Abstract: We studied the actions of lead and enzyme activators on this branch of the calcium messenger system. Helically-cut strips of rabbit mesenteric artery were mounted in muscle baths for measurement of isometric force development.Cumulative addition of lead acetate （10-10 to 10-3 mol/L ） to the muscle bath induced contractions （ED50 value = 10 -5 mol/ L）. These contractile responses to lead acetate were potentinted by protein kinase C activators, phorbol 12-myristate 13-acetate （TPA ） and mezerein as indicated by leftward shifts in the dose-response curve. H-7, a selective blocker of protcin kinase C, inhibited contractions to lead acetate. The inactive phorbol ester, phorbol 12-myristate 13-acetate 4-0-mcthyl ether, did not alter contractile responses to the metal. Arteries incubated in calcium-free solution did not contract by lead acetate and verapamil decreased lead-induced contractions. Contractile responses to lead acetate in arteries denuded of endothelium did not differ from those in intact vessels. These data indicate that lead interacts with the protein kinase C pathway of the calcium messenger system in vascular smooth muscle cells to induce contraction.