The mechanisms by which pregnancy redistributes cardiac output in an organ-specific manner are poorly understood. We propose that it is consequential to @entity172 -mediated alterations in G protein-mediated signal transduction. Aortas and uterine (UAs) and mesenteric arteries (MAs) were obtained from late-pregnant, nonpregnant, or ovariectomized @entity840 chronically treated with @entity53 . High-affinity GTPase activity was assayed enzymatically. The @entity6708 generated in response to the endothelium-dependent agonist @entity1617 was measured in UAs incubated with or without cholera toxin ( @entity3525 , which inhibits G(s)alpha). Pregnancy significantly decreased UA but not aorta or MA GTPase activity. @entity53 decreased UA GTPase activity compared with untreated ovariectomized animals. @entity1617 increased @entity6708 in pregnant but not nonpregnant UAs. Pretreatment of nonpregnant UAs with @entity3525 increased @entity1617 -induced @entity6708 levels similar to pregnancy. Thus pregnancy and @entity53 decrease the GTPase activity of a @entity3525 -sensitive G protein in UAs, increasing receptor-dependent @entity6708 release. This alteration in receptor-mediated G protein coupling in UAs may contribute to the characteristic cardiovascular adaptation to pregnancy.

Pregnancy and @entity53 decrease GTPase activity in the XXXX uterine artery.

@entity172 :: ('MESH:D004967', 'Chemical') :: ['estrogen'] @entity6708 :: ('CHEBI:16356', 'Chemical') :: ['cGMP'] @entity3525 :: ('CHEBI:36467', 'Chemical') :: ['CTX'] @entity840 :: ('10141', 'Species') :: ['guinea pigs'] @entity53 :: ('MESH:D004958', 'Chemical') :: ['17beta-estradiol', '17beta-Estradiol', 'estradiol'] @entity1617 :: ('CHEBI:22614', 'Chemical') :: ['ACh']
@entity840 :: (10141,Species) :: ['guinea pig']
