ABSTRACT
Although most vascular smooth muscles (VSMs) do not exhibit action potentials, changes in membrane potential are almost always integral to vascular responses to both constricting and dilating stimuli. Under resting conditions in vivo, the VSM membrane potential is sufficiently depolarized that Ca2þ influx through voltage-gated Ca2þ channels (VGCCs) makes an important contribution to basal tone. The opening of these channels is enhanced by depolarization and suppressed by hyperpolarization, leading to alterations in the intracellular calcium concentration ([Ca2þ]i) that correspondingly potentiate or diminish force development and therefore vascular resistance.
