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低肾素性低醛固酮血症中肾血管活性系统的研究。

Studies of the renal vasoactive systems in hyporeninemic hypoaldosteronism.

作者信息

Hahn J A, Zipser R D, Barg A, Stone R A, Zia P K, Hsueh W A, Horton R

出版信息

Prostaglandins Med. 1981 Jun;6(6):549-56. doi: 10.1016/0161-4630(81)90116-6.

Abstract

Plasma renin activity, total renin, active renin, and aldosterone were measured as well as urinary prostaglandin E2 and kallikrein in a group of patients with hyperkalemia (6.1-7.7 mEq per liter) and hyporeninemic hypoaldosteronism. Plasma renin activity and aldosterone were low and the response was markedly blunted to upright posture, and furosemide. The rise in cortisol but not aldosterone was normal following ACTH stimulation. Active renin was depressed; however, total renin was normal. Urine PGE was variable including some low values, but the mean of the group was normal (p greater than 0.1). Urine kallikrein excretion was markedly diminished and undetectable in most cases. Fludrocortisone normalized potassium but minimally increased kallikrein in the patients. The possibility exists that kallikrein deficiency in these patients may underlie the inability to generate active renin.

摘要

对一组高钾血症(血钾浓度为6.1 - 7.7毫当量/升)和低肾素性低醛固酮血症患者测定了血浆肾素活性、总肾素、活性肾素和醛固酮,以及尿前列腺素E2和激肽释放酶。血浆肾素活性和醛固酮水平较低,对直立姿势和呋塞米的反应明显减弱。促肾上腺皮质激素刺激后皮质醇升高正常,但醛固酮升高不正常。活性肾素降低;然而,总肾素正常。尿PGE变化不定,包括一些低值,但该组平均值正常(p大于0.1)。尿激肽释放酶排泄明显减少,多数情况下检测不到。氟氢可的松使患者血钾恢复正常,但激肽释放酶仅轻度增加。这些患者存在激肽释放酶缺乏的可能性,这可能是无法产生活性肾素的原因。

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