Cardiac and vascular effects of atrial natriuretic factor and sodium nitroprusside in healthy men.

Abstract

To assess the contribution of venous effects to the hemodynamic changes caused by atrial natriuretic factor (ANF), the cardiac and peripheral effects of ANF were compared with those induced by the venoarterial vasodilator sodium nitroprusside. On 3 different days, eight healthy subjects received 2-hour infusions of either ANF, sodium nitroprusside, or placebo, by a single-blind crossover design. ANF was administered at a rate of 15 ng/kg/min for hour 1 and 50 ng/kg/min for hour 2; each infusion rate was preceded by a 50-micrograms bolus. The lower ANF infusion rate increased plasma cGMP fourfold, but only modest cardiovascular effects (small decreases in left ventricular end-diastolic and end-systolic volumes) were noted. At the higher ANF infusion rate, left ventricular volumes and intravascular volume, as indirectly assessed by changes in hematocrit levels, decreased further, which resulted in decreases in stroke volume, cardiac index, and systolic blood pressure. No evidence for arterial vasodilation (no decrease in diastolic blood pressure, total peripheral resistance, or forearm resistance) was obtained, and no increase in sympathetic activity was noted. In contrast, sodium nitroprusside caused arterial vasodilation, an increase in cardiac index, and significant increases in sympathetic activity. We conclude that short-term increases in plasma ANF within the physiologic range primarily affect the venous vascular bed (by decreasing intravascular volume or by venodilation) without increasing sympathetic activity.