Hornych A, Fontaliran F, Safar M, Guyene T T, Bariety J, Milliez P
Contrib Nephrol. 1978;11:189-96. doi: 10.1159/000401802.
PG A1, B1, E2, F1,2alpha and PRA have been measured in 8 hypertensive patients with unilateral renal arterial stenosis, 7 hypertensive patients with unilateral renal atrophy and 20 control normotensive subjects. PRA and PGA1 were significantly increased in patients with renovascular hypertension but not in patients with atrophy. PGE2 and PGF1,2alpha were increased in both groups of patients, especially on the stenotic or atrophic side. The increase of PGA1 and PGE2, represents a secondary antihypertensive, diuretic and natriuretic mechanism, the increase of PGF1,2alpha a direct hypertensive mechanism.
已对8例单侧肾动脉狭窄的高血压患者、7例单侧肾萎缩的高血压患者和20名血压正常的对照者测定了PGA1、B1、E2、F1,2α和肾素活性（PRA）。肾血管性高血压患者的PRA和PGA1显著升高，但萎缩患者则不然。两组患者的PGE2和PGF1,2α均升高，尤其是在狭窄或萎缩侧。PGA1和PGE2的升高代表一种继发性降压、利尿和排钠机制，PGF1,2α的升高则是一种直接的升压机制。
