豚鼠离体心脏对神经激肽A的血管收缩和舒张反应。

Vasoconstrictor and dilator responses to neurokinin A in isolated guinea pig heart.

作者信息

Hoover D B, Hossler F E

机构信息

Department of Pharmacology, James H. Quillen College of Medicine, East Tennessee State University, Johnson City 37614.

出版信息

Peptides. 1993 Jan-Feb;14(1):29-36. doi: 10.1016/0196-9781(93)90007-4.

DOI:10.1016/0196-9781(93)90007-4

PMID:7680129

Abstract

Effects of neurokinin A (NKA) and substance P (SP) on coronary resistance vessels were studied in isolated guinea pig hearts perfused with isotonic buffer containing 20 mM KCl. Injections of NKA and SP caused dose-dependent reductions in perfusion pressure with ED50 values of 14.0 and 0.326 pmol, respectively. Blockade of nitric oxide synthesis or removal of the endothelium inhibited vasodilator responses to neurokinins. Infusions of NKA or SP caused tachyphylaxis and cross-desensitization to the other neurokinin but not to acetylcholine. Injections of 2.5 nmol NKA increased perfusion pressure by 31 +/- 8% when given after tachyphylaxis developed to infused SP (2.5 nmol/100 microliters/min). It was concluded that 1) neurokinins cause an endothelium-dependent relaxation of coronary resistance vessels by stimulating NK-1 receptors on endothelial cells, and 2) desensitization of the receptor mediating vasodilation unmasks a vasoconstrictor response to NKA.

摘要

在灌注含20 mM氯化钾等渗缓冲液的离体豚鼠心脏中，研究了神经激肽A（NKA）和P物质（SP）对冠状动脉阻力血管的影响。注射NKA和SP导致灌注压力呈剂量依赖性降低，ED50值分别为14.0和0.326 pmol。一氧化氮合成的阻断或内皮的去除抑制了对神经激肽的血管舒张反应。输注NKA或SP导致快速耐受和对另一种神经激肽的交叉脱敏，但对乙酰胆碱无此现象。在对输注的SP（2.5 nmol/100微升/分钟）产生快速耐受后，注射2.5 nmol NKA可使灌注压力升高31±8%。得出的结论是：1）神经激肽通过刺激内皮细胞上的NK-1受体引起冠状动脉阻力血管的内皮依赖性舒张；2）介导血管舒张的受体脱敏掩盖了对NKA的血管收缩反应。