The influence of vascular endothelium on angiotensin II-induced contraction and the underlying mechanisms in the rabbit renal artery were investigated. In endothelium-intact preparations, angiotensin II (3-100 nM) caused a concentration-dependent increase in tension by maximally (Emax) 0.74 +/- 0.05 g. Removal of the endothelium significantly enhanced the angiotensin II-induced contractions (Emax: 3.91 +/- 0.19 g). Indomethacin (10 microM) did not influence the angiotensin II-induced contractions. Methylene blue (10 microM) and NG-methyl-l-arginine (L-NMMA, 5 microM) significantly enhanced angiotensin II-induced contractions by 418 +/- 29% and 200 +/- 14%, respectively, in endothelium intact preparations, but not in those devoid of endothelium. L-arginine (1 mM), but not D-arginine, reversed the L-NMMA-induced enhancement of the angiotensin II-induced contraction. The present results suggest that angiotensin II-induced contractions in rabbit renal artery are largely subject to the influence of the endothelium. The endothelium-derived relaxant factor (EDRF), rather than cyclo-oxygenase products, appears to be involved in mediating the inhibitory effects of the endothelium. Nitric oxide (NO) derived from endothelium may play a major role in inhibiting angiotensin II-induced contractions in this preparation.