Hermsmeyer K
Circ Res. 1980 Oct;47(4):524-9. doi: 10.1161/01.res.47.4.524.
Electrical measurements of current flow in ventricular myocardium immersed in silicone oil showed that angiotensin II increases the cell-to-cell spread of current within seconds. The increases in current spread and conduction velocity occur without any changes in resting membrane potential or maximum rate of rise of the action potential. The concentration range was 10 nM to 10 microM, with an ED50 of 100 nM for angiotensin exposures lasting about 10 seconds. The larges effects were an apparent decrease in resistance through the cellular pathway to 50% of control and a 40% increase in conduction velocity, which returned to control in about 15 minutes. Continuous or repeated exposure to angiotensin caused desensitization to appear. These effects were found with or without denervation by 6-hydroxydopamine and beta-adrenergic blockade by 1 microM propranolol in calf, pig, sheep, and rabbit ventricular myocardium. Therefore, angiotensin appears to increase electrical conduction rapidly and directly in cardiac muscle by decreasing resistance through the cellular pathway.
对浸没在硅油中的心室心肌中电流流动进行的电学测量表明，血管紧张素II在数秒内就能增加电流在细胞间的传播。电流传播和传导速度的增加发生时，静息膜电位或动作电位的最大上升速率没有任何变化。血管紧张素暴露持续约10秒时，其浓度范围为10 nM至10 microM，半数有效浓度（ED50）为100 nM。最大的影响是通过细胞途径的电阻明显降低至对照的50%，传导速度增加40%，约15分钟后恢复到对照水平。持续或反复暴露于血管紧张素会导致脱敏现象出现。在小牛、猪、绵羊和兔的心室心肌中，无论是否用6-羟基多巴胺去神经支配以及用1 microM普萘洛尔进行β-肾上腺素能阻断，均发现了这些效应。因此，血管紧张素似乎通过降低细胞途径的电阻，在心肌中迅速且直接地增加电传导。
