Electrophysiological basis of arteriolar vasomotion in vivo
Electrophysiological basis of arteriolar vasomotion in vivo
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DOI:
10.1159/000054090
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发表时间:
2000-11-01
影响因子:
1.7
通讯作者:
Segal, SS
中科院分区:
文献类型:
--
作者:
Bartlett, IS;Crane, GJ;Segal, SS
We tested the hypothesis that cyclic changes in membrane potential (E-m) underlie spontaneous vasomotion in cheek pouch arterioles of anesthetized hamsters, Diameter oscillations (similar to3 min(-1)) were preceded (similar to3 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 m); (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 m) 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 PO2 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. Copyright (C) 2000 S. Karger AG, Basel.