Regulation of maternal placental blood flow: A review

Abstract

Summary We do not know for certain that the maternal placental circulation is under physiological control. The human placenta is hemochorial and lacks arterioles, the principal determinants of resistance and flow in other organs. Innervation of the uterine arteries does not extend to the spiral arteries and work on isolated vessels suggests that sympathetic nerves are unimportant in the control of placental blood flow. Vasodilator fibers supply the larger vessels and may use nitric oxide and substance P as neurotransmitters. Hormones such as arginine vasopressin and angiotensin II have no effect on myometrial vessels in the physiological range of plasma concentrations. Angiotensin II may be important in disease states like pre-eclampsia, however, as might the endothelium derived autacoid, endothelin-1. There may be an endothelium-derived relaxing factor in uterine arteries. It is not necessarily nitric oxide; it might be prostacyclin. Clinical studies on the effect of nitric oxide donors on umbilical artery flow velocity have yielded conflicting results. Further work is required to resolve these differences and define criteria for determining the effects of autacoids and drugs in a clinical context. There is still ample room for work on isolated vessels. We need to know if vascular reactivity to endothelin-1, atrial natriuretic peptide and other autacoids is altered in pre-eclampsia. Since such studies likely will be made on myometrial arteries taken from the lower uterine segment, it needs also to be shown that they react to autacoids in the same way as arteries from the placental site. It should be possible to obtain placental vessels at Cesarean section in cases of placenta previa. Because reduced placental perfusion is a feature of pre-eclampsia, and often is associated with fetal growth restriction, research on the control of maternal placental blood flow is of great potential benefit.