The effect of nifedipine, nimodipine and nisoldipine on agonist- and 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.