Yoshimura T, Magness R R, Rosenfeld C R
Department of Pediatrics, University of Texas, Southwestern Medical Center, Dallas 75235.
Am J Physiol. 1990 Aug;259(2 Pt 2):H473-9. doi: 10.1152/ajpheart.1990.259.2.H473.
The fetoplacental vasculature is more sensitive to angiotensin II (ANG II) than to alpha-agonists, possibly reflecting their differing effects on vascular prostaglandin (PG) production. To examine this we studied in fetal sheep (123-138 days) the effects of ANG II (n = 7; 0.057, 1.15, and 5.73 micrograms/min) and phenylephrine (PHEN, n = 7; 0.306, 1.53, and 7.64 micrograms/min) on mean arterial pressure (MAP), heart rate (HR), and simultaneous measurements of umbilical arterial and venous PGE2, 6-keto-PGF1 alpha (PGI2) and thromboxane B2 (TxB2) concentrations. ANG II increased MAP and decreased HR dose dependently (P less than 0.05). Basal umbilical venous plasma PGE2 levels exceeded PGI2 (P less than 0.001) and increased during ANG II infusions from 502 +/- 63 to 516 +/- 113, 647 +/- 188, and 1,968 +/- 541 pg/ml (mean +/- SE, P less than 0.05), as did venous-arterial concentration differences (129 +/- 26 to 179 +/- 47, 244 +/- 58, and 1,287 +/- 507 pg/ml, respectively; P less than 0.05). ANG II also increased umbilical venous PGI2 levels from 110 +/- 13 to 116 +/- 24, 144 +/- 46, and 680 +/- 147 pg/ml (P less than 0.01) and the venous-arterial concentration difference from 3 +/- 6 to 20 +/- 16, 41 +/- 27, and 405 +/- 122 pg/ml (P less than 0.05), respectively. ANG II had no effect on plasma TxB2, and no umbilical venous-arterial concentration differences existed. Although PHEN increased MAP and decreased HR, plasma eicosanoid concentrations were unaltered. The fetus is more sensitive to ANG II than PHEN; however, only ANG II increased placental PGE2 and PGI2 production.(ABSTRACT TRUNCATED AT 250 WORDS)
