INTERRELATIONSHIPS BETWEEN THE RENIN-ANGIOTENSIN SYSTEM AND UTEROPLACENTAL BLOOD-FLOW - A RECENT PERSPECTIVE

In pregnancy, the maternal circulating renin-angiotensin system (RAS) and uteroplacental tissue RAS have been thought to support maternal pl acental flow by raising maternal arterial pressure or changing placent al vascular resistance. Also, the placenta or uterus may alter materna l circulating RAS. Recent studies in the authors' laboratory using chr onically catheterized rabbits are compared with previous studies on in teractions between the RAS and uterop]acental flow. When uterine drivi ng pressure was reduced either mechanically or after converting enzyme inhibition, maternal placental flow decreased in proportion to change in driving pressure; myoendometrial flow did not change. Angiotensin II (AII) infusion to increase pressure by 21+/-2mm Hg decreased placen tal but not myoendometrial few. Thus, there is no evidence that matern al placental flow is autoregulated or supported by a specific renin-an giotensin mechanism. Normally, there is no net uterine release or upta ke of active plasma renin activity, AI, or AII, but there is a small n et release of trypsin-activated plasma renin activity (tPRA), presumab ly prorenin. Distal aortic occluder inflation produced upper-body hype rtension, and uterine release of tPRA increased. There was a significa nt uterine arteriovenous concentration difference for AII during All i nfusion. These methods are adaptable for studying interactions between uteroplacental flow and other vasoactive agents.