Uteroplacental ischemia is known to cause systemic hypertension in various species, but the mechanisms are unknown. These studies were designed to test the hypothesis that the increased systemic arterial pressure that occurs during reduced uteroplacental perfusion pressure is mediated by the renin-angiotensin system, possibly due to release of renin or angiotensin from the ischemic gravid uterus. In trained, chronically instrumented pregnant dogs (gestation age 47 ± 2 days, term = 60 days) maintained on a normal Na+ intake (~ meq/day), uterine perfusion pressure was reduced to 60 mmHg with an inflatable aortic occluder positioned distal to the renal arteries but proximal to the uterine arteries and was servo-controlled at this level for 1 h. Systemic arterial pressure rose by 14 ± 2 mmHg, from 96 ± 7 to 110 ± 8 mmHg. Plasma renin activity and angiotensin II levels did not change significantly. On another day in the same animals, the activity of the renin-angiotensin system was fixed by infusing captopril and sufficient angiotensin II to restore arterial pressure to normal (2-5 ng·kg-1·min-1 iv). Reduction of uterine artery pressure to 60 mmHg caused systemic arterial pressure to increase by 10 ± 2 mmHg with the renin-angiotensin system fixed, a response not different from that in the control experiments. These data suggest that the increase in systemic arterial pressure during reduced uteroplacental perfusion pressure is independent of the renin-angiotensin system.
|Original language||English (US)|
|Journal||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|State||Published - 1989|
ASJC Scopus subject areas
- Physiology (medical)