Angiotensin II-stimulated secretion of arginine vasopressin is inhibited by atrial natriuretic peptide in humans

2011 ◽  
Vol 300 (3) ◽  
pp. R624-R629 ◽  
Author(s):  
Toshiyoshi Matsukawa ◽  
Takenori Miyamoto
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Arginine Vasopressin ◽  
Intravenous Infusion ◽  
Ang Ii ◽  
Blood Pressure Elevation ◽  
Arterial Blood ◽  
Atrial Natriuretic

We investigated the effect of the intravenous infusion of atrial natriuretic peptide (ANP) on the response of plasma arginine vasopressin (AVP) levels to intravenous infusion of angiotensin II (ANG II) in healthy individuals. Intravenous infusion of ANP (10 ng·kg−1·min−1) slightly but significantly decreased plasma AVP levels, while intravenous infusion of ANG II (10 ng·kg−1·min−1) resulted in slightly increased plasma AVP levels. ANG II infused significant elevations in arterial blood pressure and central venous pressure (CVP). Because the elevation in blood pressure could have potentially inhibited AVP secretion via baroreceptor reflexes, the effect of ANG II on blood pressure was attenuated by the simultaneous infusion of nitroprusside. ANG II alone produced a remarkable increase in plasma AVP levels when infused with nitroprusside, whereas the simultaneous ANP intravenous infusion (10 ng·kg−1·min−1) abolished the increase in plasma AVP levels induced by ANG II when blood pressure elevation was attenuated by nitroprusside. Thus, ANG II increased AVP secretion and ANP inhibited not only basal AVP secretion but also ANG II-stimulated AVP secretion in humans. These findings support the hypothesis that circulating ANP modulates AVP secretion, in part, by antagonizing the action of circulating ANG II.

Elevated angiotensin II and vasopressin in primary hyperparathyroidism. Angiotensin II infusion studies before and after removal of the parathyroid adenoma

1989 ◽  
Vol 120 (3) ◽  
pp. 362-368 ◽  
Author(s):  
B. Jespersen ◽  
E. B. Pedersen ◽  
P. Charles ◽  
H. Danielsen ◽  
H. Juhl
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Primary Hyperparathyroidism ◽  
Atrial Natriuretic Peptide ◽  
Creatinine Clearance ◽  
Natriuretic Peptide ◽  
Arginine Vasopressin ◽  
Plasma Levels ◽  
Before And After ◽  
Atrial Natriuretic

Abstract. In order to evaluate the role of calcium metabolism in blood pressure regulation, 15 patients with primary hyperparathyroidism and 9 healthy control subjects were studied before and during angiotensin II infusion. The patients were re-investigated 2–5 months after removal of the parathyroid adenoma. Blood pressure, plasma levels of angiotensin II, aldosterone, arginine vasopressin, and atrial natriuretic peptide, and creatinine clearance were determined. Blood pressure and the blood pressure response to angiotensin II infusion were both the same before and after the operation. Angiotensin II and arginine vasopressin during basal conditions were significantly higher before than after the operation (angiotensin II: 17 (median) to 10 pmol/l, P < 0.02; arginine vasopressin: 2.9 to 1.9 pmol/l, P < 0.01), whereas aldosterone, atrial natriuretic peptide, and creatinine clearance were unchanged. During angiotensin II infusion, aldosterone, arginine vasopressin, and atrial natriuretic peptide increased to approximately the same levels before and after the operation. Blood pressure was not correlated to any of the hormones measured. Thus, patients with primary hyperparathyroidism have elevated plasma levels of angiotensin II and arginine vasopressin which may be compensatory phenomena counteracting volume depletion owing to a decreased renal concentrating ability induced by hypercalcemia, and owing to PTH-induced inhibition of renal sodium reabsorption.

Effects of angiotensin II and atrial natriuretic peptide alone and in combination on urinary water and electrolyte excretion in man

1988 ◽  
Vol 74 (4) ◽  
pp. 419-425 ◽  
Author(s):  
J. McMurray ◽  
A. D. Struthers
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Normal Male ◽  
Urinary Flow ◽  
Ang Ii ◽  
Electrolyte Excretion ◽  
Water Excretion ◽  
Background Infusion ◽  
Atrial Natriuretic

1. Atrial natriuretic peptide (ANP) has previously been shown to inhibit the renin–angiotensin–aldosterone system (RAAS) at several different levels. We have now investigated a further non-endocrine, renal interaction between ANP and the RAAS. 2. The effects of ANP and angiotensin II (ANG II) alone, and in combination, on urinary electrolyte and water excretion were studied in eight normal male subjects undergoing maximal water diuresis. 3. ANP caused a significant increase in urine flow and sodium excretion. ANG II alone was antidiuretic, antinatriuretic and antikaliuretic. When ANP was given against a background infusion of ANG II, urinary flow rate and electrolyte excretion increased from a new lower level to reach a value intermediate between that found with ANG II alone and ANP alone. 4. It is concluded that the renal effects of ANP are modified in the presence of simultaneously elevated levels of ANG II and that net water and electrolyte excretion reflect the sum of the opposing influences of each peptide. While this interplay may be non-specific, it is possible that ANP may exert some of its actions by specifically inhibiting the intrarenal effects of ANG II.

Atrial Natriuretic Peptide: Regulator of Chronic Arterial Blood Pressure

Physiology ◽  
2000 ◽  
Vol 15 (3) ◽  
pp. 143-149 ◽  
Author(s):  
Luis Gabriel Melo ◽  
Stephen C. Pang ◽  
Uwe Ackermann
Keyword(s):  
Blood Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Salt Intake ◽  
Gene Knockout ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Arterial Blood ◽  
Gene Knockout Mouse ◽  
Atrial Natriuretic

Recent findings in atrial natriuretic peptide (ANP) transgenic and gene knockout mouse models uncovered a tonic vasodilatory effect of this hormone that contributes to chronic blood pressure homeostasis. With elevated salt intake, ANP-mediated antagonism of the renin-angiotensin system is essential for blood pressure constancy, suggesting that a deficiency in ANP activity may underlie the etiology of sodium-retaining disorders.

scholarly journals Chronic Endothelium-Dependent Regulation of Arterial Blood Pressure by Atrial Natriuretic Peptide: Role of Nitric Oxide and Endothelin-1

Endocrinology ◽  
2009 ◽  
Vol 150 (5) ◽  
pp. 2382-2387 ◽  
Author(s):  
Karim Sabrane ◽  
Markus-N. Kruse ◽  
Alexandra Gazinski ◽  
Michaela Kuhn
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Methyl Ester ◽  
Atrial Natriuretic Peptide ◽  
Arterial Blood Pressure ◽  
Natriuretic Peptide ◽  
Endothelin 1 ◽  
Arterial Blood ◽  
Atrial Natriuretic

Atrial natriuretic peptide (ANP), via its guanylyl cyclase (GC)-A receptor, plays a key role in the regulation of arterial blood pressure (ABP) and volume. Endothelial-restricted deletion of GC-A in mice [endothelial cell (EC) GC-A knockout (KO)] resulted in hypervolemic hypertension, demonstrating that the endothelium participates in the hypotensive and hypovolemic actions of ANP. Published studies showed that ANP modulates the release of the vasoactive factors nitric oxide (NO) and endothelin-1 (ET-1) from cultured endothelia. Based on these observations, we examined the role of these endothelial factors in ANP-dependent vasodilatation (studied in isolated arteries) and chronic regulation of ABP (measured in awake mice by tail-cuff plethysmography). ANP induced concentration-dependent vasorelaxations of aortic, carotid, and pulmonary arteries. These responses were not different between control and EC GC-A KO mice, and were significantly enhanced after inhibition of NO synthase [by N(G)-nitro-l-arginine-methyl ester]. Intravenous administration of N(G)-nitro-l-arginine-methyl ester to conscious mice significantly increased ABP. The extent of these hypertensive reactions was similar in EC GC-A KO mice and control littermates (increases in systolic blood pressure by ∼25 mm Hg). Conversely, antagonism of ET-1/endothelin-A receptors with BQ-123 reduced ABP significantly and comparably in both genotypes (by ∼11 mm Hg). Finally, the vascular and tissue expression levels of components of the NO system and of immunoreactive ET-1 were not different in control and EC GC-A KO mice. We conclude that the endothelium, but not modulation of endothelial NO or ET-1, participates in the chronic regulation of ABP by ANP.

scholarly journals Extrarenal resistance to atrial natriuretic peptide in rats with experimental nephrotic syndrome

1998 ◽  
Vol 274 (3) ◽  
pp. F556-F563
Author(s):  
Jean-Pierre Valentin ◽  
Wei-Zhong Ying ◽  
William G. Couser ◽  
Michael H. Humphreys
Keyword(s):  
Nephrotic Syndrome ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Fluid Distribution ◽  
Ang Ii ◽  
Hypotensive Action ◽  
Heymann Nephritis ◽  
Atrial Natriuretic

Nephrotic syndrome is associated with resistance to the renal actions of atrial natriuretic peptide (ANP). We performed experiments in anesthetized, acutely nephrectomized rats 21–28 days after injection of adriamycin (7–8 mg/kg iv) or 9–14 days after injection of anti-Fx1A antiserum (5 ml/kg ip) (passive Heymann nephritis; PHN) to test whether extrarenal resistance also occurred. Proteinuria was significantly elevated in both models compared with controls before study. ANP infusion (1 μg ⋅ kg−1 ⋅ min−1) caused arterial pressure to decrease similarly in control rats, adriamycin-treated rats, and rats with PHN (by 8.2 ± 1.0, 9.4 ± 2.3, and 9.0 ± 2.0%, respectively; all P < 0.05 vs. both baseline and vehicle-infused control rats). In control rats, hematocrit increased progressively to a maximal value 9.5 ± 0.9% over baseline as a result of the infusion, an increase corresponding to a reduction in plasma volume of 16.1 ± 0.9%. The ANP-induced increase in hematocrit was preserved in adriamycin-treated rats (9.2 ± 1.3%) but was markedly blunted in rats with PHN (2.4 ± 1.3%; P < 0.0001 vs. ANP infusion in control rats). ANP infusion increased plasma ANP levels to the same extent in the three groups, whereas plasma guanosine 3′,5′-cyclic monophosphate was significantly lower in rats with PHN compared with both control and adriamycin-treated rats. Infusion of a subpressor dose of angiotensin II (ANG II, 2.5 ng ⋅ kg−1 ⋅ min−1) fully restored the ANP-induced increase in hematocrit in rats with PHN. This study demonstrates that 1) the hemoconcentrating and hypotensive actions of ANP are preserved in adriamycin-treated rats, 2) the effect of ANP on hematocrit and fluid distribution is blunted in rats with PHN while its hypotensive action is preserved, and 3) low-level ANG II infusion normalizes the hemoconcentrating effect of exogenously infused ANP in rats with PHN. Thus deficient ANG II generation in rats with PHN, but not adriamycin nephrosis, may contribute to extrarenal ANP resistance.

Atrial natriuretic peptide inhibits the aldosterone response to angiotensin II in man

1986 ◽  
Vol 70 (5) ◽  
pp. 507-512 ◽  
Author(s):  
J. V. Anderson ◽  
A. D. Struthers ◽  
N. N. Payne ◽  
J. D. H. Slater ◽  
S. R. Bloom
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Pressor Response ◽  
Endocrine System ◽  
Significant Rise ◽  
Plasma Aldosterone Concentration ◽  
Natriuretic Factor ◽  
Atrial Natriuretic

1. We have investigated the interaction between the recently discovered natriuretic factor alpha human atrial natriuretic peptide (alpha h-ANP) and the renin-angiotensin-aldosterone system in man. 2. Angiotensin II infused with placebo produced a significant rise of plasma aldosterone concentration (mean ± sem increment 352 ± 23 pmol/l, n = 7, P < 0.001). The infusion of alpha h-ANP together with angiotensin II largely abolished the aldosterone response (P < 0.001). 3. Diastolic blood pressure rose in response to the infusion of angiotensin II with placebo (mean increment 21.0 ± 0.9 mmHg, P < 0.001). Systolic blood pressure increased to a lesser degree (mean increment 12.5 ± 0.7 mmHg, P < 0.001). 4. The infusion of alpha h-ANP together with angiotensin II significantly blunted the diastolic pressor response (P < 0.01). This ability of alpha h-ANP to blunt the pressor effect of angiotensin II may be important in the control of systemic blood pressure. 5. The inhibition of angiotensin II-stimulated aldosterone release demonstrates that alpha h-ANP may not only be a circulating natriuretic factor in its own right but that it may also act as a modulator of a related endocrine system.

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