Plasma renin activity, angiotensin II, prostacyclin and thromboxane A2 concentrations in 139 preeclamptic patients.

Abstract

Plasma renin activity , plasma concentratrions of angiotensin 11(AngII), stable metabolites (6-keto-prostaglandin Fla : 6-keto-PGFIa) of prostacyclin (PGI2) and a metabolite (thromboxane B2: TXB2) of thromboxane A2 (TXA2 ) were measured with radioimmunoassay(RIA) in 107 normal pregnancy (control) and 139 preeclamptic patients in 28-41 gestational weeks. PRA and 6-ketoPGFIa were significantly higher and AngII was slightly higher in preeclampsia than in control, and TXB2 was significantly lower in preeclampsia in control. The ratio of 6-keto-PGFIa/TXB2 was significantly lower in preeclampsia than in control. These data suggest that the changes in the renin-angiotensin system may not be primary alterations in preeclampsia. It can be speculated that in preeclampsia the changes in absolute concentrations of 6-keto-PGFIa and TXB2 are less important than the decrease in the ratio of the 6-keto-PGFIa/TXB2. plasma renin activity ; angiotensin II ; prostacyclin ; tromboxane A2; preeclampsia The renin-angiotensin system is known to play an important role in the maintenance of normal blood pressure and it has been shown that women who have, or are destined to develop, preeclampsia show an increased sensitivity to infused angiotensin II (Gant et al. 1976). This effect can be abolished by the administration of prostaglandin E2 or induced by the prior administration of an inhibitor of prostaglandin synthetase (Everetta et al. 1978). It is well established that vasocon-striction in the arteriolar bed, particularly in the uterus and kidney, is a characteristic feature of preeclampsia. Thromboxane A2 (TXA2) and prostacyclin (PGI2) are potent vasoactive compounds. TXA2 causes vasoconstriction and induces platelet aggregation, whereas PGI2 has the opposite properties (Moncada and Vane 1978). Other studies with isolated tissues have shown that there

Maternal and Fetal Atrial Natriuretic Peptide Levels, Maternal Plasma Renin Activity, Angiotensin II, Prostacyclin and Thromboxane A2 Levels in Normal and Preeclamptic Pregnancies.

“…Lack of significant correlation between ANP and the severity of preeclampsia (especially blood pressure) may be an argument against a causal relationship between blood pressure and ANP level. PRA and 6-keto-PGF1 levels in preeclapmsia was significantly (p <0.05) lower than that of normal pregnancy as previously reported (Furuhashi et al 1990). The ratio of 6-keto-PGFIa/TXB2 in preeclapmsia (n=35, 0.99+0.05) was significantly (p <0.01) lower than normal pregnancy (n =19, 1.85 ± 0.35) as previously reported (Furuhashi et al 1990).…”

“…PRA and 6-keto-PGF1 levels in preeclapmsia was significantly (p <0.05) lower than that of normal pregnancy as previously reported (Furuhashi et al 1990). The ratio of 6-keto-PGFIa/TXB2 in preeclapmsia (n=35, 0.99+0.05) was significantly (p <0.01) lower than normal pregnancy (n =19, 1.85 ± 0.35) as previously reported (Furuhashi et al 1990). There was no significant difference in Ang II and TXB2 levels in normal pregnancy and preeclampsia.…”

“…PRA, Ang II, PGIZ and TXAZ assays PRA, Ang II, PGIZ and TXAZ were measured as previously reported (Furuhashi et al 1990). Plasma renin activity (PRA) was measured by a solid phase radioimmunoassay (RIA) of angiotensin I (Ikeda 1982).…”

“…For these reasons its possible pathophysiologic role has been studied in preeclapmsia (Thomsen et al 1987;Fivet et al 1988;Frohlicha 1988;Hirai et al 1988;Miyamoto et al 1988;Bond et al 1989;Hatji et al 1989;Dessi-Fulgheri et al 1990;McCane et al 1990). The renin-angiotensin system and the balance of prostacyclin (PGI2) and thromboxane A2 (TXA2) is known to play an important role in preeclampsia (Bond et al 1989;Furuhashi et al 1990). There are few published data, however, regarding to ANP, renin-angiotensin system, PGI2 and TXA2 in normal pregnant and preeclamptic women.…”

Cardiovascular risk factors regulate the expression of vascular endothelin receptors

“…In addition, plasma concentrations of angiotensin II are often elevated in patients with hypertension (Furuhashi et al, 1990). These substances unavoidably reduce the formation of endothelial NO and increase leukocyte adhesion and peripheral resistance (Vanhoutte & Boulanger, 1995).…”