Myocardial Actions of Angiotensin
Myocardial Actions of Angiotensin
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血管紧张素的心肌作用
DOI：
10.1097/00132586-196502000-00013
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发表时间：
1964
影响因子：
20.1
通讯作者：
J. Koch
中科院分区：
文献类型：
--
作者：
J. Koch
合成血管紧张素 a 对小猫的等长收缩、孤立乳头肌具有明显的正性肌力作用。在 10−10 M 至 10−5 M 范围内，反应随着药物浓度的增加而增加。张力发展的平均最大增加为 120%。血管紧张素通过增加收缩元件的激活程度来提高收缩性，而其激活状态的持续时间没有显着变化。低浓度的血管紧张素比等摩尔浓度的l-去甲肾上腺素具有更强的正性肌力作用；但左旋去甲肾上腺素可获得的最大正性肌力作用几乎是血管紧张素的两倍。血管紧张素对猫心房肌的正性肌力作用轻微，对蛙心室肌无活性。它对哺乳动物心房或心室肌肉的静息长度-张力关系没有影响。血管紧张素浓度高达 10−5 M 时，SA 结中脉冲形成的频率不会发生显着变化。与左旋肾上腺素形成鲜明对比的是，血管紧张素不会引起心房或心室肌肉中的异位脉冲形成。这表明血管紧张素对心室心肌的正性肌力作用对于药物在完整循环中的升压作用很重要。面对心脏射血阻力增加，心肌收缩力的增加往往会最小化或防止心输出量的减少，从而支持动脉压的升高。
Synthetic angiotensin a has pronounced inotropic effects on isometrically contracting, isolated papillary muscles of kittens. The response increases with drug concentration over the range from 10−10 M to 10−5 M. The mean maximum increase in tension development is 120%. Contractility is raised by angiotensin through an increase in the degree of activation of the contractile elements with no significant change in the duration of their active state. Low concentrations of angiotensin have a greater inotropic action than equimolar concentrations of l-norepinephrine; but the maximum inotropic effect obtainable with l-norepinephrine is almost twice that of angiotensin. The inotropic effects of angiotensin on cat atrial muscle are slight, and the drug is inactive on frog ventricular myocardium. It has no effect on the resting length-tension relationship of mammalian atrial or ventricular muscle. The frequency of impulse formation in the SA node is not significantly changed by concentrations of angiotensin up to 10−5 M. In marked contrast to levarterenol, angiotensin does not cause ectopic impulse formation in atrial or ventricular muscle. It is suggested that the positive inotropic effect of angiotensin on ventricular myocardium is of importance for the pressor action of the drug in the intact circulation. The increase in myocardial contractility tends to minimize or prevent decreases in cardiac output in the face of increased resistance to cardiac ejection and thus supports the elevation of arterial pressure.