Diurnal change in plasma atrial natriuretic peptide concentrations

1987 ◽  
Vol 73 (5) ◽  
pp. 489-495 ◽  
Author(s):  
A. M. Richards ◽  
G. Tonolo ◽  
R. Fraser ◽  
J. J. Morton ◽  
B. J. Leckie ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Antidiuretic Hormone ◽  
Natriuretic Peptide ◽  
Plasma Concentrations ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Diurnal Changes ◽  
Renin Angiotensin ◽  
Atrial Natriuretic

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.

Comparative Effects of Atrial Natriuretic Peptide and Brain Natriuretic Peptide on the Aldosterone and Pressor Responses to Angiotensin Ii in Man

1995 ◽  
Vol 88 (1) ◽  
pp. 81-86 ◽  
Author(s):  
Robert I. Cargill ◽  
Allan D. Struthers ◽  
Brian J. Lipworth
Keyword(s):  
Steady State ◽  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Concentrations ◽  
Plasma Aldosterone ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Atrial Natriuretic

1. Atrial natriuretic peptide and brain natriuretic peptide have similar vasodilator and natriuretic properties, although little information is available regarding their relative effects as antagonists of the renin—angiotensin—aldosterone system. We have therefore compared how atrial natriuretic peptide and brain natriuretic peptide affect the systemic pressor and aldosterone responses to angiotensin II in eight male subjects. 2. Each subject was studied on three separate occasions, when they received a 60-min infusion of placebo, atrial natriuretic peptide (10 pmol min−1 kg−1) or brain natriuretic peptide (10 pmolmin−1 kg−1), with a concomitant infusion of angiotensin II (6 ng min−1 kg−1) given for the final 30 min of the infusion period. The change in haemodynamic parameters and plasma aldosterone induced by angiotensin II was measured. Plasma concentrations of atrial natriuretic peptide (182 ± 23 pmol/l) and brain natriuretic peptide (193 ± 25 pmol/l) achieved at steady-state during the infusion on each study day were not significantly different. 3. Increases in mean arterial pressure in response to angiotensin II were significantly lowered by concomitant infusion of atrial natriuretic peptide (21.0 ± 1.7 mmHg) and brain natriuretic peptide (20.1 ± 1.9 mmHg) compared with placebo (29.0 ± 4.1 mmHg). There were similar effects on systolic and diastolic blood pressure. Cardiac output was decreased on each study day to the same extent by angiotensin II infusion. Total systemic vascular resistance showed a non-significant trend towards an attenuated response to angiotensin II when atrial natriuretic peptide or brain natriuretic peptide was infused concomitantly in comparison with placebo. 4. Plasma aldosterone increased by 326 ± 49 pmol/l when angiotensin II was infused with placebo. Both atrial natriuretic peptide and brain natriuretic peptide significantly blunted this response, although the increase with atrial natriuretic peptide (19 ± 35 pmol/l) was significantly lower than the increase with brain natriuretic peptide (133 ± 19 pmol/l). 5. Atrial natriuretic peptide and brain natriuretic peptide were therefore equally effective in blunting the systemic pressor response to angiotensin II. It was apparent, however, in view of similar plasma concentrations at steady state, that on a molar basis atrial natriuretic peptide was a more potent inhibitor of angiotensin II-induced aldosterone secretion than brain natriuretic peptide. These results suggest a dissociation between the haemodynamic and hormonal effects of atrial natriuretic peptide and brain natriuretic peptide in terms of antagonism of the renin—angiotensin—aldosterone system.

Effect of Acute Hypercapnia on Alpha Atrial Natriuretic Peptide, Renin, Angiotensin II, Aldosterone, and Vasopressin Plasma Levels in Patients With COPD

CHEST Journal ◽  
1995 ◽  
Vol 107 (3) ◽  
pp. 780-786 ◽  
Author(s):  
François Chabot ◽  
Paul M. Mertes ◽  
Nicolas Delorme ◽  
Francine V. Schrijen ◽  
Claude G. Saunier ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Plasma Levels ◽  
Renin Angiotensin ◽  
Atrial Natriuretic

Endogenous angiotensin II modulates the effect of atrial natriuretic peptide on extracellular fluid partition

1993 ◽  
Vol 264 (4) ◽  
pp. R676-R680
Author(s):  
J. P. Valentin ◽  
N. Nafrialdi ◽  
J. Ribstein ◽  
A. Mimran
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Renin Angiotensin System ◽  
Acute Administration ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Series Of Experiments ◽  
Atrial Natriuretic

Atrial natriuretic peptide (ANP) has been shown to promote a fluid shift from the intravascular toward the interstitial compartment and to interact with the renin-angiotensin system at the renal as well as the extrarenal level. In the present studies, the interaction between the renin-angiotensin system and the effects of ANP infusion (100 ng.kg-1 x min-1 for 45 min) on arterial pressure and hematocrit were assessed in bilaterally nephrectomized, anesthetized rats. In a first series of experiments, suppression of angiotensin II generation was achieved by chronic (10 days) treatment by the angiotensin-converting-enzyme inhibitor (ACEI) captopril in rats maintained on a low-sodium diet. ACEI pretreatment prevented the rise in hematocrit associated with ANP infusion (+2.1 +/- 0.1 vs. +5.8 +/- 0.2%, P < 0.05), without influencing the effect of ANP on arterial pressure. In ACEI-pretreated rats, acute administration of angiotensin II at a subpressor dose (2.5 ng.kg-1 x min-1) restored the ANP-induced increase in hematocrit. In a second series of experiments, acute blockade of the renin-angiotensin system was obtained by the ACEI enalaprilat or the nonpeptide angiotensin II receptor antagonist losartan (both 1 mg/kg i.v. bolus). In the presence of either enalaprilat or losartan, the ANP-induced increase in hematocrit was similarly prevented. These results indicate that the effect of ANP on vascular permeability is modulated by endogenous angiotensin II, possibly due to distinct influences of the two peptides at the level of pre- and postcapillary resistances.

A Proposal of Ovarian ERAANPS (Endothelin-Renin-Angiotensin-Atrial Natriuretic Peptide System) and Effects of Tokishakuyakusan, Keishibukuryogan, Shakuyakukanzoto and Unkeito on the ERAANPS

1992 ◽  
Vol 20 (01) ◽  
pp. 65-74 ◽  
Author(s):  
Satoshi Usuki ◽  
Junko Tanaka ◽  
Yumiko Kawakura ◽  
Yoshie Usuki
Keyword(s):  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Binding Site ◽  
Natriuretic Peptide ◽  
Binding Sites ◽  
Ovarian Follicle ◽  
High Concentration ◽  
Renin Angiotensin ◽  
Atrial Natriuretic

We have previously shown the presence in a high concentration of endothelin-l (ET) in the corpus luteum and renin-angiotensin system (RAS) and binding sites for atrial natriuretic peptide (ANP) in the ovarian follicle. The present study was undertaken to identify the existence of ET, renin, angiotensin II and the binding site for ANP in the ovary at proestrus and examine in vivo the effects of herbal medicines [Tokishakuyakusan (TS), Keishibukuryogan (KB), Shakuyakukanzoto (SK) and Unkeito (UT)] on them. ET, all components of RAS and binding sites for ANP were found at high levels in the ovary. TS, KB, SK and UT decreased the ET levels in ovary, while components of RAS and binding sites for ANP have the propensity to increase. However, ET, renin, angiotensin II and ANP levels in plasma were not at all affected before and after treatment with TS, KB, SK or UT. Taken together with previous observations showing the existence of ET, RAS and the binding site for ANP in the ovary, we propose here the ERAANPS (endothelin-renin-angiotensin-ANP system) in the ovary as a functional regulator. Further, these results suggest that TS, KB, SK or UT may regulate the ovarian ERAANPS.

Effects of Physiological Increments in Human α-Atrial Natriuretic Peptide and Human Brain Natriuretic Peptide in Normal Male Subjects

1994 ◽  
Vol 86 (6) ◽  
pp. 723-730 ◽  
Author(s):  
B. M. Y. Cheung ◽  
J. E. C. Dickerson ◽  
M. J. Ashby ◽  
M. J. Brown ◽  
J. Brown
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Human Brain ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Physiological Role ◽  
Sodium Balance ◽  
Urinary Flow ◽  
Male Subjects ◽  
The Brain ◽  
Atrial Natriuretic

1. Brain natriuretic peptide, closely related to atrial natriuretic peptide in structure, may be an important circulating hormone. Its physiological role is unclear. First, we studied the effects of incremental infusions of brain natriuretic peptide in six healthy men on plasma brain natriuretic peptide levels and the pharmacokinetics of brain natriuretic peptide. Synthetic human brain natriuretic peptide-32 was infused intravenously, at an initial rate of 0.4 pmol min−1 kg−1, doubling every 15 min until the dose rate reached 6.4 pmol min−1 kg−1, at which rate the infusion was maintained for 30 min. 2. The brain natriuretic peptide infusion raised the brain natriuretic peptide-like immunoreactivity from 1.4 ± 0.5 pmol/l to 21.4 ± 7.6 pmol/l. Brain natriuretic peptide-like immunoreactivity after the end of infusion was consistent with a bi-exponential decay, with half-lives of 2.1 min and 37 min. 3. Next, we studied the effects of low-dose infusion of brain natriuretic peptide to mimic physiological increments in the circulating levels in comparison with atrial natriuretic peptide. Six dehydrated male subjects received intravenous infusions of atrial natriuretic peptide and brain natriuretic peptide, separately and in combination, in a randomized double-blind, placebo-controlled, four-part cross-over design. Atrial natriuretic peptide and brain natriuretic peptide were given at the rate of 0.75 and 0.4 pmol min−1 kg−1, respectively, for 3 h. The control infusion consisted of the vehicle. 4. Analysis of variance showed that atrial natriuretic peptide and atrial natriuretic peptide plus brain natriuretic peptide, but not brain natriuretic peptide alone, increased urinary flow and decreased urinary osmolality significantly. However, urinary sodium excretion was significantly increased by atrial natriuretic peptide, brain natriuretic peptide and atrial natriuretic peptide plus brain natriuretic peptide. 5. None of the four infusates significantly altered the blood pressure, heart rate or glomerular filtration rate. 6. This study showed, for the first time, that physiological increments in brain natriuretic peptide, like those in atrial natriuretic peptide, are natriuretic. Although atrial natriuretic peptide and brain natriuretic peptide do not appear to interact synergistically, they are likely to act in concert in the physiological regulation of sodium balance.

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