RENAL PROSTACYCLIN, RENIN AND GLOMERULAR-FILTRATION IN PREGNANCY-INDUCED HYPERTENSION

Decreased renal production of prostacyclin (PgI2) might impair both renal release of renin and glomerular filtration rate (GFR) in women with pregnancy-induced hypertension (PIH). We measured renal excretion of the PgI2 metabolite 6-keto PgF1a and thromboxane B2 (TxB2) as well as plasma active renin concentration (PRC) and creatinine in 20 non-pregnant, 37 normal pregnant and 41 women with PIH (21 mild, 20 severe). Urinary 6-keto PgF1a and TxB2 excretion, the ratio 6-keto PgF1a:TxB2 and PRC were increased and plasma creatinine decreased in normal pregnancy compared with non-pregnant women. All prostanoid measurements and PRC were reduced significantly in those with severe PIH compared with normal pregnant women. Urinary 6-keto PgF1a and TxB2 were correlated negatively with both PRC and plasma creatinine in those with severe, but not mild, PIH. In a separate study, PRC was increased by head-up tilt in seven normal pregnant women and five women with PIH but urinary 6-keto PgF1a was not altered significantly by this manoeuver. These studies do not support a significant role for renal PgI2 in the control of renin release in women with PIH. However, they do provide preliminary evidence that failure of renal PgI2 production may contribute to a fall in GFR in severe PIH.