779-5 The Effect of Endothelial Stimulation on the Renal Circulation in Patients with Chronic Heart Failure

Impairment of renal blood flow (RBF) is common in pts with chronic heart failure (CHF) and may lead to renal dysfunction. Although abnormal RBF may be due to depressed cardiac output, individual correlations are weak and suggest for local vasoregulatory mechanisms. We assessed the role of endothelium (END) derived nitric oxide (NO) on the renal circulation in 12 pts with CHF. Acetylcholine (ACh) (END-dependent vasodilator) and nitroglycerin (NTG) (END-independent vasodilator) were infused in a randomized, crossover design into the renal artery (RA). Effects on renal arterial (RAP) and renal venous IRVP) pressures, RA cross sectional area (CSA), RBF and renal vascular resistance (RVR) were studied. CSA was measured by intravascular ultrasound and RA flow velocity by a Doppler flow wire. The results were as follows:RAP mmHgRVP mmHgCSA mm2RBF ml/minRVR dynes.cm-5BLl91±410±1.03.7±0.3610±4611171±1295ACh 10-8M88±410±0.93.8±0.4*1015±118*6685±723*10-7M87±410±0.83.9±0.3*l360±154*5188±805*10-6M90±411±0.94.0±0.3*1499±181*4868±660*BL291±310±1.03.5±0.3635±3010275±931NTG 10-7M91±410±1.037±0.3†782±808842±106010-6M95±410±1.03.9±0.3†753±789972±141510-5M89±310±1.13.9±0,3†755±588595±809*p < 0.05 vs Baseline 1 (BL1)†p < 0.05 vs Baseline 2 (BL2)Conclusion1) Exogenous NO (NTG) causes a vasodilatory effect on renal conductance but not on resistance vessels; 2) In contrast, stimulation of endothelium-derived NO results in a significant vasodilation of both conductance and resistance vessels. This effect leads to reduction in RVR and increase in RBF and may be an important regulatory mechanism of renal circulation in pts with CHF