ROLE OF ANGIOTENSIN-II IN POTASSIUM-MEDIATED STIMULATION OF ALDOSTERONE SECRETION IN THE DOG
ROLE OF ANGIOTENSIN-II IN POTASSIUM-MEDIATED STIMULATION OF ALDOSTERONE SECRETION IN THE DOG
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DOI：
10.1172/jci110661
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发表时间：
1982-01-01
影响因子：
15.9
通讯作者：
PRATT, JH
中科院分区：
文献类型：
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作者：
PRATT, JH
K增强血管紧张素II的醛固酮刺激作用[AII]。K与AII的这种协同作用可能代表了II作为一种刺激而增强K的作用。为了检测AII对K的这种影响，我们测量了输注Kc1前后的血浆醛固酮水平(15MEQ静脉注射)。应用血管紧张素转换酶抑制剂卡托普利预防AII的形成。此外，在接受AII加卡托普利治疗的一组狗中，测量了对K的反应。补钾后，对照组犬血清白蛋白含量增加7.7%。血浆醛固酮水平为1.90 ng/dl(P<；0.001)。相比之下，卡托普利治疗的犬对K的血浆醛固酮浓度没有变化。当给卡托普利治疗的狗注射AII时，对K的反应恢复(血浆醛固酮浓度增加7.4±-)。2.1ngdl，P<；0.002)。促肾上腺皮质激素刺激醛固酮分泌，尽管卡托普利治疗(P<；0.001)，然而，促肾上腺皮质激素在对照组比卡托普利治疗组产生更大的血浆醛固酮浓度的增加。AII可显著增强K对醛固酮分泌的刺激作用。这些刺激在调节醛固酮分泌方面的一个重要的相互依赖似乎是存在的。
K enhances the aldosterone-stimulating action of angiotensin II [AII]. Such a synergistic interaction of K with AII could represent an action by II to potentiate K as a stimulus. To examine for this effect of AII on K, plasma aldosterone levels were measured before and after an infusion of KC1 (15 meq i.v.) into dogs without and with prevention of AII formation by captopril, an angiotensin converting-enzyme inhibitor. In addition, responses to K were measured in a group of dogs receiving AII plus captopril. After K infusion, control dogs showed an increase of 7.7 .+-. 1.9 (standard error of the mean) ng/dl (P < 0.001) in the level of plasma aldosterone. In contrast, captopril-treated dogs showed no change in plasma aldosterone concentration in response to K. When AII was administered to captopril-treated dogs, responsiveness to K administration was restored (plasma aldosterone concentration increased by 7.4 .+-. 2.1 ng/dl, P < 0.002). ACTH stimulated aldosterone secretion despite captopril treatment (P < 0.001), however, ACTH produced a greater increase in the plasma aldosterone concentration in controls than in captopril-treated animals. Stimulation of aldosterone secretion by K is considerably enhanced by AII. An important interdependence of these stimuli in the regulation of aldosterone secretion appears to exist.