Central role for angiotensin in control of adrenal catecholamine secretion.

Central role for angiotensin in control of adrenal catecholamine secretion.
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血管紧张素在控制肾上腺儿茶酚胺分泌中起核心作用。

DOI:
10.1152/ajpregu.1985.248.3.r363
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发表时间:
1985
期刊:
The American journal of physiology
影响因子:
--
通讯作者:
Harrison,TS
Harrison,TS
中科院分区:
--
文献类型:
--
作者:
Corwin,EJ;Seaton,JF;Hamaji,M;Harrison,TS

文献摘要

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血管紧张素II (ANG II)是犬出血后肾上腺反射正常分泌儿茶酚胺所必需的。为了检验ANG II是否具有中枢作用,在全身麻醉下对双侧或假肾切除的狗进行实验,出血剂量为25 ml/kg。脑室池灌注ANG II或其拮抗剂saralasin通过针头插入左侧脑室和大池完成。测定出血前后平均动脉压和肾上腺儿茶酚胺分泌。切除肾脏的狗只接受人工脑脊液(脑室池灌注),与接受脑室内(IVT)的动物相比,肾上腺对出血的反应非常小(在10和100 pg)。公斤。最低为1)。这种作用也取决于IVT输注的速率。外周输注ANG II (10 pg)。公斤。Min-1)对肾上腺儿茶酚胺分泌无影响。肾完整的动物给予萨拉拉西素静脉滴注(0.06 ng/min)的反应与肾切除的狗只接受脑脊液静脉滴注相似。静脉注射萨拉拉西素并没有减弱出血的反应。因此,ANG II似乎通过中枢机制支持儿茶酚胺的分泌。这一机制在生理上具有重要意义,因为无论是肾切除术还是萨拉霉素对ANG II的功能性消除,都大大减弱了体内肾上腺髓质对出血的反应。
Angiotensin II (ANG II) is required for unimpaired adrenal reflex secretion of catecholamines after hemorrhage in the dog. To test if ANG II acts centrally, experiments were performed under general anesthesia on bilaterally or sham-nephrectomized dogs hemorrhaged at 25 ml/kg. Ventriculocisternal perfusion of ANG II or its antagonist saralasin was accomplished via needles inserted in the left lateral cerebral ventricle and cisterna magna. Mean arterial pressure and adrenal secretion of catecholamines were measured before and after hemorrhage. Nephrectomized dogs receiving only artificial cerebrospinal fluid (CSF) by ventriculocisternal perfusion had a very small adrenal response to hemorrhage compared with animals receiving ANG II intraventricularly (IVT) (at 10 and 100 pg . kg-1 . min-1). This effect of ANG II IVT also depended on the rate of IVT infusion. Peripheral infusion of ANG II (10 pg . kg-1 . min-1) had no effect on adrenal catecholamine secretion. Animals with intact kidneys given saralasin IVT (0.06 ng/min) responded similarly to nephrectomized dogs receiving only CSF IVT. Intravenous saralasin did not blunt the response to hemorrhage. Thus ANG II appears to support catecholamine secretion via a central mechanism. This mechanism is physiologically significant because either nephrectomy or functional elimination of ANG II by saralasin greatly attenuates the adrenal medullary response to hemorrhage in vivo.