As a fetus grows over gestation, virtually all of the oxygen and nutrients needed for growth are acquired from the maternal circulation through the placenta. Fetal waste products are also removed by this route. Therefore it is not surprising that conditions in which maternal uteroplacental blood flow is reduced are often associated with intrauterine growth retardation. It is clear that an understanding of the mechanisms that control uterine blood flow in pregnancy will be important in preventing such conditions. Unfortunately, the physiological regulation of the uteroplacental circulation remains -poorly understood. The renin-angiotensin system has been postulated to be involved in controlling uteroplacental blood flow in pregnancy, however the role of renin and angiotensin in regulating uterine blood flow and cardiovascular dynamics in pregnancy is still not clear. The goals of these studies are 1) to determine the extent to which uteroplacental blood flow autoregulates in the chronically instrumented pregnant dog and to test the hypotheses that the renin-angiotensin and/or prostaglandin systems mediate the autoregulatory behavior, by comparing autoregulation curves in the presence and absence of pharmacological inhibitors of these two systems, 2) to determine the role of the renin-angiotensin system in controlling uteroplacental blood flow, and to test the hypotheses that angiotensin II is purely a vasoconstrictor in the uteroplacental circulation and that captopril reduces uteroplacental blood flow by mechanisms other than by reducing arterial pressure or blockade of the renin-angiotensin system. These concepts will be tested by servo-controlling uterine perfusion pressure during infusion of angiotensin II or captopril, and also by comparing responses to other drugs that block the renin-angiotensin system, 3) to determine the relative contributions of uterine and renal renin secretion to plasma renin activity in pregnancy and to test the hypothesis that both uterine and renal renin secretion increase in response to reduced perfusion pressure in the conscious pregnant dog, and 4) to test the hypotheses that angiotensin II acts as a vasoconstrictor in isolated uterine vessels and that vascular smooth muscle (uterine and femoral) from the pregnant dog is intrinsically less sensitive to angiotensin II and norepinephrine than is that from nonpregnant animals.