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人体对沙拉新的即时升压反应:反对交感神经激活及支持内源性血管紧张素II样肌性作用的证据

The immediate pressor response to saralasin in man: evidence against sympathetic activation and for intrinsic angiotensin II-like myotropism.

作者信息

Mathias C J, Unwin R J, Pike F A, Frankel H L, Sever P S, Peart W S

出版信息

Clin Sci (Lond). 1984 May;66(5):517-24. doi: 10.1042/cs0660517.

DOI:10.1042/cs0660517
PMID:6231156
Abstract

The cardiovascular and hormonal effects of intravenous saralasin (0.5, 1 and 5 micrograms min-1 kg-1) were assessed in nine tetraplegic patients (with complete cervical spinal cord transaction above the sympathetic outflow) and in six normal subjects. In the tetraplegic patients, saralasin caused an immediate transient pressor response which was not dose-dependent and substantially greater than the pressor response in normal subjects. The pressor response in the tetraplegic patients was not accompanied by a rise in levels of plasma noradrenaline. In the tetraplegic patients, after alpha-adrenoceptor blockade with thymoxamine (1 mg kg-1 h-1), twice the dose of intravenous noradrenaline was needed to induce the same pressor response. The pressor response to saralasin (5 micrograms kg-1 min-1), however, was unaffected by thymoxamine. Saralasin caused minimal changes in levels of plasma renin activity and plasma aldosterone in both groups. There was no relationship between basal plasma renin activity and the pressor response in either group. We therefore conclude that the immediate transient pressor response to saralasin in man is not due to central sympathetic stimulation, is unlikely to be due to peripheral sympathetic activation and is probably the result of intrinsic angiotensin II-like myotropism.

摘要

在9名四肢瘫痪患者(颈髓完全横断且高于交感神经传出部位)和6名正常受试者中评估了静脉注射沙拉新(0.5、1和5微克/分钟·千克⁻¹)对心血管和激素的影响。在四肢瘫痪患者中,沙拉新引起立即的短暂升压反应,该反应不依赖剂量,且显著大于正常受试者的升压反应。四肢瘫痪患者的升压反应未伴随血浆去甲肾上腺素水平升高。在四肢瘫痪患者中,用百里胺(1毫克/千克·小时⁻¹)进行α-肾上腺素能受体阻断后,需要两倍剂量的静脉注射去甲肾上腺素才能诱导出相同的升压反应。然而,对沙拉新(5微克/千克·分钟⁻¹)的升压反应不受百里胺影响。沙拉新在两组中引起的血浆肾素活性和血浆醛固酮水平变化极小。两组中基础血浆肾素活性与升压反应之间均无关联。因此,我们得出结论,人类对沙拉新的立即短暂升压反应并非由于中枢交感神经刺激,不太可能是由于外周交感神经激活,可能是内源性血管紧张素II样肌性作用的结果。

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