| Augmented EDHF signaling in rat uteroplacental vasculature during late pregnancy. | |
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MedLine Citation:
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PMID: 20817830 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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A successful pregnancy outcome relies on extensive maternal cardiovascular adaptation, including enhanced uteroplacental vasodilator mechanisms. The objective of the present study was to determine the contribution of the endothelium-derived hyperpolarizing factor (EDHF) signaling in pregnancy-enhanced uterine vasodilation, to define the role of Ca(2+)-activated K(+) channels in mediating EDHF effects, and to explore the impact of endothelial Ca(2+) signaling in pregnancy-specific upregulation of EDHF. Fura 2-based measurements of smooth muscle cell (SMC) and endothelial cell cytosolic Ca(2+) concentration ([Ca(2+)](i)) were performed simultaneously with measurements of the diameter of uterine radial arteries from nonpregnant (NP) and late pregnant (LP) rats. Changes in SMC membrane potential of pressurized arteries from LP rats were assessed using glass microelectrodes. After blockade of nitric oxide and prostacyclin production, a cumulative application of ACh induced rapid and effective dilatation of uterine vessels from both NP and LP rats. This vasodilation was associated with SMC hyperpolarization and SMC [Ca(2+)](i) reduction and was abolished by a high-K(+) solution, demonstrating that N(G)-nitro-L-arginine (L-NNA)- and indomethacin-resistant responses are attributable to EDHF. Pregnancy significantly potentiates EDHF-mediated vasodilation in part due to enhanced endothelial Ca(2+) signaling. L-NNA- and indomethacin-resistant responses were insensitive to iberiotoxin but abolished by a combined treatment with apamin and charybdotoxin, supporting the key role of small- and intermediate-conductance K(+) channels in mediating EDHF signaling in the maternal uterine resistance vasculature. |
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Authors:
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N I Gokina; O Y Kuzina; A M Vance |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2010-09-03 |
Journal Detail:
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Title: American journal of physiology. Heart and circulatory physiology Volume: 299 ISSN: 1522-1539 ISO Abbreviation: Am. J. Physiol. Heart Circ. Physiol. Publication Date: 2010 Nov |
Date Detail:
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Created Date: 2010-11-01 Completed Date: 2010-11-29 Revised Date: 2011-11-01 |
Medline Journal Info:
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Nlm Unique ID: 100901228 Medline TA: Am J Physiol Heart Circ Physiol Country: United States |
Other Details:
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Languages: eng Pagination: H1642-52 Citation Subset: IM |
Affiliation:
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Dept. of Obstetrics, Gynecology, and Reproductive Sciences, College of Medicine, The Univ. of Vermont, Burlington, VT 05405, USA. Natalia.Gokina@uvm.edu |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apamin / pharmacology Biological Factors / physiology* Calcium Signaling / physiology Charybdotoxin / pharmacology Cyclooxygenase Inhibitors / pharmacology Female Indomethacin / pharmacology Models, Animal Nitric Oxide Synthase / antagonists & inhibitors, metabolism Placental Circulation / drug effects, physiology* Potassium Channels, Calcium-Activated / physiology Pregnancy Pregnancy, Animal / physiology* Prostaglandin-Endoperoxide Synthases / metabolism Rats Rats, Sprague-Dawley Signal Transduction / drug effects, physiology* Vasodilation / drug effects, physiology |
| Grant Support | |
ID/Acronym/Agency:
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HL-067250/HL/NHLBI NIH HHS; HL-088245/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Biological Factors; 0/Cyclooxygenase Inhibitors; 0/Potassium Channels, Calcium-Activated; 0/endothelium-dependent hyperpolarization factor; 115422-61-2/Charybdotoxin; 24345-16-2/Apamin; 53-86-1/Indomethacin; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.99.1/Prostaglandin-Endoperoxide Synthases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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