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-degrees-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.mu-g 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.mu-g-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.mu-g-1.h-1; PV PGE2 rose from 4.5 +/- 1.1 to 9.0 +/- 3.5 and 7.9 +/- 2.3 pg.mu-g-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. mu-g-1.h-1 and PGI2 from 8.7 +/- 1.0 to 12.4 +/- 2.2 and 16.2 +/- 5.2 (P < 0.05) pg.mu-g-1, h-1. Angiotensin II had no effect on MA, cotyledonary, or caruncular prostanoids. alpha-Agonist had no effect on any tissue examined. In fetal sheep, angiotensin II-induced increases in PGI2 and PGE2 are likely of vascular origin.
