Document Detail


Exercise training-enhanced, endothelium-dependent dilation mediated by altered regulation of BK(Ca) channels in collateral-dependent porcine coronary arterioles.
MedLine Citation:
PMID:  23002811     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: Test the hypothesis that exercise training increases the contribution of BK(Ca) channels to endothelium-mediated dilation in coronary arterioles from collateral-dependent myocardial regions of chronically occluded pig hearts and may function downstream of H2O2.
METHODS: An ameroid constrictor was placed around the proximal left circumflex coronary artery to induce gradual occlusion in Yucatan miniature swine. Eight weeks postoperatively, pigs were randomly assigned to sedentary or exercise training (treadmill; 14 week) regimens.
RESULTS: Exercise training significantly enhanced bradykinin-mediated dilation in collateral-dependent arterioles (~125 μm diameter) compared with sedentary pigs. The BK(Ca) -channel blocker, iberiotoxin alone or in combination with the H2O2 scavenger, polyethylene glycol catalase, reversed exercise training-enhanced dilation in collateral-dependent arterioles. Iberiotoxin-sensitive whole-cell K+ currents (i.e., BK(Ca)-channel currents) were not different between smooth muscle cells of nonoccluded and collateral-dependent arterioles of sedentary and exercise trained groups.
CONCLUSIONS: These data provide evidence that BK(Ca)-channel activity contributes to exercise training-enhanced endothelium-dependent dilation in collateral-dependent coronary arterioles despite no change in smooth muscle BK(Ca)-channel current. Taken together, our findings suggest that a component of the bradykinin signaling pathway, which stimulates BK(Ca) channels, is enhanced by exercise training in collateral-dependent arterioles and suggest a potential role for H2O2 as the mediator.
Authors:
Wei Xie; Janet L Parker; Cristine L Heaps
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Microcirculation (New York, N.Y. : 1994)     Volume:  20     ISSN:  1549-8719     ISO Abbreviation:  Microcirculation     Publication Date:  2013 Feb 
Date Detail:
Created Date:  2013-02-15     Completed Date:  2013-08-06     Revised Date:  2014-02-04    
Medline Journal Info:
Nlm Unique ID:  9434935     Medline TA:  Microcirculation     Country:  United States    
Other Details:
Languages:  eng     Pagination:  170-82     Citation Subset:  IM    
Copyright Information:
© 2012 John Wiley & Sons Ltd.
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MeSH Terms
Descriptor/Qualifier:
Animals
Arterioles / physiology*
Bradykinin / pharmacology,  physiology
Catalase / metabolism,  pharmacology
Collateral Circulation / physiology
Coronary Circulation / physiology*
Endothelium, Vascular / physiology*
Female
Hydrogen Peroxide / metabolism
Large-Conductance Calcium-Activated Potassium Channels / agonists,  antagonists & inhibitors,  physiology*
Muscle, Smooth, Vascular / physiology
Patch-Clamp Techniques
Peptides / pharmacology
Physical Conditioning, Animal / physiology*
Polyethylene Glycols / pharmacology
Potassium / metabolism
Random Allocation
Superoxide Dismutase / metabolism
Swine
Swine, Miniature
Vasodilation / physiology*
Grant Support
ID/Acronym/Agency:
R01 HL064931/HL/NHLBI NIH HHS; R01-HL064931/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Large-Conductance Calcium-Activated Potassium Channels; 0/Peptides; 0/Polyethylene Glycols; 0/catalase-polyethylene glycol; 129203-60-7/iberiotoxin; BBX060AN9V/Hydrogen Peroxide; EC 1.11.1.6/Catalase; EC 1.15.1.1/Superoxide Dismutase; RWP5GA015D/Potassium; S8TIM42R2W/Bradykinin
Comments/Corrections

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


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