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 (Em) 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- PO2 superfusion (approximately 20 Torr; arteriolar diameter 55 +/- 2 micron), Em of SMC and EC averaged -37 and -36 mV, respectively. High-PO2 superfusion ( approximately 150 Torr) depolarized SMC (to -15 +/- 1 mV) with vasoconstriction (to 24 +/- 2 micron) and diameter cycled with Em of SMC during vasomotion. In contrast, the Em of EC did not change with PO2 nor during vasomotion, yet Em depolarized by 21 +/- 2 mV when the extracellular K+ concentration ([K+]o) was raised to 55 mM. Superfusion with diltiazem (10 microM) or nifedipine (1 microM) abolished vasomotor and electrical responses to PO2 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.