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We evaluated the effects of pathophysiological levels of human brain natriuretic peptide (BNP), a recently identified cardiac hormone with natriuretic activity, by determining the hemodynamic and renal responses to low dose infusion (4 pmol/kg.min for 1 h, from 1500-1600 h) of human synthetic BNP in five healthy volunteers in a randomized placebo-controlled crossover study. Compared to placebo, BNP induced significant increases in effective renal plasma flow (para-aminohippurate clearance), glomerular filtration rate (creatinine clearance), urine flow rate, and sodium excretion without affecting blood pressure, heart rate, cardiac output (echocardiographic method), peripheral vascular resistance, PRA, plasma aldosterone, or plasma norepinephrine to any significant extent. Exploration of segmental sodium handling by the lithium clearance technique showed that the natriuretic effect of BNP was due to both an increase in filtered sodium load and a reduced distal sodium reabsorption. These results indicate that the high plasma BNP levels observed in disease states, such as heart failure, may contribute to the regulation of renal hemodynamics and sodium excretion.
Villa et al. (1994) studied this question.