Effects of incremental infusions of atrial natriuretic factor on aldosterone, renin, and blood pressure in humans.

Abstract

SUMMARY To evaluate the physiological effects of human atrial natriuretic factor-(99-126) (ANF), we infused ANF, 0.1, 0.3, and 1.0 /ig/min, or placebo for 125 minutes on different days into six sodium-deprived normal men. During the last 45 minutes of infusion, angiotensin II, 6 ng/kg/min, was infused. Blood pressure, heart rate, plasma concentrations of ANF, aldosterone, and cortisol, and plasma renin activity (PRA) were measured before and during infusion. Steady state mean plasma ANF levels during infusion were 26.2 (placebo), 68.8 (0.1 n% ANF/min), 221 (0.3 ng ANF/min), and 648 pg/ml (1.0 /ig ANF/min). Systolic blood pressure fell significantly (with 1.0 /xg ANF/min), and diastolk pressure tended to rise in a dose-dependent manner, while heart rate was unchanged. PRA and plasma aldosterone fell during ANF infusion in a dose-dependent manner (significant with 0. A TRIAL natriuretic factor (ANF) may be phys-Z.\ iologically and pathophysiologically in-J-\~ volved in ridding the body of a sodium load and in preventing central venous pressure from rising above a certain limit.1 Most of the ANF activity in human plasma seems to be due to human However, it is controversial whether the effect of ANF on aldosterone secretion occurs with near-normal plasma concentrations of the cardiac peptide and whether the effect in vivo is more or less mediated by changes in plasma renin levels. 9 -11 In the present study, we attempted to find a threshold dose of infused ANF that significantly affects aldosterone and renin secretion in sodium-deprived normal men. Subjects and Methods Six healthy men (age range, 20-29 years; body weight range, 63-87 kg; mean body weight, 73.5 ± 8.5 kg) consented to participate in the study, the protocol of which had been approved by the ethical committee of Klinikum Steglitz (Berlin, West Germany). They were studied on 4 different days (three doses of ANF, one placebo infusion) within two periods of sodium depletion, during which the men collected their urine for the calculation of sodium and potassium balances. Sodium losses were induced to facilitate studying a possible suppressive effect of ANF on elevated basal renin and aldosterone levels. A period of sodium depletion consisted of 3 days on a low sodium diet (15 mmol sodium, 70 mmol potassium per day) plus a single 40-mg dose of furosemide (Lasix, Hoechst) on the morning of the first day. Therefore, most of the sodium loss occurred during the first 24 hours of the sodium depletion period, and the cumulative negative sodium balance at the end of Day 3 was not much different from that on the morning of Day 2. Infusion of one dose of ANF or placebo was given in the afternoon on Days 2 and 3. After an interval of 3 weeks on a free diet, the procedure of sodium depletion was

Renal, endocrine and vascular effects of atrial natriuretic peptide in a novel vasopressin‐deficient genetically hypertensive strain of rat

“…The pronounced reduction in plasma aldosterone observed in response to ANP clearly suggests not only direct ANP suppression of aldosterone synthesis from the adrenal gland (Atrashi, Mulrow & Franco-Saenz, 1985;Oelkers, Kleiner & Bahr, 1988) but also ANP blockade of the stimulating action of angiotensin II on adrenal zona glomerulosa cells (Atrashi, Mulrow, Franco-Saenz, Snajdar & Rapp, 1984). This decline in plasma aldosterone is in agreement with previous observations in the vasopressin-replete NZGH and NZN rats treated with ANP (Al-Barazanji & Balment, 1989).…”

Altered sodium perception in essential hypertensive patients following rapid volume expansion

“…ANH levels vary directly with the state of sodium intake 11 and ANH infusion reduces PRA and aldosterone secretion, particularly in sodiumrestricted normal subjects. 12 Plasma and urinary dopamine increase with sodium loading and dopamine inhibits aldosterone secretion both in vivo and in vitro. [13][14][15] Levels of endogenous digitalis-like factors also increase during saline infusion 16 and ouabain inhibits aldosterone secretion in vitro.…”

B‐type natriuretic peptide measurement in heart failure

“…34,35 Both ANP and BNP also improve renal blood flow via afferent arteriolar vasodilation and efferent arteriolar vasoconstriction. 36,37 There is also a direct effect on the collecting duct, leading to increased sodium excretion. 38 C-type natriuretic peptide acts primarily through a different receptor and plays a little known role in CHF.…”