Potassium Channels and Norepinephrine-induced Contraction of Cremasteric Arteriolar Muscle Cells

Abstract

Vascular smooth muscle cells in the walls of small arteries and arterioles play an important role in the regulation of blood flow and pressure in the cardiovascular system of vertebrates. The purpose of the present study was to evaluate the function of voltage-gated (Kv), calcium activated (KCa), and ATP sensitive (KATP) potassium channels in norepinephrine-induced contraction of the muscle surrounding the testes, cremasteric, arteriolar smooth muscle cells. This was accomplished by comparing responses of these cells before and during exposure to specific inhibitors of each type of channel. The calcium channel blockers, diltiazem and nifedipine, efficiently blocked norepinephrine-induced contraction of arteriolar muscle cells, demonstrating the integral role which L-type calcium channels play in these cells. It was thought that inhibition of Kv and KCa channels would potentiate norepinephrine-induced contractions by blocking feedback inhibition of norepinephrine-induced depolarization of the cell membrane. It was observed that tetraethylamonium, a KCa channel blocker, and 4aminopyridine, a Kv channel blocker, inhibited norepinephrine-induced contraction. This may indicate that norepinephrine acts partly by modulating these channels. Alternatively, this interaction between the polar drugs and the norepinephrine may have been non-specific prevention of norepinephrine-induced cellular contractions before they were initiated. Finally, blockade of KATP channels with glibenclamide also inhibited norepinephrine-induced contraction. These results support the hypothesis that norepinephrine acts, in part, by closing KATP channels in arteriolar muscle cells. This knowledge will aid researchers in understanding better the mechanisms by which the microvasculature of the the cardiovascular system function and possibly lead to more specific therapies for diseased systems.