9 (March 1986): 3934–38. http://dx.doi.org/10.1016/s0021-9258(17)35604-1.
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Galán-Ocaña, A., M. J. Ramírez-Expósito, J. M. Martínez-Martos, S. Tellado, and C. Azorit. "Regulation of aminopeptidases by the renin - angiotensin system: monitoring seasonal variations in red deer and fallow deer from a Mediterranean ecosystem." Animal Production Science 52, no. 8 (2012): 761. http://dx.doi.org/10.1071/an12023.
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The circulating renin–angiotensin system (RAS) is well known for its systemic role in the regulation of blood pressure, renal hemodynamics and fluid homeostasis. However, in mammals several organs also contain a local RAS, including male and female reproductive tissues. In the present study we analysed serum from a free-living population of red deer (Cervus elaphus hispanicus) and fallow deer (Dama dama) to determine the activity of four RAS-regulating aminopeptidases (aminopeptidase A, aspartyl aminopeptidase, aminopeptidase N and aminopeptidase B) as part of a study of annual cycles of growth and condition. Our aim was to detect seasonal variations in the activities of these aminopeptidases and their relationship to the reproductive behaviour of both species in a Mediterranean environment. In both males and females there was a maximum peak of activity in autumn. A second peak was detected in spring for males while in females activity was also higher in summer. These changes may be related to a different endocrine status according to their seasonal cycle, the decreased photoperiod in autumn and the normal timing of the seasonal growth cycle. Thus, changes in the activity of RAS-regulating aminopeptidases could reflect the functional role of angiotensins through the annual cycle of both species, also suggesting an important role of these peptide hormones in the regulation of these biological processes.
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Takei, Yoshio, Ippei Suzuki, Marty K. S. Wong, Ryan Milne, Simon Moss, Katsufumi Sato, and Ailsa Hall. "Development of an animal-borne blood sample collection device and its deployment for the determination of cardiovascular and stress hormones in phocid seals." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 311, no. 4 (October 1, 2016): R788—R796. http://dx.doi.org/10.1152/ajpregu.00211.2016.
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An animal-borne blood sampler with data-logging functions was developed for phocid seals, which collected two blood samples for the comparison of endocrinological/biochemical parameters under two different conditions. The sampler can be triggered by preset hydrostatic pressure, acceleration (descending or ascending), temperature, and time, and also manually by light. The sampling was reliable with 39/50 (78%) successful attempts to collect blood samples. Contamination of fluids in the tubing to the next blood sample was <1%, following the prior clearance of the tubing to a waste syringe. In captive harbor seals ( Phoca vitulina), the automated blood-sampling method was less stressful than direct blood withdrawal, as evidenced by lower levels of stress hormones ( P < 0.05 for ACTH and P = 0.078 for cortisol). HPLC analyses showed that both cortisol and cortisone were circulating in seal blood. Using the sampler, plasma levels of cardiovascular hormones, atrial natriuretic peptide (ANP), AVP, and ANG II were compared in grey seals ( Halichoerus grypus), between samples collected when the animals were on land and in the water. HPLC analyses determined that [Met12] ANP (1–28) and various forms of angiotensins (ANG II, III, and IV) were circulating in seal blood. Although water immersion profoundly changes the plasma levels of cardiovascular hormones in terrestrial mammals, there were only tendencies toward an increase in ANP ( P = 0.069) and a decrease in AVP ( P = 0.074) in the seals. These results suggest that cardiovascular regulation in phocid seals may have undergone adaptation during evolution of the carnivore to a semiaquatic lifestyle.
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Clapp, Carmen, Stéphanie Thebault, Michael C. Jeziorski, and Gonzalo Martínez De La Escalera. "Peptide Hormone Regulation of Angiogenesis." Physiological Reviews 89, no. 4 (October 2009): 1177–215. http://dx.doi.org/10.1152/physrev.00024.2009.
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It is now apparent that regulation of blood vessel growth contributes to the classical actions of hormones on development, growth, and reproduction. Endothelial cells are ideally positioned to respond to hormones, which act in concert with locally produced chemical mediators to regulate their growth, motility, function, and survival. Hormones affect angiogenesis either directly through actions on endothelial cells or indirectly by regulating proangiogenic factors like vascular endothelial growth factor. Importantly, the local microenvironment of endothelial cells can determine the outcome of hormone action on angiogenesis. Members of the growth hormone/prolactin/placental lactogen, the renin-angiotensin, and the kallikrein-kinin systems that exert stimulatory effects on angiogenesis can acquire antiangiogenic properties after undergoing proteolytic cleavage. In view of the opposing effects of hormonal fragments and precursor molecules, the regulation of the proteases responsible for specific protein cleavage represents an efficient mechanism for balancing angiogenesis. This review presents an overview of the actions on angiogenesis of the above-mentioned peptide hormonal families and addresses how specific proteolysis alters the final outcome of these actions in the context of health and disease.
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Goligorsky, M. S., D. Osborne, T. Howard, K. A. Hruska, and I. E. Karl. "Hormonal regulation of gluconeogenesis in cultured proximal tubular cells: role of cytosolic calcium." American Journal of Physiology-Renal Physiology 253, no. 5 (November 1, 1987): F802—F809. http://dx.doi.org/10.1152/ajprenal.1987.253.5.f802.
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Gluconeogenic competence of primary cultures of canine renal proximal tubular cells has been examined. Cells grown in 5 mM glucose media or in glucose-free media exhibited pyruvate-stimulated glucose production, as opposed to cells grown in 20 mM glucose media. By 72 h after the last media change, confluent cells grown in 5 mM glucose medium turn from a predominantly glycolytic to an oxidative type of metabolism. By this time, glucose production exhibited pH, 3-mercaptopicolinate, and insulin sensitivity. Parathyroid hormone, angiotensin II, and phenylephrine stimulated glucose production in a nonadditive fashion. Single-cell cystolic Ca2+ measurements using microspectrofluorometric techniques revealed that all three hormones elicited Ca2+ transients in proximal tubular cells. Ionomycin stimulated glucose production by proximal tubular cells, suggesting that Ca2+ transients could represent a sufficient stimulus for glucose production. When hormone-induced Ca2+ transients were curtailed by a pretreatment with the membrane-permeant Ca2+ chelator, Maptam, hormonal stimulation of glucose production was abolished, suggesting that Ca2+ transients represent not only a sufficient, but a necessary event in the stimulation of glucose production by these hormones.
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Siqueira, Lucas C., Joabel T. dos Santos, Rogério Ferreira, Robson Souza dos Santos, Adelina M. dos Reis, João F. Oliveira, Joanne E. Fortune, and Paulo Bayard Gonçalves. "Preovulatory changes in the angiotensin II system in bovine follicles." Reproduction, Fertility and Development 25, no. 3 (2013): 539. http://dx.doi.org/10.1071/rd11316.
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The present study evaluated whether the gonadotrophin surge modulates components of the renin–angiotensin system and whether angiotensin II (Ang II) plays a role in the production of hormones by follicular cells during the ovulatory process. In Experiment 1, cows were ovariectomised at various times (0, 3, 6, 12 and 24h) after GnRH injection to obtain preovulatory follicles. The concentration of Ang II in follicular fluid increased after GnRH and reached a peak at 24h, concomitant with the peak of angiotensinogen (AGT) mRNA expression in granulosa cells. AGT mRNA was not expressed in theca cells. Ang II receptor type 2 and angiotensin-converting enzyme mRNA levels were transiently upregulated in theca cells. In Experiment 2, an in vitro culture was used to determine whether Ang II could modulate hormone production by healthy dominant follicles. In the absence of LH, Ang II did not alter hormonal production by either theca or granulosa cells. Ang II plus LH increased progesterone and prostaglandin secretion by granulosa cells. In summary, the renin–angiotensin system is actively controlled during the preovulatory period and Ang II amplifies the stimulatory effects of LH on the secretion of progesterone and prostaglandins by granulosa cells.
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Pfeilschifter, J., A. Kurtz, and C. Bauer. "Role of phospholipase C and protein kinase C in vasoconstrictor-induced prostaglandin synthesis in cultured rat renal mesangial cells." Biochemical Journal 234, no. 1 (February 15, 1986): 125–30. http://dx.doi.org/10.1042/bj2340125.
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It was the aim of the present study to find out if a common mechanism exists by which the vasoconstrictive hormones angiotension II, noradrenaline and 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine (AGEPC) increase prostaglandin E2 (PGE2) synthesis in cultures of rat renal mesangial cells. Angiotension II, noradrenaline and AGEPC stimulated PGE2 synthesis and uptake of 45Ca2+ in cultured mesangial cells. Both of these effects could be completely suppressed by the calcium channel blocker verapamil. Angiotensin II, noradrenaline and AGEPC caused a rapid breakdown of phosphatidylinositol 4,5-bisphosphate with a concomitant increase of 1,2-diacylglycerol and inositol trisphosphate, indicating an activation of phospholipase C by these hormones. Addition of verapamil had no effect on the hormone-induced stimulation of phospholipase C. The synthetic analogue of diacylglycerol, 1-oleoyl-2-acetylglycerol, and the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA), both of which are known to stimulate protein kinase C, enhanced PGE2 synthesis. Chelation of extracellular calcium with EDTA or addition of verapamil abolished the effect of 1-oleoyl-2-acetylglycerol and phorbol ester on PGE2 synthesis. 1-Oleoyl-2-acetylglycerol and phorbol ester increased the uptake of 45Ca2+ by the cells in a dose-dependent manner and this effect could be blocked by verapamil. The entirety of these data leads us to suggest that vasoconstrictor-evoked synthesis of PGE2 in rat mesangial cells is mediated by the subsequent activation of phospholipase C and protein kinase C. The activation of protein kinase C by diacylglycerol is likely to be involved in the increase of the calcium permeability of the plasma membrane which is a prerequisite for PGE2 synthesis induced by vasoconstrictive hormones.
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Ferlazzo, Adriana, Cristina Cravana, Esterina Fazio, and Pietro Medica. "The different hormonal system during exercise stress coping in horses." May-2020 13, no. 5 (2020): 847–59. http://dx.doi.org/10.14202/vetworld.2020.847-859.
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The review discusses the hormonal changes during exercise stress. The exercise generally produces a rise of adrenaline (A), noradrenaline (NA), adrenocorticotropic hormone (ACTH), cortisol, glucagon, growth hormone, arginine vasopressine, etc., and a drop of insulin. The hormonal events during reestablishment of homeostasis due to exercise stress can be divided into a catabolic phase, with decreased tolerance of effort, and reversible biochemical, hormonal and immunological changes, and an anabolic phase, with a higher adaptive capacity, and enhanced performance. The two main hormonal axes activated in the catabolic phase are sympathetic–adrenal–medullary system and hypothalamic-pituitary-adrenal (HPA) axis, while in the anabolic phase, growth hormone-insulin-like factor I axis, and gonadal axes. The hormonal responses during exercise and recovery can be regarded as regulatory and integrated endocrine responses. The increase of catecholamines and ACTH is dependent on the intensity of exercise; a marked increase in plasma A occurs during exercises with high emotional content. The response of cortisol is correlated with the duration of exercise, while the effect of exercise duration on β-endorphin changes is highly dependent on the type of exercise performed. Cortisol and β-endorphin changes usually occur in phase, but not during exercises with high emotional content. Glucocorticoids and iodothyronines are involved in meeting immediate energy demands, and a model of functional interactions between HPA axis and hypothalamic-pituitary-thyroid axis during exercise stress is proposed. A modulation of coping responses to different energy demanding physical activities required for sport activities could be hypothesized. This review supports the proposed regulation of hypophysiotropic TRHergic neurons as metabolic integrators during exercise stress. Many hormonal systems (ghrelin, leptin, glucose, insulin, and cortisol) are activated to control substrate mobilizations and utilization. The cardiovascular homeostasis, the fluid and electrolyte balance during exercise are highly dependent on vasoactive hormones (antidiuretic hormone, atrial natriuretic peptide, renin–angiotensin–aldosterone, and prostaglandins) control.
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Armando, Ines, Andrea Carranza, Yasuaki Nishimura, Marta Barontini, Takeshi Ito, and Juan M. Saavedra. "Candesartan decreases the sympatho-adrenal and hormonal response to isolation stress." Journal of the Renin-Angiotensin-Aldosterone System 2, no. 1_suppl (March 2001): S130—S135. http://dx.doi.org/10.1177/14703203010020012301.
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A change from group housing to isolation in unfamiliar metabolic cages represents, for rodents, a significant emotional stress. We studied the effect of candesartan, a peripheral and central angiotensin II AT1-receptor antagonist, on the hormonal and sympathetic response to acute isolation. We pretreated rats with 1 mg/kg/day candesartan for 13 days via subcutaneously implanted osmotic minipumps, followed by 24-hour isolation in individual metabolic cages. We measured brain, pituitary and adrenal angiotensin II (Ang II) receptor binding by quantitative autoradiography and adrenal hormones and catecholamines by RIA and HPLC. Isolation increased adrenal catecholamines, aldosterone and corticosterone, AT1-receptor binding in the zona glomerulosa and AT2-receptor binding in the adrenal medulla. Candesartan pretreatment decreased adrenal catecholamines, aldosterone and corticosterone, AT1-receptor binding in adrenal zona glomerulosa and medulla, pituitary gland and the hypothalamic paraventricular nucleus, and AT2-receptor binding in adrenal medulla, but increased AT2-receptor binding in zona glomerulosa. We conclude that peripheral and central AT1-receptor blockade with candesartan decreases the sympatho-adrenal and hormonal response to acute stress. Our results indicate that Ang II is an important stress hormone and suggest that blockade of the physiologically active AT 1-receptors could influence stress-related disorders.
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Altin, J. G., and F. L. Bygrave. "Synergistic stimulation of Ca+ uptake by glucagon and Ca2+-mobilizing hormones in the perfused rat liver. A role for mitochondria in long-term Ca2+ homoeostasis." Biochemical Journal 238, no. 3 (September 15, 1986): 653–61. http://dx.doi.org/10.1042/bj2380653.
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A perfused liver system incorporating a Ca2+-sensitive electrode was used to study the long-term effects of glucagon and cyclic AMP on the mobilization of Ca2+ induced by phenylephrine, vasopressin and angiotensin. At 1.3 mM extracellular Ca2+ the co-administration of glucagon (10 nM) or cyclic AMP (0.2 mM) and a Ca2+-mobilizing hormone led to a synergistic potentiation of Ca2+ uptake by the liver, to a degree which was dependent on the order of hormone administration. A maximum net amount of Ca2+ influx, corresponding to approx. 3800 nmol/g of liver (the maximum rate of influx was 400 nmol/min per g of liver), was induced when cyclic AMP or glucagon was administered about 4 min before vasopressin and angiotensin. These changes are over an order of magnitude greater than those induced by Ca2+-mobilizing hormones alone [Altin & Bygrave (1985) Biochem. J. 232, 911-917]. For a maximal response the influx of Ca2+ was transient and was essentially complete after about 20 min. Removal of the hormones was followed by a gradual efflux of Ca2+ from the liver over a period of 30-50 min; thereafter, a similar response could be obtained by a second administration of hormones. Dose-response measurements indicate that the potentiation of Ca2+ influx by glucagon occurs even at low (physiological) concentrations of the hormone. By comparison with phenylephrine, the stimulation of Ca2+ influx by vasopressin and angiotensin is more sensitive to low concentrations of glucagon and cyclic AMP, and can be correlated with a 20-50-fold increase in the calcium content of mitochondria. The reversible uptake of such large quantities of Ca2+ implicates the mitochondria in long-term cellular Ca2+ regulation.
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Altin, J. G., and F. L. Bygrave. "The Ca2+-mobilizing actions of vasopressin and angiotensin differ from those of the α-adrenergic agonist phenylephrine in the perfused rat liver." Biochemical Journal 232, no. 3 (December 15, 1985): 911–17. http://dx.doi.org/10.1042/bj2320911.
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A Ca2+-sensitive electrode was used to study net Ca2+-flux changes induced by the administration of phenylephrine, vasopressin and angiotensin to the perfused rat liver. The studies reveal that, although the Ca2+ responses induced by vasopressin and angiotensin are similar, they are quite different from the Ca2+ fluxes induced by phenylephrine. The administration of phenylephrine is accompanied by a stimulation of a net amount of Ca2+ efflux (140 nmol/g of liver). A re-uptake of a similar amount of Ca2+ occurs only after the hormone is removed. In contrast, the administration of vasopressin or angiotensin to livers perfused with 1.3 mM-Ca2+ induces the release of a relatively small amount of Ca2+ (approx. 40 nmol/g of liver) during the first 60 s. This is followed by a much larger amount of Ca2+ uptake (70-140 nmol/g of liver) after 1-2.5 min of hormone administration, and a slow efflux or loss of a similar amount of Ca2+ over a period of 6-8 min. At lower concentrations of perfusate Ca2+ (less than 600 microM) these hormones induce only a net efflux of the ion. These results suggest that at physiological concentrations of extracellular Ca2+ the mechanism by which alpha-adrenergic agonists mobilize cellular Ca2+ is different from that involving vasopressin and angiotensin. It seems that the hormones may have quite diverse effects on Ca2+ transport across the plasma membrane and perhaps organellar membranes in liver.
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Binet, A., B. Berthon, and M. Claret. "Hormone-induced increase in free cytosolic calcium and glycogen phosphorylase activation in rat hepatocytes incubated in normal and low-calcium media." Biochemical Journal 228, no. 3 (June 15, 1985): 565–74. http://dx.doi.org/10.1042/bj2280565.
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The action of alpha 1-adrenergic agonists (noradrenaline in the presence of propranolol), vasopressin and angiotensin on the intracellular free Ca2+ concentration, [Ca2+]i, was determined by using the fluorescent dye quin2 in isolated rat liver cells. In the presence of external Ca2+ (1.8 mM), 1 microM-noradrenaline induced an increase in [Ca2+]i up to about 800 nM without apparent delay, whereas 10 nM-vasopressin and 1 nM-angiotensin increased [Ca2+]i to values higher than 1500 nM with a lag period of about 6s. The successive addition of the hormones and of their specific antagonists indicated that the actions of the three Ca2+-mobilizing hormones occurred without apparent desensitization (over 6 min) and via independent receptors. The relative contributions of internal and external Ca2+ pools to the cell response were determined by studying the hormone-mediated [Ca2+]i increase and glycogen phosphorylase activation in low-Ca2+ media (22 microM). In this medium: (1) [Ca2+]i was lowered and the hormones initiated a transient instead of a sustained increase in [Ca2+]i; subsequent addition (2 min) of a second hormone promoted a lesser increase in [Ca2+]i; in contrast, the subsequent addition (2 min) of Ca2+ (1.8 mM) caused [Ca2+]i to increase to a value close to that initiated by the hormone in control conditions, the amplitude of the latter response being dependent on the concentration of Ca2+ added to the medium; (2) returning to normal Ca2+ (1.8 mM) restored the resting [Ca2+]i and allowed the hormone added 2 min later to promote a large increase in [Ca2+]i whose final amplitude was also dependent on the concentration of Ca2+ added beforehand. Similar results were found when the same protocol was applied to the glycogen phosphorylase activation. It is concluded that Ca2+ influx is required for a maximal and sustained response and to reload the hormone-sensitive stores.
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Wright, John W., Shigehiko Mizutani, and Joseph W. Harding. "Focus on Brain Angiotensin III and Aminopeptidase A in the Control of Hypertension." International Journal of Hypertension 2012 (2012): 1–12. http://dx.doi.org/10.1155/2012/124758.
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The classic renin-angiotensin system (RAS) was initially described as a hormone system designed to mediate cardiovascular and body water regulation. The discovery of a brain RAS composed of the necessary functional components (angiotensinogen, peptidases, angiotensins, and specific receptor proteins) independent of the peripheral system significantly expanded the possible physiological and pharmacological functions of this system. This paper first describes the enzymatic pathways resulting in active angiotensin ligands and their interaction with AT1, AT2, and mas receptor subtypes. Recent evidence points to important contributions by brain angiotensin III (AngIII) and aminopeptidases A (APA) and N (APN) in sustaining hypertension. Next, we discuss current approaches to the treatment of hypertension followed by novel strategies that focus on limiting the binding of AngII and AngIII to the AT1receptor subtype by influencing the activity of APA and APN. We conclude with thoughts concerning future treatment approaches to controlling hypertension and hypotension.
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Knox, FG, and JP Granger. "Control of Sodium Excretion: The Kidney Produces Under Pressure." Physiology 2, no. 1 (February 1, 1987): 26–29. http://dx.doi.org/10.1152/physiologyonline.1987.2.1.26.
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Sodium excretion is controlled by an integration of physical, neural, and hormonal regulatory systems. The major systems involved in retention of sodium include the renin-angiotensin-aldosterone system and the sympathetic nervous system. In response to increased sodium intake, the sodium-retaining systems are inhibited and natriuretic hormones are activated. Pressures and flows within the microcirculation of the kidney, in concert with neural and hormonal systems, are important effector mechanisms that work to regulate sodium excretion.
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Lei, Lei, and Yuanjie Mao. "Hormone treatments in congestive heart failure." Journal of International Medical Research 46, no. 6 (February 22, 2018): 2063–81. http://dx.doi.org/10.1177/0300060518761262.
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The common ultimate pathological feature for all cardiovascular diseases, congestive heart failure (CHF), is now considered as one of the main public health burdens that is associated with grave implications. Neurohormonal systems play a critical role in cardiovascular homeostasis, pathophysiology, and cardiovascular diseases. Hormone treatments such as the newly invented dual-acting drug valsartan/sacubitril are promising candidates for CHF, in addition to the conventional medications encompassing beta receptor blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and mineralocorticoid receptor antagonists. Clinical trials also indicate that in CHF patients with low insulin-like growth factor-1 or low thyroid hormone levels, supplemental treatment with growth hormone or thyroid hormone seems to be cardioprotective; and in CHF patients with volume overload the vasopressin antagonists can relieve the symptoms superior to loop diuretics. Furthermore, a combination of selective glucocorticoid receptor agonist and mineralocorticoid receptor antagonist may be used in patients with diuretic resistance. Finally, the potential cardiovascular efficacy and safety of incretin-based therapies, testosterone or estrogen supplementation needs to be prudently evaluated in large-scale clinical studies. In this review, we briefly discuss the therapeutic effects of several key hormones in CHF.
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Pidgeon, G. B., A. M. Richards, M. G. Nicholls, C. J. Charles, M. T. Rademaker, K. L. Lynn, R. R. Bailey, L. K. Lewis, and T. G. Yandle. "Chronic ouabain infusion does not cause hypertension in sheep." American Journal of Physiology-Endocrinology and Metabolism 270, no. 3 (March 1, 1996): E386—E392. http://dx.doi.org/10.1152/ajpendo.1996.270.3.e386.
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Ouabain is claimed to be a hormone of adrenal origin, capable of raising arterial pressure in rats. We infused ouabain in conscious sheep under carefully controlled circumstances to determine its effects on blood pressure, urine electrolytes, and vasoactive hormones. Eight healthy ewes were studied while taking a constant intake of dietary sodium and potassium. Ouabain infusion at 0.25 mg daily over 22 days reduced heart rate and arterial pressure and had no effect on pressor responsiveness to incremental intravenous infusions of angiotensin II. Ouabain induced minor, but statistically significant, decrements in urine volume, urinary sodium excretion, plasma renin and angiotensin II concentrations, and a rise in plasma aldosterone and cortisol. Plasma ouabain levels averaged 1.37 +/- 0.28 nmol/l during ouabain infusion. In conclusion, high-dose chronic ouabain infusion in sheep did not elevate arterial pressure or alter pressor responsiveness to angiotensin II, was antidiuretic and antinatriuretic, and induced minor perturbations in circulating renin, angiotensin II, aldosterone, and cortisol.
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Chanana, Neha, Tsering Palmo, Kavita Sharma, Rahul Kumar, Brian B. Graham, and Qadar Pasha. "Sex-derived attributes contributing to SARS-CoV-2 mortality." American Journal of Physiology-Endocrinology and Metabolism 319, no. 3 (September 1, 2020): E562—E567. http://dx.doi.org/10.1152/ajpendo.00295.2020.
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Epidemiological data in COVID-19 mortality indicate that men are more prone to die of SARS-CoV-2 infection than women, but biological causes for this sexual dimorphism are unknown. We discuss the prospective behavioral and biological differences between the sexes that could be attributed to this sex-based differentiation. The female sex hormones and the immune stimulatory genes, including Toll-like receptors, interleukins, and micro-RNAs present on X-chromosome, may impart lesser infectivity and mortality of the SARS-CoV-2 in females over males. The sex hormone estrogen interacts with the renin-angiotensin-aldosterone system, one of the most critical pathways in COVID-19 infectivity, and modulates the vasomotor homeostasis. Testosterone on the contrary enhances the levels of the two most critical molecules, angiotensin-converting enzyme 2 (ACE2) and the transmembrane protease serine-type 2 (TMPRSS2), transcriptionally and posttranslationally, thereby increasing viral load and delaying viral clearance in men as compared with women. We propose that modulating sex hormones, either by increasing estrogen or antiandrogen, may be a therapeutic option to reduce mortality from SARS-CoV-2.
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Vargas, Félix, Isabel Rodríguez-Gómez, Pablo Vargas-Tendero, Eugenio Jimenez, and Mercedes Montiel. "The renin–angiotensin system in thyroid disorders and its role in cardiovascular and renal manifestations." Journal of Endocrinology 213, no. 1 (October 31, 2011): 25–36. http://dx.doi.org/10.1530/joe-11-0349.
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Thyroid disorders are among the most common endocrine diseases and affect virtually all physiological systems, with an especially marked impact on cardiovascular and renal systems. This review summarizes the effects of thyroid hormones on the renin–angiotensin system (RAS) and the participation of the RAS in the cardiovascular and renal manifestations of thyroid disorders. Thyroid hormones are important regulators of cardiac and renal mass, vascular function, renal sodium handling, and consequently blood pressure (BP). The RAS acts globally to control cardiovascular and renal functions, while RAS components act systemically and locally in individual organs. Various authors have implicated the systemic and local RAS in the mediation of functional and structural changes in cardiovascular and renal tissues due to abnormal thyroid hormone levels. This review analyzes the influence of thyroid hormones on RAS components and discusses the role of the RAS in BP, cardiac mass, vascular function, and renal abnormalities in thyroid disorders.
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Takei, Y., Y. Hasegawa, T. X. Watanabe, K. Nakajima, and N. Hazon. "A novel angiotensin I isolated from an elasmobranch fish." Journal of Endocrinology 139, no. 2 (November 1993): 281–85. http://dx.doi.org/10.1677/joe.0.1390281.
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ABSTRACT It is believed that the renin-angiotensin system evolved initially in primitive bony fishes and is absent from elasmobranchs. We have isolated angiotensin I from the incubates of plasma and kidney extracts of an elasmobranch fish, Triakis scyllia, using eel vasopressor activity as an assay system. Its sequence was determined to be H-Asn-Arg-Pro-Tyr-Ile-His-ProPhe-Gln-Leu-OH. Dogfish angiotensin I is teleost-like because of an asparagine residue at position 1 but it is mammalian-like because of an isoleucine residue at position 5. The unique and most important substitution in dogfish angiotensin I is a proline residue at position 3 which may cause significant changes in its tertiary structure. A glutamine residue at position 9 is also unique among all angiotensin Is sequenced to date. Dogfish angiotensin I is more potent than rat angiotensin I in its vasopressor activity in the dogfish but the relationship is reversed in the rat. Thus angiotensin receptors as well as the hormone molecules appear to have evolved during vertebrate phylogeny. Our findings establish the elasmobranch renin-angiotensin system and support the hypothesis that the renin-angiotensin system is a phylogenetically old hormonal system which plays important roles in cardiovascular and fluid homeostasis. Journal of Endocrinology (1993) 139, 281–285
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Duffy, F. A., and A. M. Wallace. "How large a hormone can be measured by microencapsulated antibody?" Journal of Endocrinology 115, no. 1 (October 1987): 47–51. http://dx.doi.org/10.1677/joe.0.1150047.
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ABSTRACT The size of molecules able to be measured in immunoassays where antibody is encapsulated within semipermeable microcapsules is restricted by the pore size of the membrane. This study was performed to determine the approximate molecular weight cut-off of this membrane. Permeability was assessed by measuring which labelled hormones were able to enter and bind their respective microencapsulated antibody. Hormones with molecular weights of less than 4000 (angiotensin II, thyroxine, 17-hydroxyprogesterone, progesterone, testosterone and androstenedione) passed freely through the pores but larger molecules, with molecular weights in excess of 10 000 (parathyroid hormone, human GH, TSH) could not. Insulin, with a molecular weight of 6000 (approximate minimum diameter 3·5 nm), had restricted entry while the next smallest hormone tested, the 1–34 amino acid portion of parathyroid hormone (molecular weight 4000; diameter 1·8 nm), was able to bind encapsulated antibody, suggesting that the pore diameter is between 1·8 and 3·5 nm. It can now be predicted that the method is able to measure compounds with a diameter within this range and with a molecular weight below 6000. Microcapsules may be useful for improving specificity of assays where a cross-reactant is too large to penetrate the membrane. J. Endocr. (1987) 115, 47–51
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Cattrini, Carlo, Melissa Bersanelli, Maria Maddalena Latocca, Benedetta Conte, Giacomo Vallome, and Francesco Boccardo. "Sex Hormones and Hormone Therapy during COVID-19 Pandemic: Implications for Patients with Cancer." Cancers 12, no. 8 (August 18, 2020): 2325. http://dx.doi.org/10.3390/cancers12082325.
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The novel coronavirus disease 2019 (COVID-19) shows a wide spectrum of clinical presentations, severity, and fatality rates. The reason older patients and males show increased risk of severe disease and death remains uncertain. Sex hormones, such as estradiol, progesterone, and testosterone, might be implicated in the age-dependent and sex-specific severity of COVID-19. High testosterone levels could upregulate transmembrane serine protease 2 (TMPRSS2), facilitating the entry of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) into host cells via angiotensin-converting enzyme 2 (ACE2). Data from patients with prostate cancer treated with androgen-deprivation therapy seem to confirm this hypothesis. Clinical studies on TMPRSS2 inhibitors, such as camostat, nafamostat, and bromhexine, are ongoing. Antiandrogens, such as bicalutamide and enzalutamide, are also under investigation. Conversely, other studies suggest that the immune modulating properties of androgens could protect from the unfavorable cytokine storm, and that low testosterone levels might be associated with a worse prognosis in patients with COVID-19. Some evidence also supports the notion that estrogens and progesterone might exert a protective effect on females, through direct antiviral activity or immune-mediated mechanisms, thus explaining the higher COVID-19 severity in post-menopausal women. In this perspective, we discuss the available evidence on sex hormones and hormone therapy in patients infected with SARS-CoV-2, and we highlight the possible implications for cancer patients, who can receive hormonal therapies during their treatment plans.
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Rossi, Gian Paolo, Livia Lenzini, Brasilina Caroccia, Giacomo Rossitto, and Teresa Maria Seccia. "Angiotensin peptides in the regulation of adrenal cortical function." Exploration of Medicine 2, no. 3 (June 30, 2021): 294–304. http://dx.doi.org/10.37349/emed.2021.00047.
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The adrenal cortex plays a key role in the regulation of metabolism, salt and water homeostasis and sex differentiation by synthesizing glucocorticoid, mineralocorticoid and androgen hormones. Evidence exists that angiotensin II regulates adrenocortical function and it has been contended that angiotensin peptides of the non-canonical branch of the renin angiotensin system (RAS) might also modulate steroidogenesis in adrenals. Thus, the aim of this review is to examine the role of the RAS, and particularly of the angiotensin peptides and their receptors, in the regulation of adrenocortical hormones with particular focus on aldosterone production.
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Forhead, AJ, and AL Fowden. "Effects of thyroid hormones on pulmonary and renal angiotensin-converting enzyme concentrations in fetal sheep near term." Journal of Endocrinology 173, no. 1 (April 1, 2002): 143–50. http://dx.doi.org/10.1677/joe.0.1730143.
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In the sheep fetus, pulmonary and renal concentrations of angiotensin-converting enzyme (ACE) increase towards term in parallel with the prepartum surges in plasma cortisol and tri-iodothyronine (T(3)). The ontogenic change in pulmonary ACE has been shown to be induced, at least in part, by cortisol but the role of the thyroid hormones is unknown. Therefore, this study investigated the effects of thyroid hormones on tissue ACE concentration in fetal sheep during late gestation. Pulmonary and renal ACE concentrations were measured in sheep fetuses after experimental manipulation of thyroid hormone status by fetal thyroidectomy and exogenous hormone infusion. In intact fetuses, pulmonary and renal ACE concentrations increased between 127-132 and 142-145 days of gestation (term 145 +/- 2 days), coincident with the prepartum rises in plasma cortisol and T(3). The ontogenic increment in pulmonary ACE concentration was abolished when the prepartum surge in T(3), but not cortisol, was prevented by fetal thyroidectomy. At 143-145 days, ACE concentration in the lungs and kidneys of the thyroidectomised fetuses were both lower than those in the intact fetuses. In intact fetuses at 127-132 days, pulmonary ACE was upregulated by intravenous infusions of either cortisol (2-3 mg/kg per day) or T(3) (8-12 microg/kg per day) for 5 days. Renal ACE was unaffected by cortisol or T(3) infusion. Therefore, thyroid hormones have an important role in the developmental control of pulmonary and renal ACE concentration in the sheep fetus towards term. In addition, the prepartum rise in plasma T(3) appears to mediate, in part, the maturational effect of cortisol on pulmonary ACE concentration.
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Lipkowitz, M. S., R. D. London, J. C. Beck, and R. G. Abramson. "Hormonal regulation of rat renal proximal tubule brush-border membrane ionic permeability." American Journal of Physiology-Renal Physiology 263, no. 1 (July 1, 1992): F144—F151. http://dx.doi.org/10.1152/ajprenal.1992.263.1.f144.
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The effects on ionic permeability of toxins and hormones that activate or deactivate the guanine nucleotide regulatory (G) proteins that govern adenylate cyclase activity were examined in rat renal proximal tubule cell brush-border membranes. These studies demonstrate that activation of stimulatory G (Gs) proteins by cholera toxin or parathyroid hormone and deactivation of inhibitory (G (Gi) proteins by pertussis toxin result in a selective increase in Cl- permeability relative to that of K+ as determined with the potential-sensitive fluorescent probe 3,3'-dipropylthiadicarbocyanine iodide [diS-C3-(5)]. In contrast, activation of Gi by angiotensin II significantly decreases relative Cl- permeability. The selective increase in relative Cl- permeability induced by parathyroid hormone results in an inside-negative potential in membrane vesicles exposed to an inward NaCl gradient that is of sufficient magnitude to stimulate electrogenic, Na(+)-dependent glucose transport. These data suggest that the relative ionic permeabilities of brush-border membranes are tonically regulated by the opposing effects of hormones that act via Gs or Gi proteins. Changes in membrane potential resulting from this regulation may play an important role in modifying transport in the proximal tubule.
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Weichert, G., and C. A. Courneya. "Control of blood pressure and hindlimb conductance during hemorrhage in conscious renal hypertensive rabbits." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 6 (June 1, 1995): H2302—H2310. http://dx.doi.org/10.1152/ajpheart.1995.268.6.h2302.
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We examined the response to hemorrhage in conscious normotensive and hypertensive rabbits under control conditions and during efferent blockade of 1) the hormones vasopressin (AVP) and angiotensin II (ANG II), 2) the autonomic nervous system, and 3) autonomic and hormonal inputs. We recorded mean arterial pressure, heart rate, and hindlimb conductance. The response to hemorrhage was unchanged with hormonal blockade alone. Blockade of the autonomic nervous system caused a faster rate of blood pressure decline, but the rate of decrease in hindlimb conductance was maintained at control levels. Blocking the autonomic nervous system and the hormones resulted in rapid blood pressure decline and an increase in hindlimb conductance. Although the three types of efferent blockade had a similar pattern of effects in normotensive and hypertensive rabbits, hypertensive rabbits exhibited less cardiovascular support during hemorrhage than normotensive rabbits. During hemorrhage, hypertensive rabbits had an attenuation of hindlimb vasoconstriction, a reduction in the heart rate-mean arterial pressure relationship, and reduced ability to maintain blood pressure compared with normotensive rabbits.
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Overgaard, C. B., J. K. Walker, and D. B. Jennings. "Respiration during acute hypoxia: angiotensin- and vasopressin-receptor blocks." Journal of Applied Physiology 80, no. 3 (March 1, 1996): 810–17. http://dx.doi.org/10.1152/jappl.1996.80.3.810.
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In normoxic conscious dogs, increased angiotensin II (ANG II), or activation (disinhibition) of the renin-angiotensin system by vasopressin (AVP) V1-receptor block, increases ventilation and decreases arterial PCO2. Both hormones can be increased during hypoxia and might modulate ventilatory drive. Six conscious dogs were studied before and during hypocapnic, isocapnic, and hypercapnic hypoxia. To study potential hormonal effects during hypocapnic hypoxia, experiment 1 included three protocols in which 12.8% O2 was breathed for 60 min: protocol 1, control studies without block; protocol 2, AVP V1 receptors were blocked at the onset of hypoxia; and protocol 3, ANG II receptors were blocked 20 min before hypoxia. To study potential effects of acid-base changes during acute hypoxia, experiment 2 included two protocols (with and without AVP V1-receptor block). A 40-min period of hypocapnic hypoxia was followed by two successive 20-min periods with hypoxia maintained but inspired CO2 progressively increased. Neither hormonal block affected respiration during the hypoxic conditions. Unlike normoxia in conscious dogs, during acute hypoxia, respiratory control by ANG II is not modulated by AVP and acid-base effects on receptors do not account for this difference.
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Makary, Samy, Mohamed Abdo, Wael Abdo Hassan, and Mona K. Tawfik. "Angiotensin blockade attenuates diabetic nephropathy in hypogonadal adult male rats." Canadian Journal of Physiology and Pharmacology 97, no. 8 (August 2019): 708–20. http://dx.doi.org/10.1139/cjpp-2018-0572.
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This study examined the effect of the aromatase inhibitor letrozole (0.5 mg/kg) alone or in combination with the angiotensin-receptor blocker valsartan (30 mg/kg) against streptozocin-induced diabetic nephropathy (DN) in hypogonadal (HG) rats for 12 weeks. First, we tested the HG effect on hormone levels, inflammatory cytokines, and oxidative stress in nondiabetic (ND) and diabetic (D) rats. HG was induced with the luteinizing hormone-releasing hormone antagonist cetrorelix (0.71 mg/kg). Diabetes enhanced hormonal hypogonadism and increased inflammation and oxidative stress. Next, experiments examined the effect of early letrozole and valsartan intervention on DN in HG rats. HG-ND and HG-D rats were treated with letrozole alone or in combination with valsartan. HG-D rats developed proteinuria and had increased blood urea nitrogen and creatinine, and histopathological evidence of renal injury, including glomerular hypertrophy and mesangial expansion. Valsartan alone or in combination with letrozole reduced proteinuria, improved renal functions, and reduced diabetes-induced renal angiotensin II. Both agents ameliorated nuclear factor kappa light chain enhancer of activated B cells, interleukin 1β, interleukin 6, and tumor necrosis factor alpha levels. The combination decreased superoxide dismutase, malondialdehyde, and glutathione peroxidase levels, and prevented glomerular hypertrophy. In HG-D rats, valsartan reduced renal collagen IV and transforming growth factor-beta 1, especially when the testosterone level was corrected by letrozole. Thus, normalizing testosterone and inhibiting renal angiotensin II have a renoprotective effect against DN in HG male rats.
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Richards, A. M., G. Tonolo, R. Fraser, J. J. Morton, B. J. Leckie, S. G. Ball, and J. I. S. Robertson. "Diurnal change in plasma atrial natriuretic peptide concentrations." Clinical Science 73, no. 5 (November 1, 1987): 489–95. http://dx.doi.org/10.1042/cs0730489.
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1. Diurnal changes in plasma concentrations of atrial natriuretic peptide (ANP), renin, angiotensin II, aldosterone, Cortisol and antidiuretic hormone were investigated in seven normal volunteers studied under standardized conditions of dietary sodium, posture and physical activity. After completion of the diurnal study serial measurements of these variables were continued during, and on recovery from, a 2 day period of severe sodium depletion. 2. Clear diurnal variations in plasma concentrations of renin, angiotensin II, aldosterone, Cortisol and antidiuretic hormone were observed. 3. Plasma ANP concentrations also varied significantly over 24 h. Values peaked about mid-day and a distinct trough in peptide concentrations occurred in the early evening. However, variations in plasma ANP values were of relatively small amplitude and not clearly independent of modest parallel shifts in sodium balance. 4. Changes in plasma ANP concentrations both within the diurnal study period and during sodium deprivation were closely and positively correlated with concomitant changes in cumulative sodium balance. 5. No simple parallel or reciprocal relationships between plasma concentrations of ANP, on the one hand, and concurrent plasma concentrations of other hormones or in the rate of urinary sodium excretion, on the other, were observed during the 25 h of the diurnal study.
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Lynch, C. J., S. B. Bocckino, P. F. Blackmore, and J. H. Exton. "Calcium-mobilizing hormones and phorbol myristate acetate mediate heterologous desensitization of the hormone-sensitive hepatic Na+/K+ pump." Biochemical Journal 248, no. 3 (December 15, 1987): 807–13. http://dx.doi.org/10.1042/bj2480807.
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The Na+/K+ pump in rat hepatocytes is stimulated in response to Ca2+-mobilizing hormones such as [arginine]vasopressin (AVP), angiotensin II and adrenaline, as well as tumour promoters such as 4 beta-phorbol 12 beta-myristate 13 alpha-acetate (PMA). The ability of these agents to increase cellular contents of diacylglycerol and activate protein kinase C may be necessary to observe this response. In the present work, ouabain-sensitive 86Rb+ uptake was studied in isolated rat hepatocytes to help to explain why stimulation of the Na+/K+ pump by Ca2+-mobilizing hormones and tumour promoters is not temporally sustained relative to other hormone responses. A transient stimulation (3-4 min) of the Na+/K+ pump was observed in hepatocytes exposed to high (10 nM), but not low (0.1 nM), concentrations of AVP. Experiments with the Ca2+ chelator EGTA and the Na+ ionophore monensin indicate that the rapid secondary decrease in Na+/K+-pump activity which occurs after AVP stimulation is not due to changes in cytosolic Ca2+ and Na+ concentrations. When added after the stimulation and rapid decrease in Na+/K+-pump activity induced in hepatocytes by a high concentration of AVP, a second challenge with AVP or PMA failed to stimulate the pump. Similarly, previous exposure of hepatocytes to angiotensin, adrenaline or PMA attenuated the subsequent Na+/K+-pump responses to AVP and PMA. In contrast, previous exposure to AVP had no significant effect on subsequent stimulation of the Na+/K+-pump by monensin, glucagon, forskolin or 8-p-chlorophenylthio cyclic AMP. In addition, exposure to monensin had no effect on subsequent responses to AVP and PMA. These data indicate that high concentrations of Ca2+-mobilizing hormones and PMA result in heterologous desensitization of the hepatic Na+/K+ pump to subsequent stimulation by Ca2+-mobilizing hormones and PMA, but not by cyclic-AMP-dependent agonists or monensin.
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Burgess, W. J., and R. J. Balment. "Plasma atrial natriuretic peptide in vasopressin deficiency the effects of acute water deprivation in rats." Journal of Endocrinology 135, no. 3 (December 1992): 431–38. http://dx.doi.org/10.1677/joe.0.1350431.
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ABSTRACT Plasma concentrations of atrial natriuretic peptide (ANP) and other renally active hormones were measured in Long–Evans (LE) rats and vasopressin-deficient Brattleboro rats with diabetes insipidus (DI) in conditions of water repletion and deprivation, and in DI rats following chronic vasopressin replacement. In water-replete rats, vasopressin deficiency was associated with elevated circulating ANP and angiotensin II (AII) concentrations, while plasma adrenal steroid concentrations were depressed by comparison with LE rats. These differences were fully reversed after 7 days of vasopressin replacement in DI rats to restore normal water turnover. Water deprivation for 4 h had little effect on plasma tonicity or hormone profile in LE rats. In contrast, however, the unreplaced fluid loss during 4-h water deprivation in the DI rat was associated with a marked increase in plasma tonicity evident within 30 min. Plasma ANP concentrations fell substantially to levels below those in LE rats, coincident with a rise in adrenal steroid levels and independent of any clear change in AII. These changes in circulating ANP concentration were directly correlated with changes in plasma Na+ concentration, osmolality and tissue water content in the DI rats, underlining the importance of body fluid status in modulating the secretion of ANP. These data clearly show that plasma ANP concentration is increased in vasopressin deficiency, but emphasize the sensitivity of circulating hormone levels in vasopressin-deficient animals to acute changes in the state of hydration, underscoring the complex and labile interaction between body fluid and hormonal factors involved in the control of ANP secretion. Journal of Endocrinology (1992) 135, 431–438
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Raziq, Hammad, Humaira Fayyaz Khan, Noman Sadiq, Muhammad Athar Abdullah Baig, and Azmat Hayyat. "Association of angiotensin II levels in patients of vasovagal syncope and postural tachycardia syndrome." Professional Medical Journal 26, no. 08 (August 10, 2019): 1218–21. http://dx.doi.org/10.29309/tpmj/2019.26.08.558.
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Syncope occurs as a result of cerebral hypoperfusion. Various neuroendocrine hormones have some role in the pathogenesis of Syncope. Current study was conducted to determine the role of Angiotensin II in pathophysiology of vasovagal syncope (VVS) and Postural tachycardia syndrome (POTS). Study Design: Cross sectional analytical study. Setting: Islamic International Medical College, Rawalpindi and in Electrophysiology department (AFIC). Period: April 2017 to April 2018. Material and Methods: Sample size of this study was comprises of 80 subjects, having 35 cases of VVS and POTS each and 10 controls were also taken. Cases were collected on the basis of Head up tilt test (HUT) result and on their previous history of syncope, then their blood samples were collected and stored. Hormonal analysis of Angiotensin II was performed by ELISA technique. SPSS statistics 21 was used to evaluate result by applying ANOVA test. p value of < 0.05 was considered significant. Result: Analysis of Angiotensin II concentration in Postural tachycardia syndrome, Vasovagal and control group was found 170.93 ± 118.59 pg/ml, 152.16 ± 91.40 pg/ml and 136.93 ± 43.18 pg/ml respectively. In statistical analysis p value was 0.570 which is insignificant. Conclusion: It is concluded that Angiotensin II exerts role in the pathophysiology of VVS and POTS as shown by the difference in the value of Angiotensin II in VVS, POTS and in control group.
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Charbonneau, A., M. Leclerc, and M. G. Brunette. "Effect of angiotensin II on calcium reabsorption by the luminal membranes of the nephron." American Journal of Physiology-Endocrinology and Metabolism 280, no. 6 (June 1, 2001): E928—E936. http://dx.doi.org/10.1152/ajpendo.2001.280.6.e928.
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In the rat and the rabbit, a number of studies have reported the effects of angiotensin II (ANG II) on Na+ reabsorption by the proximal (PT) and distal (DT) convoluted tubules of the kidney. The aim of the present study was to examine the effect of ANG II on Ca2+ uptake by the luminal membranes of the PT and DT of the rabbit. Incubation of PT and DT with 10−12 M ANG II enhanced the initial Ca2+uptake in the two segments. Dose-response experiments revealed, for Ca2+ as well as for Na+ transport, a biphasic action with a maximal effect at 10−12 M. Ca2+transport by the DT luminal membrane presents a dual kinetic. ANG II action influenced the high-affinity Ca2+ channel, increasing maximal velocity from 0.72 ± 0.03 to 0.90 ± 0.05 pmol · μg−1 · 10 s−1( P < 0.05, n = 3) and leaving the Michaelis-Menten constant unchanged. The effect of ANG II was abolished by losartan, suggesting that the hormone is acting through AT1 receptors. In the PT, calphostin C inhibited the effect of the hormone. It is therefore probable that protein kinase C is involved as a messenger. In the DT, however, neither Rp cAMP, calphostin C, nor econazole (a phospholipase A inhibitor) influenced the hormone action. Therefore, the mechanisms involved in the hormone action remain undetermined. Finally, we questioned whether ANG II acts in the same DT segment as does parathyroid hormone on Ca2+transport. The two hormones increased Ca2+ transport, but their actions were not additive, suggesting that they both influence the same channels in the same segment of the distal nephron, i.e., the segment responsible for the high-affinity calcium channel.
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vom Dahl, S., P. Graf, and H. Sies. "Hepatic inositol release upon hormonal stimulation of perfused rat liver." Biochemical Journal 251, no. 3 (May 1, 1988): 843–48. http://dx.doi.org/10.1042/bj2510843.
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A sustained increase in the hepatic release of 3H radioactivity was shown to occur upon hormonal stimulation of perfused rat liver 15-20 h after intraperitoneal injection of 100 microCi of myo-[2-3H]inositol. Hormone-released radioactive material was analysed by t.l.c. and was found to consist predominantly of [3H]inositol, without further metabolites. Vasopressin (14 nM), phenylephrine (1.7 microM), angiotensin II (15 nM), glucagon (0.5 nM) and dibutyryl cyclic AMP (5 microM) exert maximal effects on hepatic inositol efflux after 10-15 min of stimulation. Omission of Ca2+ from the perfusion medium abolishes the hormone-dependent inositol release. LiCl (10 mM) does not significantly affect the basal release of [3H]inositol, but suppresses vasopressin- and angiotensin-triggered inositol release. Inositol efflux induced by glucagon, dibutyryl cyclic AMP and phenylephrine, however, remains essentially unchanged by LiCl infusion. This establishes a further metabolic difference between these two groups of agonists in that stimuli that act through cyclic AMP produce a stimulated outflow of inositol, but apparently without a Li+-sensitive phosphatase being involved in the overall process.
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Cherkasova, O. P., and V. G. Selyatitskaya. "Adrenocortical and renin-angiotensin systems in dynamics of experimental diabetes." Biomeditsinskaya Khimiya 59, no. 2 (2013): 183–91. http://dx.doi.org/10.18097/pbmc20135902183.
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Components of the adrenocortical system (adrenal and blood corticosteroid hormones and hepatic and renal 11b-hydroxysteroid dehydrogenase activity) and also activity of the most important enzyme of the renin-angiotensin system, tissue and blood angiotensin converting enzyme (ACE) have been investigated in dynamics of alloxan diabetes. The study has shown that the initial period of diabetes is characterized by activation of synthesis and secretion of adrenocortical hormones into blood. High blood glucose and glucocorticoid hormones increase activity of the renin-angiotensin system in lungs and decrease ACE secretion into blood. This is accompanied by a decrease of activity of the renin-angiotensin system in kidneys. Subsequent progression of diabetes resulted in impairments of physiologically determined correlations between the components of these systems. Development of experimental diabetes for 30 days was accompanied by sign of a decrease of the adrenal glucocorticoid function regardless of stable impairments of carbohydrate metabolism. Under these conditions increased adrenal and hepatic 11b-hydroxysteroid dehydrogenase activity may be responsible for maintenance of elevated levels of the main glucocorticoid in blood and tissues. Factor analysis revealed impairments in intersystem relationships between the adrenocortical and renin-angiotensin systems in experimental diabetes thus suggesting disintegration of regulatory systems.
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ISAAC, R. Elwyn, A. Tracy WILLIAMS, Mohammed SAJID, Pierre CORVOL, and David COATES. "Cleavage of arginyl-arginine and lysyl-arginine from the C-terminus ofpro-hormone peptides by human germinal angiotensin I-converting enzyme (ACE) and the C-domain of human somatic ACE." Biochemical Journal 328, no. 2 (December 1, 1997): 587–91. http://dx.doi.org/10.1042/bj3280587.
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Mammalian germinal angiotensin I-converting enzyme (gACE) is a single-domain dipeptidyl carboxypeptidase found exclusively in male germ cells, which has almost identical sequence and enzymic properties with the C-domain of the two-domain somatic ACE. Mutant mice that do not express gACE are infertile, suggesting a role for the enzyme in the processing of undefined peptides involved in fertilization. A number of spermatid peptides [e.g. cholecystokinin (CCK) and gastrin] are processed from pro-hormones by endo- and exo-proteolytic cleavages which might generate substrates for gACE. We have shown that peptide hormone intermediates with Lys/Arg-Arg at the C-terminus are high-affinity substrates for human gACE. gACE from human sperm cleaved Arg-Arg from the C-terminus of the CCK5-GRR (GWMDFGRR), a peptide corresponding to the C-terminus of a CCK-gastrin prohormone intermediate. Hydrolysis of CCK5-GRR by recombinant human C-domain ACE was Cl- dependent, with maximal activity achieved in 5-10 mM NaCl at pH 6.4. C-Domain ACE cleaved Lys/Arg-Arg from the C-terminus of dynorphin-(1-7), a pro-TRH peptide KRQHPGKR, and two insect peptides FSPRLGKR and FSPRLGRR. C-Domain ACE displayed high affinity towards all these substrates with Vmax/Km values between 14 and 113 times greater than the Vmax/Km for the conversion of the best known ACE substrate, angiotensin I, into angiotensin II. In conclusion, we have identified a new class of substrates for human gACE, and we suggest that gACE might be an alternative to carboxypeptidase E for the trimming of basic dipeptides from the C-terminus of intermediates generated from pro-hormones by subtilisin-like convertases in human male germ cells.
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Maric, Christine. "Vasoactive Hormones and the Diabetic Kidney." Scientific World JOURNAL 8 (2008): 470–85. http://dx.doi.org/10.1100/tsw.2008.57.
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Diabetic nephropathy is the single most common cause of end-stage renal disease (ESRD) and accounts for significant morbidity and mortality. While the incidence of ESRD increased dramatically in the 1980s and 1990s, the U.S. Renal Data System (USRDS) 2005 Annual Data Report shows that 338 out of every million Americans had kidney failure in 2003, down slightly from 340 per million in 2002. This report shows that the numbers of people developing ESRD have stabilized despite the persistent increase in the number of people diagnosed with type 2 diabetes mellitus (T2DM). These data attest to both the efficacy of the currently available therapeutic regimens for the treatment of ESRD as well as better overall patient care. Unfortunately, these encouraging statistics do not apply to all patients. According to the USRDS report, the most marked ESRD decrease was seen in young Caucasian men (<40 years of age), while in other patient groups, particularly African Americans, ESRD has not changed much at all. These observations suggest that more in-depth studies, addressing specific issues, such as race, are needed to understand the disease process fully in order to create novel therapeutic strategies to eradicate the disease completely in all patient populations.The most commonly used therapeutic treatments for diabetic nephropathy are angiotensin-converting enzyme (ACE) inhibitors and angiotensin II (Ang II) receptor blockers (ARBs), implicating the importance of the renin-angiotensin-aldosterone system (RAAS) in the pathophysiology of diabetic nephropathy. The RAAS is not the only vasoactive hormonal system that is involved in the disease process. Over the past decade, studies have suggested that other vasoactive hormones, including endothelin, urotensin II, and the kallikrein-kinin system (KKS), are instrumental in mediating structural and functional alterations in the renal vasculature and parenchyma, leading to the development and progression of diabetic nephropathy. This review will summarize our current understanding of the contribution of vasoactive hormones in the pathophysiology of diabetic nephropathy with specific emphasis on the RAAS, especially the more recently identified components of this hormonal pathway.
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Charles, Christopher J., Miriam T. Rademaker, and A. Mark Richards. "Urocortin 1 modulates the neurohumoral response to acute nitroprusside-induced hypotension in sheep." Clinical Science 112, no. 9 (April 2, 2007): 485–91. http://dx.doi.org/10.1042/cs20060303.
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In addition to haemodynamic actions, Ucn1 (urocortin 1) has been reported to affect a number of hormonal systems; however, it remains unclear whether Ucn1 modulates circulating hormones under physiological conditions. Accordingly, in the present study, we have examined the effects of Ucn1 on haemodynamics, hormones and renal indices in normal conscious sheep subjected to a nitroprusside-induced hypotensive stimulus designed to alter hormonal levels within the physiological range. Ucn1 administration did not alter the haemodynamic response to nitroprusside-induced hypotension. However, compared with the rise observed on the control day, plasma ANP (atrial natriuretic peptide; P=0.043), BNP (brain natriuretic peptide; P=0.038) and endothelin-1 (P=0.011) levels were reduced following Ucn1 administration. Associated with this significant reduction in natriuretic peptides, the increase in urinary sodium output associated with rising pressures post-nitroprusside was abolished following Ucn1 administration (P=0.048). Ucn1 had no significant effect on the response of hormones of the renin–angiotensin–aldosterone system or the hypothalamo–pituitary–adrenal axis. In conclusion, Ucn1, administered at physiologically relevant levels during nitroprusside-induced hypotension, attenuates the secretion/release of endothelin-1 and the cardiac natriuretic peptides ANP and BNP. Suppression of ANP and BNP probably led to an attenuated natriuretic response to recovery from acute hypotension. The threshold for the action of Ucn1 on the natriuretic peptides and endothelin-1 appears to be below that of other actions of Ucn1.
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Mizutani, S., K. Goto, K. Mizuno, A. Itakura, O. Kurauchi, F. Kikkawa, and Y. Tomoda. "Interaction between pregnancy-induced bioactive peptides and the placental proteases." Reproduction, Fertility and Development 7, no. 6 (1995): 1431. http://dx.doi.org/10.1071/rd9951431.
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Studies have shown that placental proteases metabolize vasoactive peptides, possibly derived from the fetus, and protect the exchange of peptide hormones across the placenta in order to maintain feto-placental homeostasis. Changes in maternal serum protease activities were useful for monitoring pre-eclampsia and predicting the onset of labour. The study showed that possible role of oxytocinase in the maintenance of gestation and the possible involvement of angiotensinase in the attenuated pressor responses to angiotensin II during pregnancy, respectively. In addition, the ratio of peak systolic over least diastolic pressure (S/D) of uterine or umbilical artery assessed by the Doppler technique was closely correlated with the concentrations of maternal serum proteases in pre-eclampsia, which suggested that placental proteases might control utero-placental circulation via the regulation of concentrations of vasoactive peptides in uteroplacental circulation.
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Sanchez-Bueno, A., and P. H. Cobbold. "Agonist-specificity in the role of Ca2+-induced Ca2+ release in hepatocyte Ca2+ oscillations." Biochemical Journal 291, no. 1 (April 1, 1993): 169–72. http://dx.doi.org/10.1042/bj2910169.
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Ca(2+)-mobilizing hormones induce oscillations in the cytoplasmic concentration of free Ca2+ (‘free Ca’) (spikes) in many cells. In hepatocytes the frequency of spiking depends on agonist dose, but the time course of an individual spike does not change with agonist concentration. Interestingly, the time course of individual spikes does depend on the hormone species, but the cellular mechanisms underlying this agonist-specificity are not understood. Here we show that ryanodine, which blocks the muscle Ca2+ channel responsible for Ca(2+)-induced Ca2+ release (‘CICR’) in the open conformation, has almost no effect on phenylephrine-induced spikes, but does, in contrast, inhibit vasopressin- or angiotensin II-induced spikes. We also show that ryanodine has no effect either on the increase in frequency or on the elevated peak free Ca induced by increased cyclic AMP on phenylephrine spikes. In contrast, ryanodine truncates the prolonged falling phases of spikes induced by vasopressin or angiotensin II in the presence of elevated cyclic AMP. A working hypothesis is proposed in which vasopressin- or angiotensin II-induced spikes consist of an Ins(1,4,5)P3-mediated symmetrical spike, identical in time course and mechanism with those induced by phenylephrine, followed by a ‘tail’ that represents CICR. The data hint at the existence of a novel signalling pathway.
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Fry, Mark, and Alastair V. Ferguson. "Ghrelin: Central Nervous System Sites of Action in Regulation of Energy Balance." International Journal of Peptides 2010 (February 15, 2010): 1–8. http://dx.doi.org/10.1155/2010/616757.
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Ghrelin, a peptide hormone secreted by the stomach, has been shown to regulate energy homeostasis by modulating electrical activity of neurons in the central nervous system (CNS). Like many circulating satiety signals, ghrelin is a peptide hormone and is unable to cross the blood-brain barrier without a transport mechanism. In this review, we address the notion that the arcuate nucleus of the hypothalamus is the only site in the CNS that detects circulating ghrelin to trigger orexigenic responses. We consider the roles of a specialized group of CNS structures called the sensory circumventricular organs (CVOs), which are not protected by the blood-brain barrier. These areas include the subfornical organ and the area postrema and are already well known to be key areas for detection of other circulating hormones such as angiotensin II, cholecystokinin, and amylin. A growing body of evidence indicates a key role for the sensory CVOs in the regulation of energy homeostasis.
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Turovsky, Egor A., Maria V. Turovskaya, and Vladimir V. Dynnik. "Deregulation of Ca2+-Signaling Systems in White Adipocytes, Manifested as the Loss of Rhythmic Activity, Underlies the Development of Multiple Hormonal Resistance at Obesity and Type 2 Diabetes." International Journal of Molecular Sciences 22, no. 10 (May 12, 2021): 5109. http://dx.doi.org/10.3390/ijms22105109.
Full textAbstract:
Various types of cells demonstrate ubiquitous rhythmicity registered as simple and complex Ca2+-oscillations, spikes, waves, and triggering phenomena mediated by G-protein and tyrosine kinase coupled receptors. Phospholipase C/IP3-receptors (PLC/IP3R) and endothelial NO-synthase/Ryanodine receptors (NOS/RyR)–dependent Ca2+ signaling systems, organized as multivariate positive feedback generators (PLC-G and NOS-G), underlie this rhythmicity. Loss of rhythmicity at obesity may indicate deregulation of these signaling systems. To issue the impact of cell size, receptors’ interplay, and obesity on the regulation of PLC-G and NOS-G, we applied fluorescent microscopy, immunochemical staining, and inhibitory analysis using cultured adipocytes of epididumal white adipose tissue of mice. Acetylcholine, norepinephrine, atrial natriuretic peptide, bradykinin, cholecystokinin, angiotensin II, and insulin evoked complex [Ca2+]i responses in adipocytes, implicating NOS-G or PLC-G. At low sub-threshold concentrations, acetylcholine and norepinephrine or acetylcholine and peptide hormones (in paired combinations) recruited NOS-G, based on G proteins subunits interplay and signaling amplification. Rhythmicity was cell size- dependent and disappeared in hypertrophied cells filled with lipids. Contrary to control cells, adipocytes of obese hyperglycemic and hypertensive mice, growing on glucose, did not accumulate lipids and demonstrated hormonal resistance being non responsive to any hormone applied. Preincubation of preadipocytes with palmitoyl-L-carnitine (100 nM) provided accumulation of lipids, increased expression and clustering of IP3R and RyR proteins, and partially restored hormonal sensitivity and rhythmicity (5–15% vs. 30–80% in control cells), while adipocytes of diabetic mice were not responsive at all. Here, we presented a detailed kinetic model of NOS-G and discussed its control. Collectively, we may suggest that universal mechanisms underlie loss of rhythmicity, Ca2+-signaling systems deregulation, and development of general hormonal resistance to obesity.
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Noguchi, A., P. A. Jett, and A. H. Gold. "cAMP-independent stimulation of glycogen phosphorylase in newborn rat hepatocytes." American Journal of Physiology-Endocrinology and Metabolism 248, no. 5 (May 1, 1985): E560—E566. http://dx.doi.org/10.1152/ajpendo.1985.248.5.e560.
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Postnatal development of glycogen phosphorylase activation by the cAMP-independent pathway was examined in isolated rat hepatocytes from control and propylthiouracil-treated congenital hypothyroid rat pups. At 5 days postnatum there was complete phosphorylase activation by beta-adrenergic stimulation, glucagon, and the calcium ionophore A23187, but no activation by alpha-adrenergic stimulation. Activation of phosphorylase by angiotensin or vasopressin was less than in hepatocytes from adult rats (P less than 0.01). At 28 days postnatum activation by all of these hormones was complete. In the propylthiouracil-treated group hormone responsiveness was similar to the control at 5 days postnatum. However, alpha-adrenergic (P less than 0.025), angiotensin, and vasopressin (P less than 0.05) activation was decreased at 28 days postnatum, and beta-adrenergic, glucagon, and A23187 activation was complete. The attenuated responses were restored by thyroxine replacement from 15 days postnatum. [32P]Pi incorporation into phosphatidylinositol by epinephrine and vasopressin in 28-day propylthiouracil-treated rats was lower than the control (P less than 0.01). We speculate that the diminished phosphorylase response of hepatocytes to alpha-adrenergic, vasopressin, or angiotensin stimuli in the early neonatal period could be related to low receptor numbers and the weaker phosphoinositide response during this period. Also, the depressed phosphorylase response to alpha-adrenergic, vasopressin, and angiotensin stimulation in congenital hypothyroidism at 28 days postnatum could be related to a decrease in number of plasma membrane receptors for these agonists.
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Hughson, R. L., A. Maillet, G. Gauquelin, P. Arbeille, Y. Yamamoto, and C. Gharib. "Investigation of hormonal effects during 10-h head-down tilt on heart rate and blood pressure variability." Journal of Applied Physiology 78, no. 2 (February 1, 1995): 583–96. http://dx.doi.org/10.1152/jappl.1995.78.2.583.
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Head-down tilt (HDT) bed rest was used in this study to achieve physiological manipulation of the plasma concentrations of atrial natriuretic peptide (ANP) and the hormones of the renin-angiotensin system. The purpose of this was to achieve a parallel with previous animal experiments in which blockade of the renin-angiotensin system caused significant increases in low-frequency spectral power of heart rate variability, presumably as a consequence of increased blood pressure variability, although this was not measured in these animal experiments. Eight healthy young men completed 10 h of seated control and 6 degrees HDT. To gain a more complete understanding of the interactions between hormonal and neural factors involved in cardiovascular regulation, we measured heart rate, systolic and diastolic pressure variabilities, plasma hormone concentrations, and blood flow to selected vascular beds by pulsed Doppler. Resting R-R interval was not significantly different between seated and HDT tests. Stroke volume and cardiac output were elevated in the first 1–2 h of HDT (P < 0.05), whereas each of systolic (P < 0.01) and diastolic (P < 0.0001) pressures was lower during HDT. Plasma ANP increased as much as 70% during HDT (P < 0.0001). Total variability in each of R-R interval and diastolic blood pressure was reduced during HDT (P < 0.001). Thus, at a time when plasma renin activity was decreased as much as 40% (P < 0.0001), there was in fact a decrease in the variability of R-R interval and diastolic blood pressure in contrast to the hypothesized increase such as found in previous animal experimentation. The data were compatible with tighter autonomic regulation of heart rate about the ideal mean value during HDT.
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Mehay, Darren, Yuval Silberman, and Amy C. Arnold. "The Arcuate Nucleus of the Hypothalamus and Metabolic Regulation: An Emerging Role for Renin–Angiotensin Pathways." International Journal of Molecular Sciences 22, no. 13 (June 30, 2021): 7050. http://dx.doi.org/10.3390/ijms22137050.
Full textAbstract:
Obesity is a chronic state of energy imbalance that represents a major public health problem and greatly increases the risk for developing hypertension, hyperglycemia, and a multitude of related pathologies that encompass the metabolic syndrome. The underlying mechanisms and optimal treatment strategies for obesity, however, are still not fully understood. The control of energy balance involves the actions of circulating hormones on a widely distributed network of brain regions involved in the regulation of food intake and energy expenditure, including the arcuate nucleus of the hypothalamus. While obesity is known to disrupt neurocircuits controlling energy balance, including those in the hypothalamic arcuate nucleus, the pharmacological targeting of these central mechanisms often produces adverse cardiovascular and other off-target effects. This highlights the critical need to identify new anti-obesity drugs that can activate central neurocircuits to induce weight loss without negatively impacting blood pressure control. The renin–angiotensin system may provide this ideal target, as recent studies show this hormonal system can engage neurocircuits originating in the arcuate nucleus to improve energy balance without elevating blood pressure in animal models. This review will summarize the current knowledge of renin–angiotensin system actions within the arcuate nucleus for control of energy balance, with a focus on emerging roles for angiotensin II, prorenin, and angiotensin-(1–7) pathways.
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Lobo, M. V., and E. T. Marusic. "Effect of angiotensin II, ATP, and ionophore A23187 on potassium efflux in adrenal glomerulosa cells." American Journal of Physiology-Endocrinology and Metabolism 250, no. 2 (February 1, 1986): E125—E130. http://dx.doi.org/10.1152/ajpendo.1986.250.2.e125.
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Angiotensin II stimulus on perifused bovine adrenal glomerulosa cells elicited an increase in 86Rb efflux from cells previously equilibrated with the radioisotope. When 45Ca fluxes were measured under similar conditions, it was observed that Ca and Rb effluxes occurred within the first 30 s of the addition of the hormone and were independent of the presence of external Ca. The 86Rb efflux due to angiotensin II was inhibited by quinine and apamin. The hypothesis that the angiotensin II response is a consequence of an increase in the K permeability of the glomerulosa cell membrane triggered by an increase in cytosolic Ca is supported by the finding that the divalent cation ionophore A23187 also initiated 86Rb or K loss (as measured by an external K electrode). This increased K conductance was also seen with 10(-4) M ATP. Quinine and apamin greatly reduced the effect of ATP or A23187 on 86Rb or K release in adrenal glomerulosa cells. The results suggest that Ca-dependent K channels or carriers are present in the membranes of bovine adrenal glomerulosa cells and are sensitive to hormonal stimulus.
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Fujita, Nobuya, Yusuke Furukawa, Naoki Itabashi, Yasushi Tsuboi, Michio Matsuda, Koji Okada, and Toshikazu Saito. "Failure of cdc2 promoter activation and G2/M transition by ANG II and AVP in vascular smooth muscle cells." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 2 (August 1, 1999): H515—H523. http://dx.doi.org/10.1152/ajpheart.1999.277.2.h515.
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The physiological role of the vasoconstrictive hormones arginine vasopressin (AVP) and angiotensin II (ANG II) in the development of vascular hyperplasia is still unclear. We examined the effects of these hormones on cell cycle regulation of cultured rat vascular smooth muscle cells (VSMC). AVP and ANG II were able to induce G1/S transition and DNA synthesis in serum-starved quiescent VSMC but failed to promote further progression into G2/M phases. AVP and ANG II enhanced the expression and activity of cdk2, cyclin E, and proliferating cell nuclear antigen but did not induce expression of cdc2/cyclin B complex, a critical regulator of G2/M transition. The failure of cdc2 mRNA induction was found to be caused by a defect in cdc2 promoter activation. Binding of free E2F-1 to the cdc2 promoter did not occur in hormone-treated VSMC, which may account for the defective induction of cdc2. The absence of cdc2 promoter activation and G2/M transition may be important for the prevention of hyperplasia under physiological conditions but underlies the hypertrophy of VSMC.
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Jayaraman, Anusha, Jenna C. Carroll, Todd E. Morgan, Sharon Lin, Liqin Zhao, Jason M. Arimoto, M. Paul Murphy, et al. "17β-Estradiol and Progesterone Regulate Expression of β-Amyloid Clearance Factors in Primary Neuron Cultures and Female Rat Brain." Endocrinology 153, no. 11 (November 1, 2012): 5467–79. http://dx.doi.org/10.1210/en.2012-1464.
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Abstract The accumulation of β-amyloid protein (Aβ) is a key risk factor in the development of Alzheimer's disease. The ovarian sex steroid hormones 17β-estradiol (E2) and progesterone (P4) have been shown to regulate Aβ accumulation, although the underlying mechanism(s) remain to be fully elucidated. In this study, we investigate the effects of E2 and P4 treatment on the expression levels of Aβ clearance factors including insulin-degrading enzyme, neprilysin, endothelin-converting enzyme 1 and 2, angiotensin-converting enzyme, and transthyretin, both in primary neuron cultures and female rat brains. Our results show that E2 and P4 affect the expression levels of several Aβ clearance factors in dose- and time-dependent manners. Most notably, expression of insulin-degrading enzyme is significantly increased by both hormones in cultured neurons and in vivo and is inversely associated with the soluble Aβ levels in vivo. These findings further define sex steroid hormone actions involved in regulation of Aβ, a relationship potentially important to therapeutic approaches aimed at reducing risk of Alzheimer's disease.
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Medina, Daniela, and Amy C. Arnold. "Angiotensin-(1-7): Translational Avenues in Cardiovascular Control." American Journal of Hypertension 32, no. 12 (September 6, 2019): 1133–42. http://dx.doi.org/10.1093/ajh/hpz146.
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Abstract Despite decades of research and numerous treatment approaches, hypertension and cardiovascular disease remain leading global public health problems. A major contributor to regulation of blood pressure, and the development of hypertension, is the renin-angiotensin system. Of particular concern, uncontrolled activation of angiotensin II contributes to hypertension and associated cardiovascular risk, with antihypertensive therapies currently available to block the formation and deleterious actions of this hormone. More recently, angiotensin-(1–7) has emerged as a biologically active intermediate of the vasodilatory arm of the renin-angiotensin system. This hormone antagonizes angiotensin II actions as well as offers antihypertensive, antihypertrophic, antiatherogenic, antiarrhythmogenic, antifibrotic and antithrombotic properties. Angiotensin-(1–7) elicits beneficial cardiovascular actions through mas G protein-coupled receptors, which are found in numerous tissues pivotal to control of blood pressure including the brain, heart, kidneys, and vasculature. Despite accumulating evidence for favorable effects of angiotensin-(1–7) in animal models, there is a paucity of clinical studies and pharmacokinetic limitations, thus limiting the development of therapeutic agents to better understand cardiovascular actions of this vasodilatory peptide hormone in humans. This review highlights current knowledge on the role of angiotensin-(1–7) in cardiovascular control, with an emphasis on significant animal, human, and therapeutic research efforts.