12063296

Source:http://linkedlifedata.com/resource/pubmed/id/12063296

Download in:

Switch to

Custom View

Named Graph Language Inference

Statements in which the resource exists as a subject.
Predicate	Object
rdf:type	pubmed:Citation
lifeskim:mentions	umls-concept:C0032961, umls-concept:C0226378, umls-concept:C0279023, umls-concept:C1280500
pubmed:issue	1
pubmed:dateCreated	2002-6-13
pubmed:abstractText	During pregnancy, maternal plasma cortisol concentrations approximately double. Given that cortisol plays an important role in the regulation of vascular reactivity, the present study investigated the potential role of cortisol in potentiation of uterine artery (UA) contractility and tested the hypothesis that pregnancy downregulated the cortisol-mediated potentiation. In vitro cortisol treatment (3, 10, or 30 ng/ml for 24 h) produced a dose-dependent increase in norepinephrine (NE)-induced contractions in both nonpregnant and pregnant (138-143 days gestation) sheep UA. However, this cortisol-mediated response was significantly attenuated by approximately 50% in pregnant UA. The 11 beta-hydroxysteroid dehydrogenase (11-beta HSD) inhibitor carbenoxolone did not change the effect of cortisol in nonpregnant UA but abolished its effect in pregnant UA by increasing the NE pD(2) in control tissues from 6.20 +/- 0.05 to 6.59 +/- 0.11. The apparent dissociation constant value of NE alpha(1)-adrenoceptors was not changed by cortisol in pregnant UA but was decreased in nonpregnant UA. There was no difference in glucocorticoid receptor density between nonpregnant and pregnant UA. Cortisol significantly decreased endothelial nitric oxide (NO) synthase protein levels and NO release in both nonpregnant and pregnant UA, but the effect of cortisol was attenuated in pregnant UA by approximately 50%. Carbenoxolone alone had no effects on NO release in nonpregnant UA but was decreased in pregnant UA. These results suggest that cortisol potentiates NE-mediated contractions by decreasing NO release and increasing NE-binding affinity to alpha(1)-adrenoceptors in nonpregnant UA. Pregnancy attenuates UA sensitivity to cortisol, which may be mediated by increasing type-2 11-beta HSD activity in UA.
pubmed:grant	http://linkedlifedata.com/resource/pubmed/grant/HD-31226, http://linkedlifedata.com/resource/pubmed/grant/HL-54094, http://linkedlifedata.com/resource/pubmed/grant/HL-57787
pubmed:language	eng
pubmed:journal	http://linkedlifedata.com/resource/pubmed/journal/100901228
pubmed:citationSubset	IM
pubmed:chemical	http://linkedlifedata.com/resource/pubmed/chemical/11-beta-Hydroxysteroid..., http://linkedlifedata.com/resource/pubmed/chemical/Carbenoxolone, http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors, http://linkedlifedata.com/resource/pubmed/chemical/Hydrocortisone, http://linkedlifedata.com/resource/pubmed/chemical/Hydroxysteroid Dehydrogenases, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type III, http://linkedlifedata.com/resource/pubmed/chemical/Norepinephrine, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Adrenergic, alpha, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Glucocorticoid
pubmed:status	MEDLINE
pubmed:month	Jul
pubmed:issn	0363-6135
pubmed:author	pubmed-author:BaeSoochanS, pubmed-author:DucsayCharles ACA, pubmed-author:HuangXiaohuiX, pubmed-author:XiaoDaliaoD, pubmed-author:ZhangLuboL
pubmed:issnType	Print
pubmed:volume	283
pubmed:owner	NLM
pubmed:authorsComplete	Y
pubmed:pagination	H238-46
pubmed:dateRevised	2007-11-14
pubmed:meshHeading	pubmed-meshheading:12063296-11-beta-Hydroxysteroid Dehydrogenases, pubmed-meshheading:12063296-Animals, pubmed-meshheading:12063296-Arteries, pubmed-meshheading:12063296-Binding, Competitive, pubmed-meshheading:12063296-Blotting, Western, pubmed-meshheading:12063296-Carbenoxolone, pubmed-meshheading:12063296-Endothelium, Vascular, pubmed-meshheading:12063296-Enzyme Inhibitors, pubmed-meshheading:12063296-Female, pubmed-meshheading:12063296-Femoral Artery, pubmed-meshheading:12063296-Hydrocortisone, pubmed-meshheading:12063296-Hydroxysteroid Dehydrogenases, pubmed-meshheading:12063296-Nitric Oxide, pubmed-meshheading:12063296-Nitric Oxide Synthase, pubmed-meshheading:12063296-Nitric Oxide Synthase Type III, pubmed-meshheading:12063296-Norepinephrine, pubmed-meshheading:12063296-Pregnancy, pubmed-meshheading:12063296-Pregnancy, Animal, pubmed-meshheading:12063296-Receptors, Adrenergic, alpha, pubmed-meshheading:12063296-Receptors, Glucocorticoid, pubmed-meshheading:12063296-Sheep, pubmed-meshheading:12063296-Uterus, pubmed-meshheading:12063296-Vasoconstriction
pubmed:year	2002
pubmed:articleTitle	Cortisol-mediated potentiation of uterine artery contractility: effect of pregnancy.
pubmed:affiliation	Center for Perinatal Biology, Department of Pharmacology and Physiology, Loma Linda University School of Medicine, Loma Linda, California 92350, USA.
pubmed:publicationType	Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't