Ma Ke-tao, Li Li, Guan Bing-cai, Li Xin-zhi, Zhu He, Zhao Lei, Si Jun-qiang
School of Medicine, Shihezi University, Shihezi, China.
Zhonghua Yi Xue Za Zhi. 2011 Dec 13;91(46):3289-92.
To observe the effects of acute hypoxia on the electrophysiological properties of vascular smooth muscle cells (VSMCs) of mesenteric artery in guinea pig.
A segment of mesenteric artery (MA) (outer diameter < 100 µm) of guinea pig was digested with collagenase A and its adventitial connective tissue cleaned subsequently with fine tweezers. Whole-cell patch clamp recordings were performed to study the effects of acute hypoxia on the whole-cell membrane current, resting membrane potential (RP), membrane input capacitance (C(input)), and membrane input resistance (R(input) or its reciprocal membrane input conductance G(input)) of VSMC embedded in arteriolar segment.
Acute hypoxia induced an outward current with an amplitude of (76 ± 23) pA at holding potential -40 mV and hyperpolarized VSMC from a RP of (-22.5 ± 1.2) mV to (-42.0 ± 2.8) mV (P < 0.01). Acute hypoxia increased the outward current of VSMC in a voltage-dependent manner. And this enhancement was more pronounced at potentials from 0 to +40 mV. The whole-cell membrane current of VSMC induced by step commands (0, +20 and +40 mV) increased from (140 ± 18) pA to (660 ± 124) pA (P < 0.01), (282 ± 23) pA to (1120 ± 186) pA (P < 0.01) and (423 ± 40) pA to (1800 ± 275) pA (P < 0.01) respectively. In the presence of 1 mmol/L tetraethylammonium (TEA, a large conductance Ca(2+)-activated K(+) channel blocker), the enhancement of VSMC membrane current by acute hypoxia was significantly reduced. Acute hypoxia increased the R(input) of VSMC in MA from (446 ± 55) MΩ to (2187 ± 290) MΩ (P < 0.01) and decreased the C(input) from (184.3 ± 75.0) pF to (17.6 ± 2.2) pF (P < 0.01). In the presence of 30 µmol/L 18β-glycyrrhetinic acid (18βGA, a gap junction blocker) and 10 mmol/L TEA, the effects of acute hypoxia on the membrane current of VSMCs were almost abolished.
Acute hypoxia causes vascular hyperpolarization and vasodilation by activating large conductance Ca(2+)-activated K(+) channels of VSMC and inhibits gap junctions between VSMCs so as to improve microcirculation and localize hypoxia-induced damage.
观察急性缺氧对豚鼠肠系膜动脉血管平滑肌细胞（VSMC）电生理特性的影响。
用胶原酶A消化豚鼠一段外径<100 µm的肠系膜动脉（MA），随后用精细镊子清理其外膜结缔组织。采用全细胞膜片钳记录技术，研究急性缺氧对嵌入小动脉段的VSMC全细胞膜电流、静息膜电位（RP）、膜输入电容（C(input)）和膜输入电阻（R(input)或其倒数膜输入电导G(input)）的影响。
急性缺氧在-40 mV的钳制电位下诱导出幅度为（76±23）pA的外向电流，并使VSMC的RP从（-22.5±1.2）mV超极化至（-42.0±2.8）mV（P<0.01）。急性缺氧以电压依赖性方式增加VSMC的外向电流。这种增强在0至+40 mV的电位下更为明显。由阶跃指令（0、+20和+40 mV）诱导的VSMC全细胞膜电流分别从（140±18）pA增加至（660±124）pA（P<0.01）、（282±23）pA增加至（1120±186）pA（P<0.01）和（423±40）pA增加至（1800±275）pA（P<0.01）。在1 mmol/L四乙铵（TEA，一种大电导钙激活钾通道阻滞剂）存在的情况下，急性缺氧对VSMC膜电流的增强作用显著降低。急性缺氧使MA中VSMC的R(input)从（446±55）MΩ增加至（2187±290）MΩ（P<0.01），并使C(input)从（184.3±75.0）pF降低至（17.6±2.2）pF（P<0.01）。在30 µmol/L 18β-甘草次酸（18βGA，一种缝隙连接阻滞剂）和10 mmol/L TEA存在的情况下，急性缺氧对VSMCs膜电流的影响几乎被消除。
急性缺氧通过激活VSMC的大电导钙激活钾通道导致血管超极化和血管舒张，并抑制VSMCs之间的缝隙连接，从而改善微循环并限制缺氧诱导的损伤。
