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

We tested whether O2-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 O2. During low-[Formula: see text] superfusion (∼20 Torr; arteriolar diameter 55 ± 2 μm), E m of SMC and EC averaged -37 and -36 mV, respectively. High-[Formula: see text] superfusion (∼150 Torr) depolarized SMC (to -15 ± 1 mV) with vasoconstriction (to 24 ± 2 μm) and diameter cycled with E m of SMC during vasomotion. In contrast, the E m of EC did not change with [Formula: see text] 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 μM) or nifedipine (1 μM) abolished vasomotor and electrical responses to[Formula: see text] 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[Formula: see text] are mediated through L-type Ca2+ channels without corresponding electrical activity in EC.