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[Acute hypoxia increases outward current and decreases gap junction of VSMCs in guinea-pig anterior inferior cerebellar artery.] [Article in Chinese]

LI Xin-Zhi, SI Jun-Qiang, ZHANG Zhong-Shuang, ZHAO Lei, LI Li, MA Ke-Tao^*

The Key Laboratory of Xinjiang Endemic and Ethnic Diseases； Department of Physiology, School of Medicine, Shihezi University, Shihezi 832002, China

Abstract

The aim of the present study was to investigate the effects of acute hypoxia on the electrophysiological properties of vascular smooth muscle cells (VSMCs) in arteriole. Guinea-pig anterior inferior cerebellar artery (AICA) segments were isolated, and outer layer connective tissue was removed by collagenase A digestion and microforceps. By perfusion with physical saline solution containing no glucose and low oxygen, VSMC model of acute hypoxia was established. The model was studied by whole-cell patch clamp recording technique. Results were shown as below: (1) Acute hypoxia induced an outward current with amplitude of (36.4 ± 9.2) pA at holding potential of −40 mV, and the rest potential (RP) of the VSMCs was hyperpolarized from (−33.2 ± 1.9) mV to (−38.4 ± 1.5) mV. Acute hypoxia increased the outward current of VSMCs in a voltage-dependent manner, this enhancing effect being more pronounced at potentials ranging from 0 to +40 mV. The whole-cell membrane current of VSMCs induced by step command (+40 mV) increased from (650 ± 113) pA to (1 900 ± 197) pA. In the presence of 1 mmol/L tetraethylammonium (TEA), the enhancement of the VSMC membrane current by acute hypoxia was significantly reduced. (2) Acute hypoxia increased the membrane resistance (Rinput) of the VSMCs in AICA from (234 ± 63) MΩ to (1 211 ± 201) MΩ, and decreased the membrane capacitance (Cinput) from (279.3 ± 83.2) pF to (25.4 ± 1.9) pF. In the presence of 30 μmol/L 18β-glycyrrhetinic acid (18βGA) and 10 mmol/L TEA, the effects of acute hypoxia on the membrane current of VSMCs were nearly abolished. These results suggest that acute hypoxia causes vascular hyperpolarization and vasodilation, possibly by activating big conductance Ca2+-activated K+ channels (BKCa) of the VSMCs, and inhibits gap junctions between VSMCs, thus improving microcirculation and localizing the hypoxia-induced damage.

Key words: acute hypoxia; anterior inferior cerebellar artery; gap junction; big conductance calcium-activated potassium channel

Received: 2011-04-11　　Accepted: 2011-08-22

Corresponding author: 马克涛　　E-mail: maketao@shzu.edu.cn

Citing This Article：

LI Xin-Zhi, SI Jun-Qiang, ZHANG Zhong-Shuang, ZHAO Lei, LI Li, MA Ke-Tao. [Acute hypoxia increases outward current and decreases gap junction of VSMCs in guinea-pig anterior inferior cerebellar artery.] [Article in Chinese]. Acta Physiol Sin 2011; 63 (6): 533-539 (in Chinese with English abstract).