Document Detail


Pregnancy enhances endothelium-dependent relaxation of ovine uterine artery: role of NO and intracellular Ca(2+).
MedLine Citation:
PMID:  11406484     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The present study tested the hypothesis that the pregnancy-associated increase in endothelium-dependent relaxation of the uterine artery was mediated primarily by an increase in nitric oxide (NO) release, resulting in a reduction in smooth muscle intracellular Ca(2+) concentration ([Ca(2+)](i)). Uterine arteries obtained from nonpregnant and near-term (140 days gestation) pregnant sheep were used. The Ca(2+) ionophore A23187 induced endothelium-dependent relaxations in both nonpregnant and pregnant uterine arteries, with an increased relaxation in the pregnant tissue. In contrast, endothelium-independent relaxations induced by sodium nitroprusside were the same in nonpregnant and pregnant arteries. In addition, removal of the endothelium significantly increased noradrenaline-induced contractions in pregnant, but not nonpregnant, uterine arteries. In accordance, pregnancy increased both basal and A23187-stimulated NO releases in the uterine artery. Simultaneous measurement of tension and [Ca(2+)](i) in the smooth muscle demonstrated a linear correlation with the slope of unity between A23187-induced relaxation and the reduction of [Ca(2+)](i) in both nonpregnant and pregnant uterine arteries. The A23187-induced reduction of [Ca(2+)](i) was significantly enhanced in pregnant, compared with nonpregnant, uterine arteries. The results indicate that pregnancy increases NO release, which, through decreasing [Ca(2+)](i) in the smooth muscle, accounts for the increased endothelium-dependent relaxation of the uterine artery. Signal transduction pathways distal to NO production are not changed by pregnancy.
Authors:
D Xiao; W J Pearce; L Zhang
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  281     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2001 Jul 
Date Detail:
Created Date:  2001-06-14     Completed Date:  2001-07-26     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H183-90     Citation Subset:  IM    
Affiliation:
Center for Perinatal Biology, Department of Pharmacology and Physiology, Loma Linda University School of Medicine, Loma Linda, California 92350, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Arteries / drug effects,  physiology
Calcimycin / pharmacology
Calcium / physiology
Endothelium, Vascular / physiology*
Female
Intracellular Membranes / metabolism
Ionophores / pharmacology
Nitric Oxide / physiology
Nitroprusside / pharmacology
Norepinephrine / pharmacology
Pregnancy
Pregnancy, Animal / physiology*
Reference Values
Sheep
Uterus / blood supply*
Vasoconstrictor Agents / pharmacology
Vasodilation / physiology*
Vasodilator Agents / pharmacology
Grant Support
ID/Acronym/Agency:
HD-31226/HD/NICHD NIH HHS; HL-54094/HL/NHLBI NIH HHS; HL-57787/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Ionophores; 0/Vasoconstrictor Agents; 0/Vasodilator Agents; 10102-43-9/Nitric Oxide; 15078-28-1/Nitroprusside; 51-41-2/Norepinephrine; 52665-69-7/Calcimycin; 7440-70-2/Calcium

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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