RENAL VASODILATORY EFFECT OF ENDOTHELIAL STIMULATION IN PATIENTS WITHCHRONIC CONGESTIVE-HEART-FAILURE

Objectives. This study sought to examine the vasodilatory response of the renal circulation to endothelial stimulation in patients with chro nic heart failure. Background. Renal blood flow is often reduced in pa tients with chronic congestive heart failure and may lead to deteriora tion of renal function. Stimulation of renal endothelium has been show n to cause renal vasodilation in animals and in isolated human renal a rtery. The vasoregulatory role of the renal endothelium in patients wi th heart failure has not been evaluated. Methods. Renal vasodilatory e ffect of endothelial stimulation with acetylcholine was assessed and c ompared with that of endothelial independent vasodilation with nitrogl ycerin. Both drugs were infused into the main renal artery. Renal arte ry cross-sectional area was measured with intravascular ultrasound and renal blood flow velocity with the aid of an intravascular Doppler te chnique. Results. Both drugs caused a significant and comparable incre ase in renal artery cross-sectional area (maximal increase [mean +/- S E] 14 +/- 5% with acetylcholine, 15 +/- 58 with nitroglycerin; both ch anges <0.05 vs, baseline). Acetylcholine also caused a significant red uction in renal vascular resistance (maximal reduction 55 +/- 6%) and increase in renal blood flow (maximal increase 136 +/- 54%), In contra st, nitroglycerin administration showed no significant effect on renal vascular resistance and blood flow. Conclusions. Stimulation of endot helium derived nitric oxide with acetylcholine results in a significan t vasodilatory effect on both conductance and resistance renal blood v essels and leads to a marked reduction in renal vascular resistance an d enhancement of renal blood flow. Nitroglycerin, an exogenous nitric oxide donor, caused a selective vasodilatory effect on renal conductan ce but not on resistance blood vessels and failed to increase renal bl ood how. These data suggest the possibility that stimulation of endoge nous nitric oxide production in the kidney could be used as a therapeu tic target for enhancement of renal flow in patients with heart failur e.