Membrane Potential and Arteriolar Tone at Rest

Arterioles in the microcirculation at rest display substantial tone largely due to the impact of blood pressure on the smooth muscle. Under these conditions, smooth muscle and endothelial cells have a membrane potential of about -30 mV. This relatively depolarized membrane potential results from the outward flow of K+ through K+ channels (a hyperpolarizing current) that is balanced by efflux of Cl- ions and inward flow of Na+ and Ca2+ ions (all depolarizing currents). There appear to be substantial regional and species differences in the specific ion channels that contribute to resting membrane potential. However, general patterns appear.

In arteriolar smooth muscle cells at rest, membrane potential is determined by K+ efflux through KV channels, cation (Na+ and Ca2+) influx through SOC, and probably Cl-efflux through ClSW channels. In skeletal muscle and coronary vascular beds, KATP channels also contribute to resting membrane potential. In vivo studies suggest that voltage-gated Ca2+ channels and BKCa channels may not be active at rest. The mechanisms responsible for the apparent lack of activity of voltage-gated Ca2+ channels at rest in vivo have not been established. However, it is likely that the low resting activity of arteriolar BKCa channels in vivo reflects the low activity of voltage-gated Ca2+ channels, with which the BKCa channels are functionally coupled (Figure 1), along with a high Ca2+ threshold of microvascular BKCa channels. Inward rectifier K+ channels do not contribute to resting potential because of the relatively depolarized membrane potential (-30mV) found in arteriolar smooth muscle cells. Calcium-activated Cl- channels appear silent at rest due to their high Ca2+ threshold.

The ion channels that contribute to resting membrane potential in arteriolar endothelial cells have not been established. However, similar to the overlying smooth muscle cells, KV channels, Clsw channels and nonselective cation channels probably contribute to the relatively depolarized membrane potential in endothelial cells in resting arterioles (-30 mV). In addition, blood flow over the endothelium may activate endothelial KIR channels through a shear-stress dependent mechanism, such that these K+ channels may also contribute to resting membrane potential of arteriolar endothelial cells. Also, because smooth muscle and endothe-lial cells may be electrically coupled by myoendothelial gap junctions in some arterioles, both smooth muscle and endothelial ion channels may contribute to the membrane potential of the other cell type.

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