Tan S Y, Bravo E, Mulrow P J
Prostaglandins Med. 1978 Jul;1(1):76-85. doi: 10.1016/0161-4630(78)90079-4.
Urinary Prostaglandin E2 (PGE2), a known indicator of renal production, was measured by specific radioimmunoassay in 111 normal volunteers, 85 patients with essential hypertension, 6 with renovascular hypertension, and 23 patients with primary aldosteronism. Women excreted less PGE2 than men in both normotensive and hypertensive groups. When compared to normals, essential hypertensives demonstrated significantly lower PGE2 levels, with one third excreting less than 100 ng/24 hr, values usually seen only in subjects receiving the prostaglandin synthetase inhibitor, indomethacin. Normal PGE2 was seen in patients with renovascular hypertension, and levels were uninfluenced by treatment with the converting enzyme inhibitor SQ14225, Despite normalization of blood pressure and increased plasma renin activity. Normal PGE2 was also encountered in primary aldosteronism. These data indicate that impaired renal PGE2 biosynthesis is specific for human essential hypertension, and is not secondary to the elevated blood pressure. Although PGE2 excretion tends to be lower in low-renin hypertension, a constant relationship between PGE2 and renin is not always apparent.
采用特异性放射免疫分析法，对111名正常志愿者、85名原发性高血压患者、6名肾血管性高血压患者及23名原发性醛固酮增多症患者检测了尿前列腺素E2（PGE2），PGE2是已知的肾脏生成指标。在血压正常和高血压组中，女性排泄的PGE2均少于男性。与正常人相比，原发性高血压患者的PGE2水平显著降低，三分之一的患者排泄量低于100 ng/24小时，此值通常仅见于接受前列腺素合成酶抑制剂吲哚美辛治疗的患者。肾血管性高血压患者的PGE2正常，尽管血压恢复正常且血浆肾素活性升高，但使用转换酶抑制剂SQ14225治疗对其水平无影响。原发性醛固酮增多症患者也出现PGE2正常。这些数据表明，肾脏PGE2生物合成受损是人类原发性高血压所特有的，并非继发于血压升高。虽然低肾素性高血压患者的PGE2排泄量往往较低，但PGE2与肾素之间的恒定关系并不总是明显。
