Krishna G G, Chusid P, Hoeldtke R D
Department of Medicine, Temple University School of Medicine, Philadelphia, Pa.
Nephron. 1987;47(3):184-9. doi: 10.1159/000184488.
The pathogenesis of acquired hypoaldosteronism, a frequent cause of hyperkalemia in patients with chronic renal failure, is poorly understood. The present studies were undertaken to investigate the role of dopamine in suppressing mineralocorticoid secretion in this syndrome. We studied the plasma aldosterone response to dopaminergic blockade with metoclopramide in 11 patients with chronic renal failure (5 of whom were hyperkalemic) and 7 normal controls. Following repetitive doses of metoclopramide, the normokalemic chronic renal failure patients showed an exaggerated aldosterone response (peak aldosterone 50 +/- 5 ng/dl or 1,385 +/- 138 pmol/l) compared to normal controls (24 +/- 4 ng/dl or 665 +/- 110 pmol/l). In the hyperkalemic chronic renal failure patients, however, metoclopramide failed to induce a significant increase in plasma aldosterone (peak aldosterone 13 +/- 3 ng/dl or 360 +/- 83 pmol/l). By contrast, metoclopramide stimulated prolactin secretion in both normokalemic and hyperkalemic chronic renal failure patients. The plasma renin activity and serum potassium values were unchanged in all 3 groups. Our data show that dopaminergic blockade with metoclopramide fails to stimulate aldosterone secretion in patients with acquired hypoaldosteronism. Thus this syndrome does not result from enhanced dopaminergic inhibition of aldosterone, but rather from an independent abnormality in aldosterone biosynthesis.
获得性醛固酮减少症是慢性肾衰竭患者高钾血症的常见病因，但其发病机制尚不清楚。本研究旨在探讨多巴胺在该综合征中抑制盐皮质激素分泌的作用。我们研究了11例慢性肾衰竭患者（其中5例有高钾血症）和7例正常对照者对甲氧氯普胺多巴胺能阻滞的血浆醛固酮反应。重复给予甲氧氯普胺后，血钾正常的慢性肾衰竭患者的醛固酮反应增强（醛固酮峰值为50±5 ng/dl或1385±138 pmol/l），而正常对照者为24±4 ng/dl或665±110 pmol/l。然而，在高钾血症的慢性肾衰竭患者中，甲氧氯普胺未能使血浆醛固酮显著增加（醛固酮峰值为13±3 ng/dl或360±83 pmol/l）。相比之下，甲氧氯普胺刺激了血钾正常和高钾血症的慢性肾衰竭患者的催乳素分泌。所有3组的血浆肾素活性和血清钾值均无变化。我们的数据表明，甲氧氯普胺多巴胺能阻滞未能刺激获得性醛固酮减少症患者的醛固酮分泌。因此，该综合征并非由多巴胺对醛固酮的抑制增强所致，而是由醛固酮生物合成的独立异常引起。
