In experiments performed in anesthetized monkeys in the third trimester of pregnancy, mean maternal arterial blood pressure was continuously monitored, the uterine artery blood flow was measured with an electromagnetic flow probe, and prostaglandin levels were assayed in the uterine venous effluent. After inhibition of prostaglandin synthesis with indomethacin, the mean arterial blood pressure in response to angiotensin II was greater than the response prior to indomethacin treatment, and an increase in uterine artery blood flow was prevented. These findings are consistent with the suggestion that prostaglandins mediate the uterine artery blood flow response to angiotensin II, as well as modifying the maternal systemic blood pressure response.