Document Detail


Contribution of BK(Ca) channels to local metabolic coronary vasodilation: Effects of metabolic syndrome.
MedLine Citation:
PMID:  20044440     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
This investigation was designed to examine the hypothesis that impaired function of coronary microvascular large-conductance Ca(2+)-activated K(+) (BK(Ca)) channels in metabolic syndrome (MetS) significantly attenuates the balance between myocardial oxygen delivery and metabolism at rest and during exercise-induced increases in myocardial oxygen consumption (MVo(2)). Studies were conducted in conscious, chronically instrumented Ossabaw swine fed a normal maintenance diet (11% kcal from fat) or an excess calorie atherogenic diet (43% kcal from fat, 2% cholesterol, 20% kcal from fructose) that induces many common features of MetS. Data were collected under baseline/resting conditions and during graded treadmill exercise before and after selective blockade of BK(Ca) channels with penitrem A (10 microg/kg iv). We found that the exercise-induced increases in blood pressure were significantly elevated in MetS swine. No differences in baseline cardiac function or heart rate were noted. Induction of MetS produced a parallel downward shift in the relationship between coronary venous Po(2) and MVo(2) (P < 0.001) that was accompanied by a marked release of lactate (negative lactate uptake) as MVo(2) was increased with exercise (P < 0.005). Inhibition of BK(Ca) channels with penitrem A did not significantly affect blood pressure, heart rate, or the relationship between coronary venous Po(2) and MVo(2) in lean or MetS swine. These data indicate that BK(Ca) channels are not required for local metabolic control of coronary blood flow under physiological (lean) or pathophysiological (MetS) conditions. Therefore, diminished function of BK(Ca) channels does not contribute to the impairment of myocardial oxygen-supply demand balance in MetS.
Authors:
Léna Borbouse; Gregory M Dick; Gregory A Payne; Brittany D Payne; Mark C Svendsen; Zachary P Neeb; Mouhamad Alloosh; Ian N Bratz; Michael Sturek; Johnathan D Tune
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-12-31
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  298     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-02-25     Completed Date:  2010-04-02     Revised Date:  2013-05-31    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H966-73     Citation Subset:  IM    
Affiliation:
Dept. of Cellular and Integrative Physiology, Indiana Univ. School of Medicine, Indianapolis, 46202, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Coronary Vessels / physiopathology*
Disease Models, Animal
Heart Rate / physiology
Metabolic Syndrome X / physiopathology*
Mycotoxins / pharmacology
Myocardium / metabolism
Oxygen Consumption / physiology
Physical Conditioning, Animal / physiology
Potassium Channels, Calcium-Activated / antagonists & inhibitors,  physiology*
Regional Blood Flow / physiology
Swine
Vasodilation / physiology*
Grant Support
ID/Acronym/Agency:
HL-092245/HL/NHLBI NIH HHS; HL-62552/HL/NHLBI NIH HHS; RR-13223/RR/NCRR NIH HHS; UL1 RR-025761/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Mycotoxins; 0/Potassium Channels, Calcium-Activated; 37203-49-9/tremortin
Comments/Corrections

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


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