The placental vascular bed is normally fully dilated. Therefore, changes in vascular resistance elsewhere in the body can affect uteroplacental blood flow (UBF). For example, antihypertensive drugs, such as diazoxide, hydralazine and the angiotensin-converting enzyme inhibitor captopril, cause falls in arterial pressure and, hence, in UBF. 2. Angiotensin II (AngII), prostacyclin and nitric oxide (NO) all influence uteroplacental vascular tone. Angiotensin II in a pharmacological dose (62.5 micrograms/h) had a biphasic effect on UBF in the sheep. Initially, there was a rise in UBF as pressure rose; however, by 16-24 h, UBF had fallen. The AngII-induced fall in UBF caused severe foetal hypoxia and hypercapnia. 3. Prostacyclin may protect the uteroplacental circulation from vasoconstrictors such as AngII, as the vasoconstrictor effect of AngII in the uteroplacental circulation is enhanced following indomethacin. 4. Oestrogen-induced uterine artery vasodilation is nitrergic dependent. As well, nitrergic nerves alter the responsiveness of pregnant uterine arteries to noradrenaline. 5. Thus, both systemic and local factors are important in the control of UBF and in promoting foetal health and growth.
