The effects of elgodipine, a new dihydropyridine derivative, were compared to those of nisoldipine on contractile responses in various isolated artery rings and on mechanical activity in portal vein segments. Arteries used were: rabbit aorta, mesenteric (fifth branch), femoral and basilar, and sheep coronary arteries. Elgodipine and nisoldipine (10(-16)-3 x 10(-6) M) produced a concentration-dependent inhibition of the contractile responses induced by high K+ (80 mM), 5-hydroxytryptamine (10(-5) M) or noradrenaline (10(-6) M or 10(-4) M) in all the arteries studied. The inhibitory effect of elgodipine was greater in mesenteric resistance vessels (IC50 = 8.0 +/- 2.1 x 10(-12) M and 2.0 +/- 0.5 x 10(-13) M for the depression of high K(+)- and agonist-induced contraction, respectively), and in coronary arteries (IC50 = 2.6 +/- 0.3 x 10(-10) M and 9.0 +/- 1.4 x 10(-8) M for the inhibition of high K(+)- and agonist-induced contraction, respectively). In addition, the action of elgodipine in peripheral resistance vessels and in the coronary artery was more prominent than in aorta or femoral arteries, and this tissue selectivity was more apparent for elgodipine than for nisoldipine. In rat portal vein elgodipine (IC50 = 6.5 +/- 0.9 x 10(-8) M) and nisoldipine (IC50 = 8.5 +/- 1.3 x 10(-8) M) reduced in a concentration-dependent manner the development of mechanical activity. Furthermore, contractile responses produced by the addition of Ca2+ (1-5 mM) to Ca(2+)-free high K+ solution were also concentration dependently inhibited by elgodipine. However, elgodipine did not modify noradrenaline-induced contractions attributed to intracellular Ca2+ release. The results of this study indicate that elgodipine has potent vasodilator properties and vascular selectivity. The mechanisms through which elgodipine relaxes vascular smooth fibres seem to be related to its ability to inhibit the entry of extracellular Ca2+ into the cell.