Xiao X H, Bevan J A
Department of Pharmacology, University of Vermont, College of Medicine, Burlington.
J Pharmacol Exp Ther. 1994 Jan;268(1):25-31.
Flow-induced contraction depends upon extracellular Ca++, but the underlying Ca++ entry pathway involved is unknown. We chose the rabbit facial vein to carry out this study because, in addition to contracting to a number of pharmacological agents and developing myogenic tone in response to stretch in vitro, flow-induced contraction also can be consistently demonstrated. Our goal was to determined whether the Ca++ entry pathway for flow-induced contraction could be distinguished from that involved in K(+)-, histamine- and stretch-induced contraction through the use of a Ca++ entry activator: Bay K 8644 and the Ca++ entry blockers nifedipine, diltiazem and verapamil and also cobalt and manganese. All four types of contractions studied are dependent on extracellular Ca++ Flow- and K(+)-induced contraction were equally sensitive to inhibition by nifedipine, verapamil and diltiazem. Those to histamine and stretch were not. Furthermore, the flow- and K(+)-induced contractions were enhanced equivalently by the calcium channel activator, Bay K 8644, but to a lesser degree than those to histamine and stretch. The inorganic calcium channel blockers, Co++ and Mn++ effected equally flow-, K(+)- and histamine-induced contraction. They were more potent in their inhibition of stretch-induced contraction. Our results suggest that flow- and K(+)-induced contractions depend on a similar Ca++ entry system into vascular smooth muscle: probably a voltage-gated Ca++ entry pathway, which is different from that utilized by histamine and stretch.
