Importance of prostaglandins in hypertension during reduced uteroplacental perfusion pressure

Abstract

Uteroplacental ischemia causes hypertension in various species but the mechanisms involved are not known. These studies were designed to test the hypothesis that the systemic hypertension that occurs during reduced uteroplacental perfusion pressure is mediated by the prostaglandin system. Trained chronically instrumented pregnant dogs in the last third of gestation were studied. When uterine perfusion pressure was reduced to 60 mmHg for 60 min using an inflatable aortic occluder placed distal to the renal but proximal to the uterine and ovarian arteries, systemic arterial pressure increased from 95 +/- 5 to 110 +/- 7 mmHg. On another day in the same animals, the prostaglandin system was blocked with meclofenamate. Subsequent reduction of uterine arterial pressure caused no significant change in systemic pressure, from 96 +/- 4 to 99 +/- 6 mmHg, suggesting an important role for the prostaglandin system in mediating the normal response. In additional experiments, the thromboxane receptor antagonist SQ 29,548 was given. Arterial pressure averaged 94 +/- 5 mmHg after administration of SQ 29,548 and did not change significantly when uterine perfusion pressure was reduced during SQ 29,548. These data suggest that at least one component of the prostaglandin system, thromboxane, contributes to the rise in systemic arterial pressure during reduced uteroplacental perfusion pressure.