Guo Hui-Shu, Cai Zheng-Xu, Zheng Hai-Feng, Li Xiang-Lan, Cui Yi-Feng, Wang Zuo-Yu, Xu Wen-Xie, Lee Sang-Jin, Kim Young-Chul
Department of Physiology, College of Medicine, Yanbian University, Yanji 133000, Jilin Province, China.
World J Gastroenterol. 2003 Sep;9(9):2054-9. doi: 10.3748/wjg.v9.i9.2054.
To investigate ion channel mechanism in CNP-induced relaxation of gastric circular smooth muscle in guinea pigs.
Spontaneous contraction of gastric smooth muscle was recorded by a four -channel physiograph. The whole cell patch-clamp technique was used to record calcium-activated potassium currents and membrane potential in the gastric myocytes isolated by collagenase.
C-type natriuretic peptide (CNP) markedly inhibited the spontaneous contraction in a dose-dependent manner in gastric circular smooth muscle in guinea pigs. Ly83583, an inhibitor of guanylate cyclase, weakened CNP-induced inhibition on spontaneous contraction but Zaparinast, an inhibitor of cGMP sensitive phosphoesterase, potentiated CNP-induced inhibition in gastric circular smooth muscles. The inhibitory effects of CNP on spontaneous contraction were blocked by tetrathylammonium (TEA), a nonselective potassium channel blocker. CNP hyperpolarized membrane potential from -60.0 mV+/-2.0 mV to -68.3 mV+/-3.0 mV in a single gastric myocyte. CNP increased calcium-activated potassium currents (I(K(ca))) in a dose-dependent manner in gastric circular myocytes. CNP also increased the spontaneously transient outward currents (STOCs). Ly83583 partly blocked CNP-induced increase of calcium-activated potassium currents, but Zaparinast potented the effect.
CNP inhibits spontaneous contraction, and potassium channel may be involved in the process in gastric circular smooth muscle of guinea pigs. CNP-induced increase of I(K(ca)) is mediated by a cGMP dependent pathway.
研究C型利钠肽（CNP）诱导豚鼠胃环行平滑肌舒张的离子通道机制。
采用四通道生理记录仪记录胃平滑肌的自发收缩活动。应用全细胞膜片钳技术记录经胶原酶分离的胃肌细胞的钙激活钾电流和膜电位。
C型利钠肽（CNP）可明显抑制豚鼠胃环行平滑肌的自发收缩，且呈剂量依赖性。鸟苷酸环化酶抑制剂Ly83583可减弱CNP对自发收缩的抑制作用，而cGMP敏感性磷酸二酯酶抑制剂扎普司特可增强CNP对胃环行平滑肌自发收缩的抑制作用。非选择性钾通道阻滞剂四乙铵（TEA）可阻断CNP对自发收缩的抑制作用。在单个胃肌细胞中，CNP可使膜电位从-60.0 mV±2.0 mV超极化至-68.3 mV±3.0 mV。CNP可使胃环行肌细胞的钙激活钾电流（I(K(ca))）呈剂量依赖性增加。CNP还可增加自发瞬时外向电流（STOCs）。Ly83583可部分阻断CNP诱导的钙激活钾电流增加，而扎普司特可增强该作用。
CNP抑制豚鼠胃环行平滑肌的自发收缩，钾通道可能参与其中。CNP诱导的I(K(ca))增加是由cGMP依赖性途径介导的。
