Abstract
We have suggested that cyclopiazonic acid (CPA), a Ca2+-ATPase inhibitor, produces nitric oxide (NO) by triggering a Ca2+-influx resulting from Ca2+-depletion in the endoplasmic reticulum of endothelial cells. The tyrosine kinase inhibitor methyl 2, 5-dihydroxycinnamate, while having no effect on relaxations induced by A23187 or Na nitroprusside, did inhibit the CPA-induced relaxation and cyclic GMP formation in rat aorta. Tyrosine kinase may participate in endothelial NO synthesis through activation of a Ca2+ entry mechanism.
