The contractile effect of lead on rat aortic rings was examined. Lead (0.1-
3.1 mM) elicited concentration-dependent but endothelium-independent contra
ctions, which were unaffected by prazosin (1 muM), The contractile effects
of lead were similar when the aortic rings were bathed either in the absenc
e or presence of external Ca2+. Lanthanum (1 mM) but not verapamil (1 muM)
inhibited the lead contractions; hence non-L-calcium channels are involved
in such effect. In addition, lead induced contractions on aortic rings incu
bated in Ca2+-free EGTA-containing solution for 70 min., an experimental co
ndition in which intracellular Ca2+-stores are depleted. Finally, the contr
actile effect of lead was not modified by calphostin C (an inhibitor of pro
tein kinase C). In conclusion, the present results suggest that in rat aort
a, the lead-induced contraction is independent of extra- and intracellular
calcium stores. In addition, the effect of lead is independent of either ca
techolamines or protein kinase C. It is likely that in rat aorta, lead ente
rs into the smooth muscle cells through non-L-calcium channels, and when ac
ting like calcium on the contractile machinery it produces contraction. The
differences observed between our results and those obtained by other autho
rs may indicate that the mechanism of the contractile effect of lead varies
among the different blood vessels.