Coronary vasoconstrictor effects of atriopeptin II.
Coronary vasoconstrictor effects of atriopeptin II.
复制标题
atriopeptin II 的冠状血管收缩作用。
DOI：
10.1126/science.2931801
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Chimoskey,JE
中科院分区：
文献类型：
--
作者：
Wangler,RD;Breuhaus,BA;Otero,HO;Hastings,DA;Holzman,MD;Saneii,HH;SparksJr,HV;Chimoskey,JE
心房利钠肽降低动脉压、心脏充盈压和心输出量。在离体的兰根多夫灌注豚鼠心脏中，心房钠肽II，一种含有23个氨基酸的心房钠肽，也是一种有效的冠状血管收缩剂。心房肽II在豚鼠心脏中的中位有效剂量为26纳摩尔，收缩阈值剂量为5纳摩尔，在恒压下灌注的心脏中，当剂量为100纳摩尔时，血流几乎停止。在大鼠和狗的心脏制剂中，相似浓度的心房肽II也可引起冠状动脉收缩。二硫桥是血管收缩活性所必需的；这个桥的减少消除了心房利钠肽的活性，正如它消除了心房利钠肽的其他生物活性一样。
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.