心房肽II的冠状动脉收缩作用。

Coronary vasoconstrictor effects of atriopeptin II.

作者信息

Wangler R D, Breuhaus B A, Otero H O, Hastings D A, Holzman M D, Saneii H H, Sparks H V, Chimoskey J E

出版信息

Science. 1985 Nov 1;230(4725):558-61. doi: 10.1126/science.2931801.

Abstract

Atrial natriuretic peptides lower arterial pressure, cardiac filling pressure, and cardiac output. In isolated, Langendorff-perfused guinea pig hearts, atriopeptin II, the 23-amino acid atrial natriuretic peptide, is also a potent coronary vasoconstrictor. The median effective dose for atriopeptin II in guinea pig hearts is 26 nanomoles, the threshold constrictor dose is 5 nanomoles, and flow nearly ceases at a dose of 100 nanomoles in perfused hearts at constant pressure. Similar concentrations of atriopeptin II also cause coronary vasoconstriction in rat and dog heart preparations. The disulfide bridge is necessary for vasoconstrictor activity; reduction of this bridge abolishes the activity, as it does the other biological activities of atrial natriuretic peptides.

摘要

心房利钠肽可降低动脉压、心脏充盈压和心输出量。在离体的、经Langendorff灌注的豚鼠心脏中，23个氨基酸的心房利钠肽——心钠素II，也是一种强效的冠状动脉血管收缩剂。心钠素II在豚鼠心脏中的半数有效剂量为26纳摩尔，阈收缩剂量为5纳摩尔，在恒压灌注的心脏中，剂量为100纳摩尔时血流几乎停止。相似浓度的心钠素II在大鼠和犬心脏标本中也会引起冠状动脉血管收缩。二硫键对于血管收缩活性是必需的；该二硫键的还原会消除其活性，心房利钠肽的其他生物学活性也是如此。