Key result
Pregnancy blunts the pressor response to angiotensin II, but estradiol and progesterone fail to reproduce it.
Why the study?
The mechanisms underlying reduced pressor responsiveness to angiotensin II during pregnancy were unclear, specifically the roles of estradiol and progesterone.
Does pregnancy or administration of estradiol/progesterone alter pressor responsiveness to angiotensin II in rats?
Population
Conscious pregnant Long-Evans rats and ovariectomized rats
Comparison
Pregnancy at days 7, 14, and 21 vs virgin rats; estradiol, progesterone, or both vs saline-injected controls
Design
Preclinical experimental study
Follow-up
21 days for pregnancy; 10 days for hormone injections
Authors
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Confirms rat model utility for gestational vascular studies; leaves open mechanisms beyond estradiol or progesterone alone.
Does pregnancy or administration of estradiol/progesterone alter pressor responsiveness to angiotensin II in rats?
The rat is an appropriate model for studying pregnancy-induced changes in angiotensin responsiveness, which are not mediated by estradiol or progesterone alone.
Novak et al. (1991) studied Pregnancy. Estradiol, progesterone, or a combination vs. saline-injected controls was evaluated on Pressor response to angiotensin II. Pregnancy significantly reduced the pressor response to angiotensin II in rats, but neither estradiol nor progesterone administration in ovariectomized rats reproduced this effect.
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