Different inhibition by vasodilators of coronary artery contraction

Actions of a variety of vasodilators were compared in helical strips of the dog coronary artery, previously soaked in Ca2+-free medium under severe hypoxia. Ca2+ entry blockers, such as nifedipine and flunarizine, did not affect the PGF2 alpha-induced contraction in Ca2+-free medium, but strongly reduced the Ca2+-induced contraction under severe hypoxia in the strips stimulated by PGF2 alpha. The contraction obtained following reoxygenation was also reduced by the Ca2+ blockers. Nitroglycerin and isoproterenol inhibited the PGF2 alpha- and Ca2+-induced contractions as well as the reoxygenation-induced contraction. PGI2 methylester and TRK-100, stable analogues of PGI2, attenuated the PGF2 alpha-induced contraction in Ca2+-free medium, but not the Ca2+-induced contraction under hypoxia. PGI2 analogues inhibited the contraction due to reoxygenation to a greater extent than Ca2+ entry blockers, nitroglycerin and isoproterenol. The present study differentiated the inhibitory actions of various vasodilator agents on coronary artery contractions, possibly associated with the release of Ca2+, influx of Ca2+ through receptor-operated channel, and reoxygenation-induced facilitation of Ca2+ influx. Suppression by the vasodilators of the reoxygenation-induced coronary vasoconstriction may participate in the prophylaxis of no-reflow phenomena elicited by severe hypoxia.