Angiotensin II and α-agonist. III. In vitro fetal-maternal placental prostaglandins

In fetal sheep, angiotensin II, but not phenylephrine, increases umbilical venous concentrations of prostaglandin E₂ (PGE₂) and prostacyclin (PGI₂); however, their source(s) is unknown. We sought to determine the tissue source(s) of this increase in prostanoids and to compare responses in fetal and maternal tissues. Fetal placental arteries (PA) and veins (PV), mesenteric arteries (MA) and cotyledons, and maternal caruncles and uterine arteries (UA) from eight pregnant ewes [127 ± 3 (SE) days] were incubated (37°C, 1 h) in Krebs-Henseleit (95% O₂-5% CO₂) with or without angiotensin II, phenylephrine, or norepinephrine (5 X 10^-10 and 5 X 10^-8 M). Basal PGE₂ production exceeded PGI₂ in PA, cotyledons, and caruncles (P < 0.05), whereas PGE₂ < PGI₂ only in UA; production of both prostanoids was greatest in MA with 34.8 ± 5.0 and 27.4 ± 3.7 pg·μg protein^-1·h^-1, respectively (P < 0.001). Caruncles produced little of either prostanoid. Angiotensin II increased PA PGE₂ production from 6.5 ± 1.5 to 8.4 ± 3.0 and 10.8 ± 4.5 pg·μg^-1·h^-1 (P = 0.001) and PGI₂ from 3.3 ± 0.5 to 5.5 ± 1.5 (P < 0.05) and 3.7 ± 0.9 pg·μg^-1·h^-1; PV PGE₂ rose from 4.5 ± 1.1 to 9.0 ± 3.5 and 7.9 ± 2.3 pg·μg^-1·h^-1 (P < 0.05); PV PGI₂ was unchanged. Angiotensin II increased UA PGE₂ from 1.5 ± 0.3 to 3.4 ± 1.2 (P < 0.05) and 2.4 ± 0.8 pg·μg^-1·h^-1 and PGI₂ from 8.7 ± 1.0 to 12.4 ± 2.2 and 16.2 ± 5.2 (P < 0.05) pg·μg^-1·h^-1. Angiotensin II had no effect on MA, cotyledonary, or caruncular prostanoids. α-Agonist had no effect on any tissue examined. In fetal sheep, angiotensin II-induced increases in PGI₂ and PGE₂ are likely of vascular origin.