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原发性高血压患者尿前列环素代谢产物减少。

Diminished urinary prostacyclin metabolite in essential hypertension.

作者信息

Grose J H, Lebel M, Gbeassor F M

出版信息

Clin Sci (Lond). 1980 Dec;59 Suppl 6:121s-123s. doi: 10.1042/cs059121s.

Abstract
  1. Urinary excretion rate of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), a stable nonenzymatic transformation product of prostacyclin (PGI2), was measured in 13 patients with sustained essential hypertension and in nine normotensive control subjects by a specific radioimmunoassay. 2. Patients with essential hypertension had significantly lower 6-keto-PGF1 alpha excretion rates irrespective of their sex, but in both groups urinary 6-keto-PGF1 alpha was lower in females. 3. Sodium excretion was significantly correlated with urinary 6-keto-PGF1 alpha only in hypertensive subjects. There was also a positive correlation between 6-keto-PGF1 alpha and urine volume in control subjects and in hypertensive patients. 4. If diminished urinary 6-keto-PGF1 alpha reflects suppressed endogenous PGI2 production, a deficiency in this important vasodepressor substance in essential hypertension may contribute to the pathogenesis of this disease.
摘要
  1. 通过特定放射免疫分析法,对13例持续性原发性高血压患者和9例血压正常的对照受试者测定了前列环素(PGI2)的稳定非酶促转化产物6-酮-前列腺素F1α(6-酮-PGF1α)的尿排泄率。2. 原发性高血压患者的6-酮-PGF1α排泄率显著较低,无论其性别如何,但两组中女性的尿6-酮-PGF1α均较低。3. 仅在高血压受试者中,钠排泄与尿6-酮-PGF1α显著相关。在对照受试者和高血压患者中,6-酮-PGF1α与尿量之间也呈正相关。4. 如果尿6-酮-PGF1α减少反映内源性PGI2生成受抑制,那么原发性高血压中这种重要血管舒张物质的缺乏可能促成该病的发病机制。

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