Renal vasodilatory effect of endothelial stimulation in patients with chronic congestive heart failure

Objectives. This study sought to examine the vasodilatory response of the renal circulation to endothelial stimulation in patients with chronic heart failure. Background. Renal blood flow is often reduced in patients with chronic congestive heart failure and may lead to deterioration of renal function. Stimulation of renal endothelium has been shown to cause renal vasodilation in animals and in isolated human renal artery. The vasoregulatory role of the renal endothelium in patients with heart failure has not been evaluated. Methods. Renal vasodilatory effect of endothelial stimulation with acetylcholine was assessed and compared with that of endothelial-independent vasodilation with nitroglycerin. Both drugs were infused into the main renal artery. Renal artery cross-sectional are was measured with intravascular ultrasound and renal blood flow velocity with the aid of an intravascular Doppler technique. Results. Both drugs caused significant and comparable increase in renal artery cross-sectional are (maximal increase [mean ± SE] 14 ± 5% with acetylcholine, 15 ± 5% with nitroglycerin; both changes <0.05 vs. baseline). Acetylcholine also caused significant reduction in renal vascular resistance (maximal reduction 55 ± 6%) and increase in renal blood flow (maximal increase 136 ± 54%). In contrast, nitroglycerin administration showed no significant effect on renal vascular resistance and blood flow. Conclusions. Stimulation of endothelium-derived nitric oxide with acetylcholine results in significant vasodilatory effect on both conductance and resistance renal blood vessels and leads to marked reduction in renal vascular resistance and enhancement of renal blood flow. Nitroglycerin, an exogenous nitric oxide donor, caused selective vasodilatory effect on renal conductance but not on resistance blood vessels and failed to increase renal blood flow. These dat suggest the possibility that stimulation of endogenous nitric oxide production in the kidney could be used as therapeutic target for enhancement of renal flow in patients with heart failure.