Acute regional circulatory and renal hemodynamic effects of converting-enzyme inhibition in patients with congestive heart failure

The acute effects of the angiotensin converting-enzyme inhibitor captopril on regional blood flow, renal hemodynamics and sodium excretion were studied in 12 patients with severe congestive heart failure. Converting-enzyme inhibition decreased systemic vascular resistance by 27% and increased cardiac index by 16%. Estimated hepatic blood flow decreased 17%, but renal blood flow increased 60%. The ratio of renal-systemic blood flow increased from 0.10 ± 0.01 to 0.14 ± 0.02 (p = 0.031). Although renal plasma flow increased from 202.8 ± 28.8 to 323.7 ± 42.7 ml/min (p = 0.008), the glomerular filtration rate did not change significantly from the mean pretreatment value of 82.1 ± 12.3 ml/min. The filtration fraction decreased from 41.3 ± 3.8% to 33.4 to 33.4 ± 4.5% (p = 0.050), while urinary sodium excretion doubled, from 34.5 ± 9.6 to 68.2 ± 19.6 μEq/min. The plasma renin activity increased from 12.6 ± 5.0 to 29.9 ± 8.4 ng/ml/hr (p = 0.030) as plasma aldosterone concentration decreased from 30.5 ± 6.5 to 11.3 ± 1.2 ng/dl (p = 0.010) and norepinephrine concentration decreased from 774 ± 105 to 618 ± 85 pg/ml (p = 0.020). We conclude that converting-enzyme inhibition reverses renal vasoconstriction in congestive heart failure and redistributes regional blood flow. The natriuresis may be mediated by one or more of the following: improved renal plasma flow, reduction in filtration fraction, suppression of hyperaldosteronism, and lowering of circulatory catecholamine concentrations.