肾小球滤过率正常的高血压和高钾血症综合征：是否存在血管舒张性前列腺素缺乏？

The syndrome of hypertension and hyperkalaemia with normal glomerular filtration rate: is there a deficiency in vasodilator prostaglandins?

Klemm S A, Hornych A, Tunny T J, Gordon R D

Endocrine-Hypertension Research Unit, Greenslopes Hospital, Brisbane, Queensland, Australia.

Clin Exp Pharmacol Physiol. 1991 May;18(5):309-13. doi: 10.1111/j.1440-1681.1991.tb01452.x.

Abstract

In Gordon's syndrome (GS; a syndrome of hypertension and hyperkalaemia with normal glomerular filtration rate), excessive proximal sodium reabsorption leads to suppression of renin and aldosterone, hyperkalaemia and hyperchloraemic acidosis. 2. Low urinary levels of vasodilator prostaglandins (PG) have been reported in GS, suggesting renal hypoprostaglandinism as a pathophysiological mechanism. 3. In four cases of GS, levels of vasodilator prostaglandins PGE2 and 6-keto-PGF1 alpha were low. 4. In one case of GS, low PGE2 levels were normalized by dietary salt restriction or diuretic therapy.

摘要

在戈登综合征（GS；一种肾小球滤过率正常的高血压和高钾血症综合征）中，近端肾小管对钠的过度重吸收导致肾素和醛固酮分泌受抑制、高钾血症和高氯性酸中毒。2. 据报道，GS患者尿中血管舒张性前列腺素（PG）水平较低，提示肾前列腺素合成减少是一种病理生理机制。3. 在4例GS患者中，血管舒张性前列腺素PGE2和6-酮-PGF1α水平较低。4. 在1例GS患者中，通过饮食限盐或利尿治疗，低水平的PGE2恢复正常。