Electrophysiological Basis of Arteriolar Vasomotion in vivo

We tested the hypothesis that cyclic changes in membrane potential (E m ) underlie spontaneous vasomotion in cheek pouch arterioles of anesthetized hamsters. Diameter oscillations (∼3 min –1 ) were preceded (∼3 s) by oscillations in E m of smooth muscle cells (SMC) and endothelial cells (EC). Oscillations in E m were resolved into six phases: (1) a period (6 ± 2 s) at the most negative E m observed during vasomotion (–46 ± 2 mV) correlating (r = 0.87, p < 0.01) with time (8 ± 2 s) at the largest diameter observed during vasomotion (41 ± 2 µm); (2) a slow depolarization (1.8 ± 0.2 mV s –1 ) with no diameter change; (3) a fast (9.1 ± 0.8 mV s –1 ) depolarization (to –28 ± 2 mV) and constriction; (4) a transient partial repolarization (3–4 mV); (5) a sustained (5 ± 1 s) depolarization (–28 ± 2 mV) correlating (r = 0.78, p < 0.01) with time (3 ± 1 s) at the smallest diameter (27 ± 2 µm) during vasomotion; (6) a slow repolarization (2.5 ± 0.2 mV s –1 ) and relaxation. The absolute change in E m correlated (r = 0.60, p < 0.01) with the most negative E m . Sodium nitroprusside or nifedipine caused sustained hyperpolarization and dilation, whereas tetraethylammonium or elevated PO 2 caused sustained depolarization and constriction. We suggest that vasomotion in vivo reflects spontaneous, cyclic changes in E m of SMC and EC corresponding with cation fluxes across plasma membranes.