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β-肾上腺素能受体和血管紧张素II受体对内脏神经诱发肾上腺髓质儿茶酚胺释放的调节作用。

Modulation by beta-adrenoceptors and angiotensin II receptors of splanchnic nerve evoked catecholamine release from the adrenal medulla.

作者信息

Foucart S, de Champlain J, Nadeau R

机构信息

Département de physiologie, Faculté de médecine, Université de Montréal, Québec, Canada.

出版信息

Can J Physiol Pharmacol. 1991 Jan;69(1):1-7. doi: 10.1139/y91-001.

DOI:10.1139/y91-001
PMID:1674668
Abstract

In the present study, we have evaluated the effect of both facilitatory beta 2-adrenoceptor and angiotensin II receptor on the release of adrenal catecholamines induced by electrical stimulation of the splanchnic nerve in anaesthetized and vagotomized dog. In these experiments, individual or combined treatments with the beta 2-adrenoceptor antagonist ICI 118551 (0.3 mg/kg i.v.), the converting enzyme inhibitor captopril (2 mg/kg i.v.), or the angiotensin II receptor antagonist saralasin (2 micrograms.kg-1.min-1 i.v.) were found to significantly decrease the release of adrenal catecholamines during splanchnic nerve stimulation (5-V pulses of 2 ms duration for 3 min at 1 Hz) whatever the order of administration of the drugs. On the other hand, the infusion of angiotensin II (20 ng.kg-1.min-1) was shown to potentiate the release of adrenal catecholamines in response to electrical stimulation, and this effect was totally blocked by treatment with saralasin (4 micrograms.kg-1.min-1 i.v.). This facilitating angiotensin mechanism differed from beta-adrenoceptor facilitating mechanism, since following beta-blockade with ICI 118551, angiotensin II infusion still significantly potentiated the release of catecholamines during splanchnic nerve stimulation. These observations thus suggest that both facilitating beta 2-adrenoceptors and angiotensin II receptors can independently modulate the release of adrenal catecholamines.

摘要

在本研究中,我们评估了易化性β2 -肾上腺素能受体和血管紧张素II受体对麻醉和迷走神经切断犬内脏神经电刺激诱导的肾上腺儿茶酚胺释放的影响。在这些实验中,发现单独或联合使用β2 -肾上腺素能受体拮抗剂ICI 118551(静脉注射0.3 mg/kg)、转化酶抑制剂卡托普利(静脉注射2 mg/kg)或血管紧张素II受体拮抗剂沙拉新(静脉注射2 μg·kg-1·min-1),无论药物给药顺序如何,均可显著降低内脏神经刺激(1 Hz下持续2 ms的5 - V脉冲,持续3 min)期间肾上腺儿茶酚胺的释放。另一方面,输注血管紧张素II(20 ng·kg-1·min-1)可增强对电刺激的肾上腺儿茶酚胺释放,且这种作用可被沙拉新(静脉注射4 μg·kg-1·min-1)治疗完全阻断。这种血管紧张素易化机制不同于β -肾上腺素能受体易化机制,因为在用ICI 118551进行β -受体阻断后,输注血管紧张素II在内脏神经刺激期间仍能显著增强儿茶酚胺的释放。因此,这些观察结果表明,易化性β2 -肾上腺素能受体和血管紧张素II受体均可独立调节肾上腺儿茶酚胺的释放。

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