Effect of morphine on the cat middle cerebral artery.

Morphine (up to 3 X 10(-4) M) elicited concentration-dependent contractions in cat middle cerebral arteries, higher concentrations induced vasodilation. These responses were annulled in the presence of 1-methyl-3-isobutylxanthine, but unaffected by diphenhydramine, cimetidine, phentolamine or naloxone. Ca2+ suppression blocked the morphine-evoked contractions and Ca2+ addition antagonized its vasodilatory effects. Nifedipine induced a marked relaxation in arteries previously contracted with morphine. Preincubation with nifedipine induced a decrease in the contraction elicited by morphine while it increased the vasodilatory phase. Morphine did not produce a significant effect in femoral arteries. In cerebral arteries previously submitted to an active tone, the opioid-induced vasodilation was unchanged by naloxone, cimetidine, diphenhydramine or ouabain, whereas Ca2+ addition antagonized this effect. These results indicate: that the opioid effects are mediated neither by opiate receptors nor by noradrenaline or histamine release; and that an antagonism exists between Ca2+ and the vasodilation caused by morphine.