title: [Effects of acute hypoxia on the electrophysiological properties of vascular smooth muscle cells of mesenteric artery in guinea pig].
abstract: OBJECTIVE
  To observe the effects of acute hypoxia on the electrophysiological properties of vascular smooth muscle cells (VSMCs) of mesenteric artery in guinea pig.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: School of Medicine, Shihezi University, Shihezi, China.
authors.forename: Ke-tao
authors.initials: KT
authors.lastname: Ma
authors.forename: Li
authors.initials: L
authors.lastname: Li
authors.forename: Bing-cai
authors.initials: BC
authors.lastname: Guan
authors.forename: Xin-zhi
authors.initials: XZ
authors.lastname: Li
authors.forename: He
authors.initials: H
authors.lastname: Zhu
authors.forename: Lei
authors.initials: L
authors.lastname: Zhao
authors.forename: Jun-qiang
authors.initials: JQ
authors.lastname: Si
mesh_terms: D000818:Animals; D015687:Cell Hypoxia / Q000502:physiology; D005260:Female; D006168:Guinea Pigs; D008297:Male; D008564:Membrane Potentials; D008638:Mesenteric Arteries / Q000166:cytology* / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000166:cytology; D032389:Myocytes, Smooth Muscle / Q000502:physiology*; D018408:Patch-Clamp Techniques; D024642:Potassium Channels, Voltage-Gated / Q000502:physiology
chemical_list: D024642:Potassium Channels, Voltage-Gated