蛋白激酶C参与毒蕈碱激动剂诱导的豚鼠回肠纵肌收缩。

Involvement of protein kinase C in muscarinic agonist-induced contractions of guinea pig ileal longitudinal muscle.

Honda K, Takano Y, Kamiya H

Department of Pharmacology, Faculty of Pharmaceutical Sciences, Fukuoka University, Japan.

Gen Pharmacol. 1996 Sep;27(6):957-61. doi: 10.1016/0306-3623(95)02124-8.

Abstract

Carbachol (10(-5) M) caused an initial transient contraction (phasic contraction) and a subsequent late contraction (tonic contraction) in the guinea pig ileum. The phasic contraction was markedly suppressed by calmodulin antagonist W-7, but not by protein kinase C inhibitor H-7. 2. The tonic contraction was suppressed by H-7, but not by W-7. 3. The carbachol-induced phasic contraction in the absence of extracellular Ca2+ was suppressed by both W-7 and H-7. 4. Carbachol (10(-5) M) stimulated the formation of inositol phosphates (IPs) in the guinea pig ileum. The carbachol-induced IPs formation was dependent on the extracellular Ca2+ concentration.

摘要

卡巴胆碱（10⁻⁵ M）可引起豚鼠回肠先出现短暂收缩（相性收缩），随后出现晚期收缩（紧张性收缩）。相性收缩明显受到钙调蛋白拮抗剂W-7的抑制，但不受蛋白激酶C抑制剂H-7的抑制。2. 紧张性收缩受到H-7的抑制，但不受W-7的抑制。3. 在无细胞外Ca²⁺的情况下，卡巴胆碱诱导的相性收缩受到W-7和H-7两者的抑制。4. 卡巴胆碱（10⁻⁵ M）刺激豚鼠回肠中肌醇磷酸（IPs）的形成。卡巴胆碱诱导的IPs形成依赖于细胞外Ca²⁺浓度。