The effect of nifedipine, nimodipine and nisoldipine on agonistand trauma-stimulated vascular prostacyclin synthesis in vitro

The present study shows that nifedipine, nimodipine and nisoldipine inhibit in vitro agonist-induced prostacyclin (PGI₂) release from rat aortic rings. The agonists used were: U46619 (a thromboxane A₂ analogue); A23187 (a calcium ionophore) and adrenaline. In contrast, these calcium channel blockers did not inhibit in vitro trauma-or arachidonic acid (AA)-induced PGI₂ release. Therefore, in vitro PGI₂ release, models may be calcium channel dependent (adrenaline, U46619, A23187) or independent (trauma, AA), a property which is relevant to calcium channel blocker research. It is suggested that calcium channel dependent PGI₂ release is relevant to modulating the relaxation phase of muscle contraction, while calcium channel independent PGI₂ release is relevant to limiting the extension of thrombi following local vascular trauma.