Alfentanil was reported to relax the rat aorta by direct action on the vascular smooth muscle. The aims of this in vitro study were to examine the effect of alfentanil on phenylephrine-induced contractions in the rat aorta and to determine the cellular mechanism associated with this process.

Endothelium-denuded aortic rings were suspended in order to record isometric tension. In the rings with or without 10−6 mol naloxone or 10−5 mol verapamil, the concentration–response curves for phenylephrine and potassium chloride were generated in the presence or absence of alfentanil (10−6, 5 × 10−5, 10−4 mol). In the rings exposed to a calcium-free isotonic depolarizing solution, the contractile response induced by the addition of calcium was assessed in the presence or absence of alfentanil (5 × 10−5, 10−4 mol).

Alfentanil (5 × 10−5, 10−4 mol) attenuated (P < 0.05) the phenylephrine-induced contraction in the ring with or without 10−6 mol naloxone but had no effect on the phenylephrine-induced contraction in the rings pretreated with verapamil. Alfentanil (5 × 10−5, 10−4 mol) produced a significant rightward shift (P < 0.01) in the potassium chloride dose–response curve, and attenuated the contractile response (P < 0.001) induced by calcium in the calcium-free isotonic depolarizing solution in a dose-dependent manner.

A supraclinical dose of alfentanil attenuates the phenylephrine-induced contraction via an inhibitory effect on calcium influx by blocking the l-type calcium channels in the rat aortic vascular smooth muscle.