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C型利钠肽在离体猪冠状动脉及冠状动脉血管平滑肌细胞中的血管作用

Vascular actions of C-type natriuretic peptide in isolated porcine coronary arteries and coronary vascular smooth muscle cells.

作者信息

Wei C M, Hu S, Miller V M, Burnett J C

机构信息

Cardiorenal Research Laboratory, Mayo Clinic and Foundation, Rochester, MN 55905.

出版信息

Biochem Biophys Res Commun. 1994 Nov 30;205(1):765-71. doi: 10.1006/bbrc.1994.2731.

Abstract

C-type natriuretic (CNP) caused concentration-dependent relaxations in porcine coronary arteries with a maximal relaxation (10(-6)M) of 46%. Relaxations to CNP in isolated coronary arteries were significantly attenuated with potassium channel antagonists charybdotoxin (10(-7)M) and glibenclamide (10(-7)M). Membrane potential and K+ currents were measured in enzymatically dissociated smooth muscle cells from porcine coronary arteries with patch-clamp techniques in a whole-cell mode (n = 5). CNP caused K+ channel activation and membrane hyperpolarization in a dose-dependent manner. This hyperpolarization was markedly suppressed by the potassium channel inhibitor tetraethylammonium (TEA, 5 mM). These results demonstrate that CNP relaxes porcine coronary arterial smooth muscle by hyperpolarization of vascular smooth muscle through potassium channel stimulation.

摘要

C型利钠肽(CNP)可使猪冠状动脉产生浓度依赖性舒张,最大舒张率(10⁻⁶M)为46%。在分离的冠状动脉中,钾通道拮抗剂蝎毒素(10⁻⁷M)和格列本脲(10⁻⁷M)可显著减弱对CNP的舒张反应。采用全细胞模式的膜片钳技术,在酶解分离的猪冠状动脉平滑肌细胞中测量膜电位和钾电流(n = 5)。CNP以剂量依赖性方式引起钾通道激活和膜超极化。钾通道抑制剂四乙铵(TEA,5 mM)可显著抑制这种超极化。这些结果表明,CNP通过刺激钾通道使血管平滑肌超极化,从而舒张猪冠状动脉平滑肌。

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