We tested the hypothesis that cyclic changes in membrane potential (E-m) un
derlie spontaneous vasomotion in cheek pouch arterioles of anesthetized ham
sters, Diameter oscillations (similar to3 min(-1)) were preceded (similar t
o3 s) by oscillations in E-m of smooth muscle cells (SMC) and endothelial c
ells (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 d
iameter observed during vasomotion (41 +/- 2 <mu>m); (2) a slow depolarizat
ion (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 transie
nt partial repolarization (3-4 mV); (5) a sustained (5 +/- 1 s) depolarizat
ion (-28 +/- 2 mV) correlating (r = 0.78, p < 0.01) with time (3 +/- 1 s) a
t the smallest diameter (27 +/- 2 <mu>m) during vasomotion; (6) a slow repo
larization (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 nitrop
russide or nifedipine caused sustained hyperpolarization and dilation, wher
eas tetraethylammonium or elevated PO2 caused sustained depolarization and
constriction. We suggest that vasomotion in vivo reflects spontaneous, cycl
ic changes in E-m of SMC and EC corresponding with cation fluxes across pla
sma membranes. Copyright (C) 2000 S. Karger AG, Basel.