MacLean M R, Ungar A
J Physiol. 1986 Apr;373:343-52. doi: 10.1113/jphysiol.1986.sp016051.
We have studied the influence of the renin-angiotensin system on the control of catecholamine release from innervated and denervated adrenal glands of anaesthetized dogs. Captopril reduced the resting release of catecholamines and inhibited release evoked either by lowering carotid sinus pressure or by stimulating the peripheral end of the cut splanchnic nerve. Both responses were restored by exogenous angiotensin II, and the reflex response could also be restored by corticotrophin. Cycloheximide, in the presence of captopril, further reduced the resting release of catecholamines and prevented the restoration of the reflex response by angiotension II. Plasma renin activity did not rise during baroreceptor tests lasting 10 min, but catecholamine release was evoked from the first minute. We conclude that the response of the adrenal medulla to sympathetic activity requires a minimum circulating concentration of angiotensin II. It is severely impaired by inhibition of the renin-angiotensin system but function can be restored either by exogenous angiotensin II or by corticotrophin.
我们研究了肾素-血管紧张素系统对麻醉犬去神经和未去神经肾上腺髓质儿茶酚胺释放调控的影响。卡托普利降低了儿茶酚胺的静息释放,并抑制了因降低颈动脉窦压力或刺激切断的内脏神经外周端所诱发的释放。两种反应均能通过外源性血管紧张素II恢复,且反射反应也能通过促肾上腺皮质激素恢复。在卡托普利存在的情况下,环己酰亚胺进一步降低了儿茶酚胺的静息释放,并阻止了血管紧张素II对反射反应的恢复。在持续10分钟的压力感受器测试期间,血浆肾素活性并未升高,但从第一分钟起就诱发了儿茶酚胺释放。我们得出结论,肾上腺髓质对交感神经活动的反应需要血管紧张素II的最低循环浓度。肾素-血管紧张素系统的抑制会严重损害其功能,但外源性血管紧张素II或促肾上腺皮质激素均可恢复其功能。