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-$P{O}_2$ superfusion (∼20 Torr; arteriolar diameter 55 ± 2 μm),E_m of SMC and EC averaged −37 and −36 mV, respectively. High-$P{O}_2$ superfusion (∼150 Torr) depolarized SMC (to −15 ± 1 mV) with vasoconstriction (to 24 ± 2 μm) and diameter cycled withE_m of SMC during vasomotion. In contrast, theE_m of EC did not change with $P{O}_2$ nor during vasomotion, yetE_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$P{O}_2$ 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$P{O}_2$ are mediated through L-type Ca²⁺ channels without corresponding electrical activity in EC.