Magness R R, Rosenfeld C R, Faucher D J, Mitchell M D
Department of Pediatrics, University of Texas, Southewestern Medical Center, Dallas 75235.
Am J Physiol. 1992 Jul;263(1 Pt 2):H188-97. doi: 10.1152/ajpheart.1992.263.1.H188.
The ovine and human uteroplacental vascular beds are more refractory to angiotensin II (ANG II)-induced vasoconstriction than the systemic vasculature. ANG II increases in vitro prostacyclin (PGI2) production by uterine but not omental arteries from pregnant sheep. Thus vasodilator prostaglandins may account for this difference in vascular responsiveness. We measured uterine and systemic eicosanoid production and hemodynamic responses in pregnant sheep before and during intravenous ANG II (1.15 and 11.5 micrograms/min). ANG II caused dose-related increases in arterial pressure and systemic and uterine vascular resistance (P less than 0.05). PGI2 metabolite (6-keto-PGF1 alpha) in the uterine vein rose from 166 +/- 70 (SE) to 223 +/- 114 and 631 +/- 323 pg/ml, respectively (P less than 0.05), and arterial levels increased from 67 +/- 24 to 145 +/- 78 and 312 +/- 173 pg/ml, respectively (P less than 0.05). Basal uterine venoarterial differences of 6-keto-PGF1 alpha were 99 +/- 43 pg/ml and increased during 11.5 micrograms ANG II/min to 295 +/- 181 pg/ml (P less than 0.05) but not during 1.15 micrograms/min (64 +/- 30 pg/ml). Responses were similar in gravid and nongravid uterine horns. Unilateral uterine prostaglandin inhibition with indomethacin did not alter basal uterine blood flow or systemic responses to ANG II (0.573-11.5 micrograms/min); however, ipsilateral uterine prostaglandin production fell and uterine vasoconstrictor responses increased (P less than 0.05). During ovine pregnancy ANG II increases uterine PGI2 production. PGI2 appears in part to attenuate ANG II-induced uterine vasoconstriction.
与全身血管系统相比，绵羊和人类的子宫胎盘血管床对血管紧张素II（ANG II）诱导的血管收缩更具耐受性。ANG II可增加妊娠绵羊子宫动脉而非网膜动脉的体外前列环素（PGI2）生成。因此，血管舒张性前列腺素可能是造成这种血管反应性差异的原因。我们在静脉注射ANG II（1.15和11.5微克/分钟）之前及期间，测量了妊娠绵羊的子宫和全身类花生酸生成以及血流动力学反应。ANG II导致动脉压以及全身和子宫血管阻力呈剂量依赖性增加（P<0.05）。子宫静脉中的PGI2代谢物（6-酮-PGF1α）分别从166±70（SE）升至223±114和631±323 pg/ml（P<0.05），动脉水平分别从67±24升至145±78和312±173 pg/ml（P<0.05）。6-酮-PGF1α的基础子宫静脉动脉差异为99±43 pg/ml，在ANG II 11.5微克/分钟时增加至295±181 pg/ml（P<0.05），但在1.15微克/分钟时未增加（64±30 pg/ml）。妊娠和未妊娠子宫角的反应相似。用吲哚美辛单侧抑制子宫前列腺素并未改变基础子宫血流量或对ANG II（0.573 - 11.5微克/分钟）的全身反应；然而，同侧子宫前列腺素生成减少，子宫血管收缩反应增加（P<0.05）。在绵羊妊娠期间，ANG II增加子宫PGI2生成。PGI2似乎部分减弱了ANG II诱导的子宫血管收缩。
