Effects of synthetic atrial natriuretic peptide on renal function and renin release in acute experimental heart failure

Studies were performed in anesthetized control dogs (n = 6) and in dogs (n = 6) with acute low-output heart failure produced by inflation of a balloon in the thoracic inferior vena cava. Studies were designed to determine the effects of synthetic atrial natriuretic peptide on renal function and renin release in this acute high-renin, sodium-retaining preparation. Intrarenal infusion of synthetic atrial natriuretic peptide (0.3 μg·kg^-1·min^-1) resulted in decreases in arterial pressure and renal blood flow in both groups. Glomerular filtration rate increased in both low-output (Δ + 10.7 ± 3.1 ml/min) and control (Δ + 8.7 ± 2.9 ml/min) groups. Fractional lithium excretion, a marker of proximal tubule reabsorption, also increased in both low-output (Δ + 12.0 ± 4.6%) and control (Δ + 14.3 ± 5.0%) groups. Renin secretory rate decreased in the low-output group from 852.8 ± 183.0 to 149.5 ± 73.7 ng/min and in the control group from 308.5 ± 84.5 to 44.5 ± 27.5 ng/ml. Intrarenal infusion of atrial natriuretic peptide resulted in an attenuated increase in both urinary sodium excretion (Δ + 42.3 ± 10.7 vs Δ + 201.2 ± 37.9 μeq/min) and fractional excretion of sodium (Δ + 0.48 ± 0.13% vs Δ + 2.85 ± 0.45%) in the low-output as compared with the control group. Our studies demonstrate that administration of synthetic atrial natriuretic peptide results in an increase in glomerular filtration rate and a decrease in proximal tubule reabsorption, as estimated by lithium excretion, in both control dogs and those with acute low-output heart failure. Furthermore, despite a decrease in arterial pressure, synthetic atrial natriuretic peptide markedly inhibits renin secretion under control conditions and in the high-renin state. Despite similar increases in glomerular filtration rate and decreases in proximal tubule reabsorption and renin release, the natriuretic response to synthetic atrial natriuretic peptide, although present, is markedly attenuated in this preparation of acute experimental heart failure.