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.

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.

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.

Overlapping distributions of receptors for atrial natriuretic peptide and angiotensin II visualized by in vitro autoradiography: morphological basis of physiological antagonism

1987 ◽  
Vol 65 (8) ◽  
pp. 1517-1521 ◽  
Author(s):  
F. A. O. Mendelsohn ◽  
A. M. Allen ◽  
S. Y. Chai ◽  
P. M. Sexton ◽  
R. Figdor
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Area Postrema ◽  
Angiotensin Ii Receptors ◽  
Electrolyte Balance ◽  
Outer Cortex ◽  
Morphological Basis ◽  
Atrial Natriuretic

Atrial natriuretic peptides exert actions on many key organs involved in blood pressure and water and electrolyte balance. Many of these actions result in a physiological antagonism of angiotensin. To investigate the morphological basis of this interaction, we have mapped the distribution of receptors for atrial natriuretic peptide and angiotensin II in a number of target organs, using 125I-labelled rat atrial natriuretic peptide (99–126) and 125I-labelled [Sar1,Ile8]angiotensin II. In the kidney both atrial natriuretic peptide and angiotensin II receptors were observed overlying glomeruli, vasa recta bundles (high densities), and the outer cortex (moderate density). In the other tissues studied, atrial natriuretic peptide and angiotensin II receptors were codistributed in the adrenal zona glomerulosa, cerebral circumventricular organs including the subfornical organ, organum vasculosum of the lamina terminalis and area postrema, and the external plexiform layer of the olfactory bulb. The concurrent distribution of specific receptors for both peptides at these sites provides the basis for atrial natriuretic peptide to exert a functional antagonism of the actions of angiotensin II on blood pressure and water and electrolyte homeostasis at multiple sites.

Effects of centrally administered atrial natriuretic peptide on renal functions

1987 ◽  
Vol 115 (4) ◽  
pp. 433-440 ◽  
Author(s):  
M. Shoji ◽  
T. Kimura ◽  
K. Matsui ◽  
K. Ota ◽  
K. Iitake ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Glomerular Filtration Rate ◽  
Atrial Natriuretic Peptide ◽  
Glomerular Filtration ◽  
Natriuretic Peptide ◽  
Filtration Rate ◽  
Significant Rise ◽  
Arterial Blood ◽  
Control Study ◽  
Atrial Natriuretic

Abstract. In order to assess the effects of centrally administered atrial natriuretic peptide (ANP) on renal water and electrolytes handling, arterial blood pressure, plasma vasopressin, renin activity, aldosterone, and ANP concentrations, synthetic α-human ANP (α-hANP) was administered intracerebroventricularly at a dose of 2.6 pmol · kg−1 · min−1 for 30 min in pentobarbitalanaesthetized dogs (N = 6). In the control study (N = 6), artificial cerebrospinal fluid was infused. Intracerebroventricular administration of α-hANP increased significantly urine flow from 178 ± 37 to 303 ± 43 μl/min (mean ± sem), sodium excretion from 27.3 ± 8.9 to 54.4 ± 10.5, μmol/min, potassium excretion from 16.1 ± 3.7 to 24.0 ± 5.1 μmol/min, and osmolar and negative free water clearances, accompanied by a significant rise in renal blood flow from 77.0 ± 14.6 to 94.9 ± 16.9 ml/min. Whereas glomerular filtration rate fell significantly, blood pressure and heart rate did not change. Plasma ANP, aldosterone, and PRA did not change significantly during the experiment, but plasma AVP were slightly but significantly decreased from 52 ± 11 to 34 ± 6 nmol/l. On the other hand, these parameters showed no changes in the control study, except a significant fall in glomerular filtration rate and a significant rise in PRA. Thus, it has been confirmed that ANP centrally brings about diuresis, natriuresis, and kaliuresis via some unknown mechanisms independent of the release of these hormones.

Responses of vasopressin, atrial natriuretic peptide, and blood pressure to central osmotic stimulation

1989 ◽  
Vol 257 (4) ◽  
pp. E611-E616 ◽  
Author(s):  
K. Iitake ◽  
T. Kimura ◽  
K. Ota ◽  
M. Shoji ◽  
M. Inoue ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Pressor Response ◽  
Intracerebroventricular Infusion ◽  
Artificial Cerebrospinal Fluid ◽  
Osmotic Stimulation ◽  
3Rd Ventricle ◽  
Slight Rise ◽  
Atrial Natriuretic

To assess whether intracerebroventricular osmoreceptors are involved in vasopressin (AVP) and atrial natriuretic peptide (ANP) release and in the pressor response to centrally administered hypertonic NaCl, artificial cerebrospinal fluid (ACSF) or ACSF made hypertonic by adding 0.2 M NaCl, 0.4 M mannitol, and 0.4 M glucose in isotonic ACSF or 0.4 M urea was infused into the 3rd ventricle of conscious rats. In addition, intravenous infusion of [1-(beta-mercapto-beta,beta-cyclopentamethylenepropionic acid),2-(O-methyl)tyrosine]AVP (TMeAVP), a V1-AVP antagonist, was given in rats receiving intracerebroventricular infusion of 0.2 M NaCl in isotonic ACSF. Intracerebroventricular 0.2 M NaCl, 0.4 M mannitol, and 0.4 M glucose in isotonic ACSF increased plasma AVP and mean arterial pressure (MAP) without changing heart rate (HR) or plasma ANP. Urea at 0.4 M decreased plasma AVP and ANP with a slight rise in MAP but no change in HR. ACSF alone did not affect plasma AVP, ANP, MAP, or HR. Intravenous TMeAVP attenuated the pressor response to infusion of 0.2 M NaCl in isotonic ACSF, decreased plasma ANP, but did not affect HR. These results indicate that central osmoreceptors are involved in the release of AVP and in the pressor response to centrally administered hypertonic NaCl.

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