[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.

CONCLUSION:

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: Ke-tao Ma, Li Li, Bing-cai Guan, Xin-zhi Li, He Zhu, Lei Zhao, Jun-qiang Si
• Journal: Zhonghua yi xue za zhi (Zhonghua Yi Xue Za Zhi) Vol. 91 Issue 46 Pg. 3289-92 (Dec 13 2011) ISSN: 0376-2491 [Print] China
• PMID: 22333153 (Publication Type: English Abstract, Journal Article, Research Support, U.S. Gov't, Non-P.H.S.)

Chemical References

• Potassium Channels, Voltage-Gated

Topics

• Animals
• Cell Hypoxia (physiology)
• Female
• Guinea Pigs
• Male
• Membrane Potentials
• Mesenteric Arteries (cytology, physiology)
• Muscle, Smooth, Vascular (cytology)
• Myocytes, Smooth Muscle (physiology)
• Patch-Clamp Techniques
• Potassium Channels, Voltage-Gated (physiology)