Angiotensin II facilitation of pressor responses to adrenal field stimulation in pithed rats.
Angiotensin II facilitation of pressor responses to adrenal field stimulation in pithed rats.
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血管紧张素 II 促进髓大鼠肾上腺场刺激的升压反应。
DOI：
10.1152/ajpregu.1988.254.1.r95
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Fluharty,SJ
中科院分区：
文献类型：
--
作者：
Vollmer,RR;Corey,SP;Fluharty,SJ
在去髓雄性Sprague-Dawley大鼠中评估血管紧张素II对肾上腺电场刺激（1-32 Hz）的升压反应的影响。刺激引起频率相关的升压反应和血浆儿茶酚胺的增量。阻断肾素-血管紧张素系统与转换酶抑制剂卡托普利或受体拮抗剂saralasin显着减弱升压反应肾上腺刺激和注射肾上腺素在同等程度上。这一观察结果，沿着发现，卡托普利并不改变肾上腺刺激产生的血浆儿茶酚胺增量，表明内源性产生的血管紧张素II并不影响肾上腺儿茶酚胺释放。相反，血管紧张素II似乎在血管平滑肌水平上相互作用，因为血管紧张素II（20 ng.kg-1.min-1 iv）在卡托普利治疗的动物中的再输注恢复了对刺激和肾上腺素的反应性。加压素输注也恢复了卡托普利后的升压活性;因此，这种相互作用似乎不是血管紧张素II特异性的，但可能取决于血管平滑肌的背景张力。此外，硝普钠降低血压可逆地减弱肾上腺刺激和肾上腺素的升压反应。结果表明，内源性血管紧张素II通过增加血管张力促进肾上腺素的血管收缩活性。
The effects of angiotensin II on pressor responses to electrical field stimulation (1-32 Hz) of the adrenal gland were assessed in pithed male Sprague-Dawley rats. Stimulation elicited frequency-related pressor responses and increments in plasma catecholamines. Interruption of the renin-angiotensin system with the converting enzyme inhibitor captopril or the receptor antagonist saralasin significantly attenuated the pressor responses to adrenal stimulation and injected epinephrine to an equivalent extent. This observation, along with the finding that captopril did not alter the plasma catecholamine increments produced by adrenal stimulation, suggested that endogenously generated angiotensin II was not affecting adrenal catecholamine release. Instead angiotensin II appears to interact at the level of the vascular smooth muscle, because reinfusion of angiotensin II (20 ng.kg-1.min-1 iv) in captopril-treated animals restored responsiveness to stimulation and epinephrine. Infusion of vasopressin also restored pressor activity after captopril; therefore the interaction does not appear to be specific for angiotensin II but may depend on the background tone of the vascular smooth muscle. Moreover, decreasing blood pressure with sodium nitroprusside reversibly attenuated the pressor responses to both adrenal stimulation and epinephrine. The results suggest that endogenously formed angiotensin II facilitates the vasoconstrictor activity of epinephrine by increasing vascular tone.