Lokhandwala M F, Amelang E, Buckley J P
Eur J Pharmacol. 1978 Dec 1;52(3-4):405-9. doi: 10.1016/0014-2999(78)90299-6.
Intravenous infusion of two separate doses of angiotensin II in pentobarbital-anesthetized, desipramine-treated animals produced dose-related increases in arterial blood pressure and caused significant potentiation of the cardioacceleration observed during the stimulation of the right postganglionic cardiac sympathetic nerve fibers. Positive chronotropic effects of intravenous norepinephrine were not altered during angiotensin II infusion. Prior administration of Saralasin, an angiotensin receptor antagonist, caused significant attenuation of the pressor action of angiotensin II, and also significantly antagonized the facilitatory effect of angiotensin II on sympathetic transmission to the myocardium. These results suggest that angiotensin II can cause facilitation of sympathetic nerve function to the myocardium via an action on angiotensin receptors which may be located on sympathetic nerve terminals.
在戊巴比妥麻醉、地昔帕明处理的动物中,静脉注射两剂不同剂量的血管紧张素II可使动脉血压呈剂量依赖性升高,并显著增强刺激右侧节后心脏交感神经纤维时观察到的心脏加速作用。静脉注射去甲肾上腺素的正性变时作用在输注血管紧张素II期间未改变。预先给予血管紧张素受体拮抗剂沙拉新可显著减弱血管紧张素II的升压作用,并且也显著拮抗血管紧张素II对交感神经向心肌传递的促进作用。这些结果表明,血管紧张素II可通过作用于可能位于交感神经末梢的血管紧张素受体,促进对心肌的交感神经功能。