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.