scholarly journals Atrial Natriuretic Peptide Modifies Arterial Blood Pressure Through Nitric Oxide Pathway in Rats

Hypertension ◽  
2000 ◽  
Vol 35 (5) ◽  
pp. 1119-1123 ◽  
Author(s):  
María de los Angeles Costa ◽  
Laura V. González Bosc ◽  
Mónica P. Majowicz ◽  
Norberto A. Vidal ◽  
Ana M. Balaszczuk ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Atrial Natriuretic Peptide ◽  
Arterial Blood Pressure ◽  
Natriuretic Peptide ◽  
Arterial Blood ◽  
Nitric Oxide Pathway ◽  
Atrial Natriuretic

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 Erythropoietin-induced hypertension in rat is not mediated by alterations of plasma endothelin, vasopressin, or atrial natriuretic peptide levels.

1997 ◽  
Vol 8 (6) ◽  
pp. 901-905
Author(s):  
X J Zhou ◽  
D Pandian ◽  
X Q Wang ◽  
N D Vaziri
Keyword(s):  
Blood Pressure ◽  
Atrial Natriuretic Peptide ◽  
Arterial Blood Pressure ◽  
Natriuretic Peptide ◽  
Clinical Studies ◽  
Controlled Study ◽  
Recombinant Erythropoietin ◽  
Arterial Blood ◽  
Induced Hypertension ◽  
Atrial Natriuretic

Regular administration of recombinant erythropoietin (EPO) in patients with chronic renal failure (CRF) is frequently complicated by a rise in arterial blood pressure. Clinical studies intended to discern the possible role of endothelin (ET) in the pathogenesis of EPO-induced hypertension have produced contradictory results. Given the limitations of the clinical studies, this placebo-controlled study was carried out in CRF (5/6 nephrectomized) rats treated with either EPO, 150 U/kg intraperitoneally, or the vehicle alone twice weekly for 6 wk. Plasma ET was measured at baseline, and weeks 2, 4, and 6. In addition, plasma arginine vasopressin (AVP) and atrial natriuretic peptide (ANP) were determined at the conclusion of the study period. As expected, blood pressure rose markedly after 1 wk of EPO therapy as compared with the placebo therapy. However, there was no significant difference in plasma ET levels between the EPO- and placebo-treated groups during the study period. Likewise, EPO therapy had no effect on plasma ANP level but depressed plasma AVP concentration. Thus, this placebo-controlled animal study revealed that EPO therapy markedly raised arterial blood pressure but had no effect on plasma ET in the CRF rats. This observation suggests that EPO-induced hypertension in this model is not mediated by an increased circulating ET level. However, the possible effect, if any, of EPO on local vascular tissue ET level is uncertain and awaits further investigation.

Effect of vasopressin on atrial natriuretic peptide release and renal function in dogs

1988 ◽  
Vol 255 (4) ◽  
pp. E449-E455 ◽  
Author(s):  
M. Inoue ◽  
T. Kimura ◽  
K. Ota ◽  
K. Iitake ◽  
M. Shoji ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Atrial Natriuretic Peptide ◽  
Arterial Blood Pressure ◽  
Natriuretic Peptide ◽  
Saline Infusion ◽  
Arterial Blood ◽  
Peptide Release ◽  
Anesthetized Dogs ◽  
Vasopressor Activity ◽  
Atrial Natriuretic

To assess the effect of arginine vasopressin (AVP) and 1-deamino-8-D-AVP (DDAVP) on atrial natriuretic peptide (ANP) release, renal water and electrolyte excretion, and cardiovascular function, AVP and DDAVP were administered at a dose of 10 ng.kg-1.min-1 iv for 30 min into anesthetized dogs receiving saline infusion at a rate of 1 ml.kg-1.min-1 (n = 12). In the control study, saline was infused alone (n = 6). AVP potentiated the plasma ANP response to an increase in plasma volume produced by saline infusion, increased mean arterial blood pressure (MAP), and exaggerated the natriuresis and kaliuresis. DDAVP did not potentiate the increase in plasma ANP but enhanced the natriuresis without any rise in MAP. Saline alone increased plasma ANP as well as sodium and potassium excretion with no changes in MAP. Inulin and p-aminohippuric acid clearances did not change during these studies. The results suggest that in hydrated dogs, AVP may increase ANP release and arterial blood pressure via the vasopressor activity of AVP and potentiate the natriuresis and kaliuresis, but the increased ANP may play little role in the natriuresis.

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.

Renal actions of atrial natriuretic peptide in spontaneously hypertensive rats: the role of nitric oxide as a key mediator

2012 ◽  
Vol 302 (11) ◽  
pp. F1385-F1394 ◽  
Author(s):  
Rosana Elesgaray ◽  
Carolina Caniffi ◽  
Lucía Savignano ◽  
Mariana Romero ◽  
Myriam Mac Laughlin ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Calmodulin Inhibitors ◽  
Nos Isoforms ◽  
Atrial Natriuretic

Atrial natriuretic peptide (ANP) is an important regulator of blood pressure (BP). One of the mechanisms whereby ANP impacts BP is by stimulation of nitric oxide (NO) production in different tissues involved in BP control. We hypothesized that ANP-stimulated NO is impaired in the kidneys of spontaneously hypertensive rats (SHR) and this contributes to the development and/or maintenance of high levels of BP. We investigated the effects of ANP on the NO system in SHR, studying the changes in renal nitric oxide synthase (NOS) activity and expression in response to peptide infusion, the signaling pathways implicated in the signaling cascade that activates NOS, and identifying the natriuretic peptide receptors (NPR), guanylyl cyclase receptors (NPR-A and NPR-B) and/or NPR-C, and NOS isoforms involved. In vivo, SHR and Wistar-Kyoto rats (WKY) were infused with saline (0.05 ml/min) or ANP (0.2 μg·kg−1·min−1). NOS activity and endothelial (eNOS), neuronal (nNOS), and inducible (iNOS) NOS expression were measured in the renal cortex and medulla. In vitro, ANP-induced renal NOS activity was determined in the presence of iNOS and nNOS inhibitors, NPR-A/B blockers, guanine nucleotide-regulatory (Gi) protein, and calmodulin inhibitors. Renal NOS activity was higher in SHR than in WKY. ANP increased NOS activity, but activation was lower in SHR than in WKY. ANP had no effect on expression of NOS isoforms. ANP-induced NOS activity was not modified by iNOS and nNOS inhibitors. NPR-A/B blockade blunted NOS stimulation via ANP in kidney. The renal NOS response to ANP was reduced by Gi protein and calmodulin inhibitors. We conclude that ANP interacts with NPR-C, activating Ca-calmodulin eNOS through Gi protein. NOS activation also involves NPR-A/B. The NOS response to ANP was diminished in kidneys of SHR. The impaired NO system response to ANP in SHR participates in the maintenance of high blood pressure.

Sign in / Sign up

Export Citation Format

Share Document