Pregnancy and estradiol decrease GTPase activity in the guinea pig uterine artery.
The mechanisms by which pregnancy redistributes cardiac output in an organ-specific manner are poorly understood. We propose that it is consequential to estrogen-mediated alterations in G protein-mediated signal transduction. Aortas and uterine (UAs) and mesenteric arteries (MAs) were obtained from late-pregnant, nonpregnant, or ovariectomized guinea pigs chronically treated with 17beta-estradiol. High-affinity GTPase activity was assayed enzymatically. The cGMP generated in response to the endothelium-dependent agonist ACh was measured in UAs incubated with or without cholera toxin (CTX, which inhibits G(s)alpha). Pregnancy significantly decreased UA but not aorta or MA GTPase activity. 17beta-Estradiol decreased UA GTPase activity compared with untreated ovariectomized animals. ACh increased cGMP in pregnant but not nonpregnant UAs. Pretreatment of nonpregnant UAs with CTX increased ACh-induced cGMP levels similar to pregnancy. Thus pregnancy and estradiol decrease the GTPase activity of a CTX-sensitive G protein in UAs, increasing receptor-dependent cGMP release. This alteration in receptor-mediated G protein coupling in UAs may contribute to the characteristic cardiovascular adaptation to pregnancy.
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Related Subject Headings
- Vasodilator Agents
- Uterus
- Second Messenger Systems
- Pregnancy, Animal
- Pregnancy
- Ovariectomy
- Nitric Oxide
- Guinea Pigs
- GTP Phosphohydrolases
- Female
Citation
Published In
DOI
ISSN
Publication Date
Volume
Issue
Start / End Page
Location
Related Subject Headings
- Vasodilator Agents
- Uterus
- Second Messenger Systems
- Pregnancy, Animal
- Pregnancy
- Ovariectomy
- Nitric Oxide
- Guinea Pigs
- GTP Phosphohydrolases
- Female