Document Detail


Effects of acute transmural pressure elevation on endothelium-dependent vasodilation in isolated rat mesenteric veins.
MedLine Citation:
PMID:  24280957     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND/AIMS: The vascular regulatory function of the endothelium can be impaired by increases in transmural pressure (TMP). We tested the hypothesis that increasing TMP impairs the endothelial dilator function of rat mesenteric small veins (MSVs).
METHODS: In PGF2α-preconstricted MSVs, bradykinin (BK), sodium nitroprusside (SNP) and S-Nitroso-N-acetylpenicillamine (SNAP) concentration-response curves were generated at intermediate (6 mm Hg) and high (12 mm Hg) pressures. BK-induced vasodilation was examined in the absence and presence of nitric oxide synthase inhibitor [N(ω)-nitro-L-arginine (L-NNA), 100 µM], cyclooxygenase inhibitor (indomethacin, 1 µM), and large (BKCa, paxilline, 500 nM) and small (SKCa, apamin, 300 nM) conductance Ca(2+)-activated K(+) channel blockers.
RESULTS: BK, SNP and SNAP responses were not altered by TMP increases. BK-induced vasodilation was significantly reduced by L-NNA, indomethacin, apamin and paxilline at 6 mm Hg and L-NNA at 12 mm Hg, and was further reduced by coapplication of apamin and/or paxilline with L-NNA compared with responses obtained with either blocker. Endothelium removal completely abolished BK-induced vasodilation.
CONCLUSION: Venous endothelial dilator function is not affected by TMP elevation. BK-induced vasodilation is completely dependent on the presence of functional endothelial cells and mediated in part by nitric oxide, BKCa and SKCa channels, while the participation of prostacyclin may be important at intermediate pressures.
Authors:
Saad Enouri; Gabrielle Monteith; Ron Johnson
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2013-11-21
Journal Detail:
Title:  Journal of vascular research     Volume:  51     ISSN:  1423-0135     ISO Abbreviation:  J. Vasc. Res.     Publication Date:  2014  
Date Detail:
Created Date:  2014-01-17     Completed Date:  2014-03-13     Revised Date:  2014-07-31    
Medline Journal Info:
Nlm Unique ID:  9206092     Medline TA:  J Vasc Res     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  27-36     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Cyclooxygenase Inhibitors / pharmacology
Dose-Response Relationship, Drug
Endothelium, Vascular / drug effects,  metabolism,  physiology*
Epoprostenol / metabolism
Large-Conductance Calcium-Activated Potassium Channels / metabolism
Male
Mechanotransduction, Cellular / drug effects
Mesenteric Veins / drug effects,  metabolism,  physiology*
Nitric Oxide / metabolism
Nitric Oxide Donors / pharmacology
Nitric Oxide Synthase / antagonists & inhibitors,  metabolism
Potassium Channel Blockers / pharmacology
Rats
Rats, Sprague-Dawley
Small-Conductance Calcium-Activated Potassium Channels / metabolism
Time Factors
Vasoconstrictor Agents / pharmacology
Vasodilation* / drug effects
Vasodilator Agents / pharmacology
Venous Pressure* / drug effects
Chemical
Reg. No./Substance:
0/Cyclooxygenase Inhibitors; 0/Large-Conductance Calcium-Activated Potassium Channels; 0/Nitric Oxide Donors; 0/Potassium Channel Blockers; 0/Small-Conductance Calcium-Activated Potassium Channels; 0/Vasoconstrictor Agents; 0/Vasodilator Agents; 31C4KY9ESH/Nitric Oxide; DCR9Z582X0/Epoprostenol; EC 1.14.13.39/Nitric Oxide Synthase

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


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