Vasopressin-Stimulated Release of Atriopeptin: Endocrine Antagonists in Fluid Homeostasis

Manning, Pamela T.; Schwartz, David B.; Katsube, Nobuo; Holmberg, Sandra; Needleman, Philip

doi:10.1126/science.2990050

Cited by 314 publications

(139 citation statements)

References 22 publications

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“…It has been shown that ANP secretion increases in response to vasopressin analogs and pressor agents. 33 High activity in the sympathetic nervous system decreases RBF by alpha-1-adrenergic receptors and increases sodium reabsorption and renin secretion by beta-1-adrenergic receptors in the juxtaglomerular cells. 34,35 The decrease in norepinephrine therefore contributes to the increased perfusion and increased sodium excretion.…”

Section: Discussionmentioning

confidence: 99%

Terlipressin improves renal function in patients with cirrhosis and ascites without hepatorenal syndrome

et al. 2007

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Patients with advanced cirrhosis and ascites are characterized by circulatory dysfunction with splanchnic vasodilatation and renal vasoconstriction, which often lead to ascites. The vasoconstrictor terlipressin improves renal function in hepatorenal syndrome (HRS). The aim of this study was to evaluate if terlipressin also improves renal function in patients with ascites without HRS. Twenty-three patients with cirrhosis participated; 15 with nonrefractory ascites were randomized to either terlipressin (N group, n ‫؍‬ 11) or a placebo (P group, n ‫؍‬ 4), and 8 had refractory ascites and received terlipressin (R group). The glomerular filtration rate (GFR), sodium clearance (C Na ), lithium clearance (C Li ), osmolal clearance (C Osm ), and urine sodium concentration (U Na ) were assessed before and after the injection of 2 mg of terlipressin or the placebo. GFR increased in the N group (69 ؎ 19 versus 92 ؎ 25 mL/min, P < 0.005) and in the R group (31 ؎ 19 versus 41 ؎ 31 mL/min, P < 0.05) after terlipressin. In the N group, terlipressin induced an increase in C Na (0.89 ؎ 0.21 versus 1.52 ؎ 1.45 mL/min, P < 0.05), C Li (17.3 ؎ 8.9 versus 21.5 ؎ 11.6 mL/min, P < 0.05), and C Osm (2.10 ؎ 0.81 versus 3.06 ؎ 2.0 mL/min, P < 0.05). In the R group, terlipressin induced an increase in C Na (0.11 ؎ 0.18 versus 0.35 ؎ 0.40 mL/min, P < 0.05) and C Li (5.5 ؎ 4.2 versus 9.5 ؎ 8.55 mL/min, P < 0.05). U Na increased in both groups after terlipressin (P < 0.005). Plasma norepinephrine (P < 0.05) and renin (P < 0.05) decreased after terlipressin. All parameters remained unchanged after the placebo. A scites is a serious complication of cirrhosis, occurring in about 50% of patients within 10 years after diagnosis, and it is associated with 50% mortality in 2 years. 1,2 Patients with ascites have hyperdynamic circulation, which is characterized by peripheral and splanchnic arterial vasodilatation and reduced arterial blood pressure and systemic vascular resistance. 3 Portal hypertension and splanchnic vasodilatation are major factors in the development of ascites. 4,5 Secondary to vasodilatation, vasoactive hormones, such as the reninangiotensin-aldosterone system and the sympathetic nervous system, are activated. This leads to renal vasoconstriction and reduced renal perfusion and filtration pressure. The current standard treatment of ascites involves diuretics and paracentesis, which are not designed to improve the underlying pathophysiology. The changes in the renal handling of water and salt seem to develop stepwise from a stage that can be controlled by diuretics to a stage refractory to diuretics and finally to full-blown renal failure, which is known as hepatorenal syndrome (HRS) type 1. 6 Several clinical studies have evaluated the efficacy of the long-term administration of terlipressin [a vasopressin 1 (V1) receptor agonist] in patients with HRS, [7][8][9][10][11][12][13] and there is evidence that terlipressin may improve renal

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Section: Discussionmentioning

confidence: 99%

Terlipressin improves renal function in patients with cirrhosis and ascites without hepatorenal syndrome

et al. 2007

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“…A direct role of the adenohypophysis has not been clearly demonstrated and there is evidence that our surgical procedure to induce diabetes insipidus spares the adenohypophysis (see methods of Baisset & Montastruc, 1957). On the contrary, vasopressin has been shown to stimulate atrial natriuretic factor release directly or secondarily to its effect on blood volume (Manning et al, 1985;Ogawa et al, 1986). Therefore, in our control animals, at least three different factors could explain the rise in atrial natriuretic factor plasma levels: the rises in blood pressure, noradrenaline and vasopressin plasma levels.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular effects of central injection of acetylcholine in anaesthetized dogs: a role for vasopressin release

Rascol

Montastruc

Gauquelin³

et al. 1990

British J Pharmacology

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1 The effect of an intracisternal injection of 20Ougkg-' of acetylcholine was studied on systolic and diastolic blood pressures, heart rate, and plasma levels of noradrenaline, adrenaline, vasopressin, plasma renin activity and atrial natriuretic factor in chloralose-anaesthetized dogs, 8 of which were normal and 7 with diabetes insipidus (deprived of vasopressin secretion by surgical lesion of the hypothalamoneurohypophysial system). 2 Acetylcholine significantly increased systolic and diastolic blood pressures in both groups of animals. However, the rise in blood pressure was significantly shorter lived in the dogs with diabetes insipidus. 3 Acetylcholine significantly increased plasma levels of noradrenaline but not adrenaline in control animals and in dogs with diabetes insipidus. Noradrenaline and adrenaline responses after acetylcholine were not different in the two groups of animals. 4 Acetylcholine induced a significant increase in vasopressin plasma levels only in control animals while in dogs with diabetes insipidus vasopressin remained at nearly undetectable levels. 5Acetylcholine significantly increased atrial natiuretic factor plasma levels only in control dogs. 6 Although plasma renin activity increased in both groups of animals after the i.c. injection of acetylcholine, this change was not significant in any group. 7 These results suggest that, in the anaesthetized dog, the central injection of acetylcholine induces a rise in blood pressure through both an increase in sympathetic outflow and a release of vasopressin.

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“…Little is known about other factors that may influence ANP release. Adrenaline, noradrenaline, vasopressin and other agents have been shown to increase the release of ANP into the circulation both in man and experimental animals, probably via their pressor effects (Manning et al, 1985;Uehlinger et al, 1986;Ruskoaho et al, 1987;Sanfield et al, 1987). In addition, clonidine, an a2-agonist, has been shown to increase plasma levels of ANP in conscious rats (Baranowska et al, 1987a,b,c).…”

Section: Introductionmentioning

confidence: 99%

The effect of medetomidine, an α₂‐adrenoceptor agonist, on plasma atrial natriuretic peptide levels, haemodynamics and renal excretory function in spontaneously hypertensive and Wistar‐Kyoto rats

Ruskoaho

Leppäluoto

1989

British J Pharmacology

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1 The effects of the selective a2-adrenoceptor agonist, medetomidine, were assessed on plasma levels of immunoreactive atrial natriuretic peptide (IR-ANP), haemodynamics and on urine water and solute excretion in conscious, chronically cannulated, 7 month-old spontaneously hypertensive (SHR) and age-matched Wistar-Kyoto (WKY) rats, in order to examine the role of a2-adrenoceptors in the control of ANP secretion.2 A 60min i.v. infusion of medetomidine (0.2 or 0.6.ugkg-1min-') decreased heart rate dosedependently in both strains. Medetomidine infusion (0.6pgkg-1min-1) resulted in an increase in mean arterial pressure in WKY, whereas both doses decreased blood pressure in SHR. There was a slight increase in the right atrial pressure in both strains (WKY: + 1.18 + 0.26 mmHg; SHR: +1.64 + 0.64 mmHg, NS) in response to infusion of 0.6 pg kg-min-of medetomidine. 3 No differences were found in resting plasma IR-ANP levels between WKY (114 + 8 pg ml-, n = 19) and SHR (117 ± 10pgmlP, n = 21). Infusion of equibradycardic doses of medetomidine increased dose-dependently plasma IR-ANP levels in WKY, but did not affect the plasma IR-ANP concentration in SHR rats. 4 Despite the different effect of medetomidine on ANP release in WKY and SHR rats, i.v. administration of medetomidine affected renal excretory functions similarly in both strains; urine flow and sodium excretion increased and urine osmolality decreased significantly, while there was no consistent change in urinary potassium excretion. Urine osmolality decreased to hypo-osmotic levels during the infusion of 0.6 yg kg-1 min1 of medetomidine, suggesting a possible interaction between a2-adrenoceptor stimulation and the vasopressin system. 5 These results show that the a2-adrenoceptor agonist medetomidine increased plasma levels of ANP in WKY rats, probably through an increase in mean arterial and right atrial pressures, whereas the SHR had attenuated ANP release to a2-adrenoceptor stimulation. Our findings, that medetomidine caused marked natriuretic and diuretic effects in both strains and that these effects on the excretory functions of the kidneys were not related to changes in plasma levels of IR-ANP, demonstrate that changes in plasma ANP levels alone do not account for the diuretic and natriuretic effect of x2-agonists.

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Vasopressin-Stimulated Release of Atriopeptin: Endocrine Antagonists in Fluid Homeostasis

Cited by 314 publications

References 22 publications

Terlipressin improves renal function in patients with cirrhosis and ascites without hepatorenal syndrome

Terlipressin improves renal function in patients with cirrhosis and ascites without hepatorenal syndrome

Cardiovascular effects of central injection of acetylcholine in anaesthetized dogs: a role for vasopressin release

The effect of medetomidine, an α₂‐adrenoceptor agonist, on plasma atrial natriuretic peptide levels, haemodynamics and renal excretory function in spontaneously hypertensive and Wistar‐Kyoto rats

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Vasopressin-Stimulated Release of Atriopeptin: Endocrine Antagonists in Fluid Homeostasis

Cited by 314 publications

References 22 publications

Terlipressin improves renal function in patients with cirrhosis and ascites without hepatorenal syndrome

Terlipressin improves renal function in patients with cirrhosis and ascites without hepatorenal syndrome

Cardiovascular effects of central injection of acetylcholine in anaesthetized dogs: a role for vasopressin release

The effect of medetomidine, an α2‐adrenoceptor agonist, on plasma atrial natriuretic peptide levels, haemodynamics and renal excretory function in spontaneously hypertensive and Wistar‐Kyoto rats

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The effect of medetomidine, an α₂‐adrenoceptor agonist, on plasma atrial natriuretic peptide levels, haemodynamics and renal excretory function in spontaneously hypertensive and Wistar‐Kyoto rats