Changes in Atrial Natriuretic Peptide (ANP) and Plasma Renin Activity (PRA) Following Changes in Right Atrial Pressure (RAP) in Patients with Chronic Renal Failure (CRF)

1992 ◽  
Vol 83 (s27) ◽  
pp. 24P-24P
Author(s):  
S Y Tan ◽  
K Craig ◽  
J Nolan ◽  
C P Swainson
1993 ◽  
Vol 265 (1) ◽  
pp. R76-R81
Author(s):  
A. U. Sheikh ◽  
L. K. Washburn ◽  
R. K. Jaekle ◽  
J. C. Rose

In adults, renin secretion is stimulated by reductions in arterial pressure and inhibited by increases in atrial pressure. In the late gestation fetus, a fall in arterial pressure stimulates renin secretion, but it is unknown whether elevation of atrial pressure will alter such an increase. Therefore we studied the effect of elevated atrial pressure on renin secretion in the presence of nitroprusside-induced arterial hypotension. Thirteen fetal lambs at 127.9 +/- 0.9 days of gestation were prepared 5 days before study with inflatable pulmonary artery occluders and right atrial, vascular, and amniotic catheters. Each fetus underwent two protocols (hypotension and hypotension with occlusion) using a randomized block design. Nitroprusside reduced arterial pressure by 34% in both groups. Right atrial pressure during the course of hypotension was significantly higher in the occlusion group (F = 14.2, P = 0.001). Plasma renin activity increased similarly in both groups during hypotension (F = 6.0, P = 0.003). Elevated right atrial pressure did not alter hypotension-induced renin secretion in the fetus.


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.


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.


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

1987 ◽  
Vol 72 (1) ◽  
pp. 19-24 ◽  
Author(s):  
Robert G. Walker ◽  
Charles P. Swainson ◽  
Tim G. Yandle ◽  
M. Gary Nicholls ◽  
Eric A. Espiner

1. Plasma levels of immunoreactive alpha human atrial natriuretic peptide (IR-ANP) were measured in nine patients with chronic renal failure before and after removal of 1.3–3.7 litres of fluid by ultrafiltration and again during volume repletion with intravenous sodium chloride solution (150 mmol/l: saline). 2. Baseline levels of IR-ANP were elevated but fell by 22% during ultrafiltration. 3. Saline infusion induced a rapid and steep rise in IR-ANP levels which were 150% of baseline while body weight was still 2% below baseline. 4. Changes in plasma renin, angiotensin II, aldosterone and vasopressin during the study were slight compared with the change in IR-ANP, but noradrenaline levels rose threefold during ultrafiltration. 5. There was a significant positive relationship between arterial pressure and IR-ANP levels before and after ultrafiltration. 6. These results lend support to the suggestion that atrial peptides are of physiological importance, especially in states of chronic fluid overload such as chronic renal failure.


Sign in / Sign up

Export Citation Format

Share Document