The contractile response of renal arterial muscle to porcine endothelin (ET-1) was studied by measuring vessel diameters and vascular smooth muscle transmembrane potentials in small arteries (300–600μm inside diameter) isolated from dog kidneys and cannulated with micropipettes connected to a pressurized reservoir system. Endothelin (10−12to 10−8M) was a potent constrictor of these vessels and caused a concentration-dependent contraction at a mean EC50(median effective concentration) of 3.1 (±1.15)×10−10M. Endothelin also produced a modest depolarization of arterial smooth muscle much smaller than had previously been demonstrated to occur in these vessels in response to norepinephrine or transmural pressure elevation. Endothelin-induced contractions were partially inhibited by 10−6M nifedipine and abolished by Ca2+-free solution. Although the influx of extracellular Ca2+ions through dihydropyridine-sensitive pathways contributes to endothelin-induced contractions of these vessels, electromechanical coupling does not appear to be the sole determinant of the magnitude of endothelin-induced constriction in canine small renal arteries.