Atrial natriuretic peptide inhibits the effect of endogenous angiotensin II on plasma aldosterone in conscious sodium-depleted rats

1987 ◽  
Vol 72 (1) ◽  
pp. 31-35 ◽  
Author(s):  
Lynn Chartier ◽  
Ernesto L. Schiffrin

1. Previous studies have shown that atrial natriuretic peptide (ANP) inhibits the secretion of aldosterone by isolated adrenal glomerulosa cells stimulated by angiotensin II, adrenocorticotropic hormone and potassium in vitro. We have also demonstrated that this inhibitory effect of ANP on plasma aldosterone induced by angiotensin II and adrenocorticotropic hormone can be reproduced in vivo in conscious unrestrained rats. In this study, we have investigated the effect of an intravenous infusion of ANP on plasma aldosterone in conscious unrestrained sodium-depleted rats. 2. During sodium depletion, the rise in plasma renin activity which determines an increment in the circulating concentration of angiotensin II was accompanied by a rise in aldosterone secretion as expected. ANP infused intravenously at a dose which increased the plasma concentration of the peptide three- to five-fold, produced a significant decrement in the concentration of aldosterone in plasma after an infusion period of 120 min. There was no significant effect of ANP on plasma renin activity and plasma corticosterone concentration. 3. Since the increase in plasma aldosterone levels in sodium-depleted rats is mainly dependent on the activation of the renin–angiotensin system, we conclude that ANP may modulate the effect of endogenous as well as exogenous angiotensin II on plasma aldosterone secretion.

1997 ◽  
Vol 92 (3) ◽  
pp. 255-260 ◽  
Author(s):  
C. M. Florkowski ◽  
A. M. Richards ◽  
E. A. Espiner ◽  
T. G. Yandle ◽  
E. Sybertz ◽  
...  

1. To assess the threshold dose for bioactivity of brain natriuretic peptide and the role of endopeptidase 24.11 in metabolism of brain natriuretic peptide at physiological plasma levels, we studied eight normal men receiving 2 h infusions of low-dose brain natriuretic peptide [0.25 and 0.5 pmol min−1 kg−1 with and without pretreatment with an endopeptidase inhibitor (SCH 32615, 250 mg intravenously)] in placebo-controlled studies. 2. Plasma brain natriuretic peptide increased 2-fold during the infusion of 0.25 pmol min−1 kg−1 (mean increment above control 3.9 pmol/l, P < 0.001), and tripled (P < 0.001) with 0.5 pmol min−1 kg−1. Plasma renin activity was inhibited by both doses (14.8%, P < 0.01, and 20%, P < 0.001, respectively). A significant natriuresis (56% increase in urine sodium/creatinine ratio, P < 0.02) occurred with the higher dose. Blood pressure, haematocrit, plasma cGMP, atrial natriuretic peptide and aldosterone were unaffected by either dose. 3. Compared with brain natriuretic peptide (0.5 pmol min−1 kg−1) alone, SCH 32615 pretreatment increased peak plasma brain natriuretic peptide (13.4±0.78 versus 12.4±0.86 pmol/l, P < 0.05), ANP (7.5±0.96 versus 5.9±0.4 pmol/l, P < 0.01) and cGMP (4.8 ± 1.7 versus 3.9 ± 1.4 nmol/l, P < 0.001). Plasma renin activity was further suppressed with SCH 32615 pretreatment (29% compared with 20%, P < 0.001). 4. Small acute increments in plasma brain natriuretic peptide (4 pmol/l) have significant biological effects in normal men without altering plasma atrial natriuretic peptide or cGMP.


1990 ◽  
Vol 31 (5) ◽  
pp. 671-682 ◽  
Author(s):  
Tetsuya NAKAMURA ◽  
Shuichi ICHIKAWA ◽  
Tetsuo SAKAMAKI ◽  
Futao AIZAWA ◽  
Toshiaki KURASHINA ◽  
...  

1972 ◽  
Vol 71 (1) ◽  
pp. 153-159 ◽  
Author(s):  
Fred H. Katz ◽  
Peggy Romfh ◽  
Judith A. Smith

ABSTRACT The increase in plasma aldosterone and reduction in plasma renin activity induced by 30 to 60 minutes of mildly pressor angiotensin II infusion in man can be largely abolished when recent prior stimulation of the adrenal cortex by upright posture has been applied. A similar prevention of the ACTH-induced increase in plasma aldosterone can be achieved by previous upright ambulation. These results indicate the intermittent refractoriness of aldosterone secretion and that care must be exerted in the timing of any tests of aldosterone stimulation.


Sign in / Sign up

Export Citation Format

Share Document