Regulation of collecting tubule adenosine triphosphatases by aldosterone and potassium.

Regulation of collecting tubule adenosine triphosphatases by aldosterone and potassium.
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醛固酮和钾对集合管三磷酸腺苷酶的调节。

DOI:
10.1172/jci116471
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发表时间:
1993
期刊:
The Journal of clinical investigation
影响因子:
--
通讯作者:
Sabatini,S
Sabatini,S
中科院分区:
--
文献类型:
--
作者:
Eiam-Ong,S;Kurtzman,NA;Sabatini,S

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为了研究钾和醛固酮对酸碱组成和集合小管ATP酶的确切作用,用零、生理或药理剂量的醛固酮替代糖皮质激素充足的肾上腺切除大鼠,并喂食不同的钾饮食以产生低钾血症、正常钾血症或高钾血症。放化法测定收集小管H/K-ATP酶活性,发现H/K-ATP酶活性与钾呈负相关,而与醛固酮无相关性; H-ATP酶活性与醛固酮呈正相关,而与钾无相关性。当这两种酶在同一方向变化时,酸碱组成的变化是深刻的;然而,当这两种酸化酶在相反的方向变化或当只有一种酶变化时,对酸碱平衡的影响是适度的。当醛固酮高而钾低时,血清碳酸氢盐约为45 meq/L;当醛固酮高而钾正常或醛固酮正常而钾低时,血清碳酸氢盐仅为29 meq/L。我们的观察可能有助于解释原发性醛固酮增多症的代谢性酸中毒,其中醛固酮过多和低钾血症相结合,以及醛固酮缺乏症的代谢性酸中毒,其中低醛固酮血症和高钾血症配对。本研究还表明,醛固酮在控制皮质集合小管Na/K-ATP酶活性方面起主要作用。低钾血症刺激延髓集合小管的Na/K-ATP酶活性;低钾血症的这种刺激作用支持了该酶存在于该部位顶膜上的假设。图片
To examine the precise role of potassium and aldosterone on acid-base composition and on collecting tubule ATPases, glucocorticoid-replete adrenalectomized rats were replaced with zero, physiological, or pharmacological doses of aldosterone and were fed varying potassium diets to produce hypokalemia, normokalemia, or hyperkalemia. Radiochemical measurement of ATPase activities showed that collecting tubule H/K-ATPase changed inversely with potassium and not with aldosterone whereas H-ATPase changed directly with aldosterone but not with potassium. When both enzymes changed in the same direction, alterations in acid-base composition were profound; however, when these two acidifying enzymes changed in opposite directions or when only one enzyme changed, the effect on acid-base balance was modest. Serum bicarbonate was approximately 45 meq/liter when aldosterone was high and potassium was low; it was only 29 meq/liter when aldosterone was high but potassium was normal or when aldosterone was normal and potassium was low. Our observations may help explain the metabolic alkalosis of primary aldosteronism in which aldosterone excess and hypokalemia are combined and the metabolic acidosis of aldosterone deficiency in which hypoaldosteronism and hyperkalemia are paired. The present study also demonstrated that aldosterone plays the major role in controlling Na/K-ATPase activity in cortical collecting tubule. Hypokalemia stimulates Na/K-ATPase activity in the medullary collecting tubule; this stimulatory effect of hypokalemia supports the hypothesis that the enzyme is present on the apical membrane at this site.Images