Renin-angiotension-aldosterone system, urinary prostaglandins and kallikrein in pregnancy-induced hypertension: evidence for a dysregulation of the renin-angiotensin-prostacyclin loop.

Plasma renin activity (PRA) and aldosterone concentrations were measured simultaneously with urinary excretion of kallikrein and of four prostaglandins (PGE2, PGF2 alpha, 6-keto-PGF1 alpha and TXB2) in 23 patients with pregnancy-induced hypertension (PIH; 17 with permanent PIH (PH) and six with labile PIH (LH), i.e. patients whose hypertension was controlled only by home bed-rest) and in 16 normotensive pregnant women. Plasma renin activity was lower in PH than in controls or in LH. No difference between the three groups was observed for plasma aldosterone and urinary excretion of kallikrein and prostaglandins except that TXB2 was higher in LH than in PH. Thus patients with LH have a different biological profile from that of PH, since they have higher PRA and higher TXB2 excretion, an association that suggests a more pronounced ureteral compression by the gravid uterus in this group. Although no decreased synthesis of vasodilating prostaglandins was found in PH, a dysregulation of the renin-angiotensin-prostacyclin loop is suggested by a negative correlation between PRA and 6-keto-PGF1 alpha. An independent vasopressive substance which would stimulate PGI2 and suppress renin secretion is therefore postulated.