Wei C M, Hu S, Miller V M, Burnett J C
Cardiorenal Research Laboratory, Mayo Clinic and Foundation, Rochester, MN 55905.
Biochem Biophys Res Commun. 1994 Nov 30;205(1):765-71. doi: 10.1006/bbrc.1994.2731.
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.
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。