Oxygen induces electromechanical coupling in arteriolar smooth muscle cells:: a role for L-type Ca2+ channels

We tested whether O-2-induced vasomotor responses of arterioles correspond to changes in membrane potential (E-m) of cells in the arteriolar wall. The cheek pouches of anesthetized male hamsters were prepared for intravital microscopy and intracellular recording. Microelectrodes containing Lucifer yellow dye were used to label smooth muscle cells (SMC) or endothelial cells (EC) during arteriolar responses to O-2. During low-Pot superfusion (similar to 20 Torr; arteriolar diameter 55 +/- 2 mu m), E-m of SMC and EC averaged -37 and -36 mV, respectively. High-Po-2 superfusion (similar to 150 Torr) depolarized SMC (to -15 +/- 1 mV) with vasoconstriction (to 24 +/- 2 mu m) and diameter cycled with E-m of SMC during vasomotion. In contrast, the E-m of EC did not change with Po, nor during vasomotion, yet E-m depolarized by 21 +/- 2 mV when the extracellular K+ concentration ([K+](o)) was raised to 55 mM. Superfusion with diltiazem (10 mu M) or nifedipine (1 mu M) abolished vasomotor and electrical responses to Po, in SMC but did not eliminate depolarizations to elevated [K+](o). We conclude that, under physiological conditions, electrical and mechanical responses of arteriolar SMC to changes in PO2 are mediated through L-type Ca2+ channels without corresponding electrical activity in EC.