Document Detail

Low-intensity interval exercise training attenuates coronary vascular dysfunction and preserves Ca²⁺-sensitive K⁺ current in miniature swine with LV hypertrophy.
MedLine Citation:
PMID:  21841018     Owner:  NLM     Status:  MEDLINE    
Coronary vascular dysfunction has been observed in several models of heart failure (HF). Recent evidence indicates that exercise training is beneficial for patients with HF, but the precise intensity and underlying mechanisms are unknown. Left ventricular (LV) hypertrophy can play a significant role in the development of HF; therefore, the purpose of this study was to assess the effects of low-intensity interval exercise training on coronary vascular function in sedentary (HF) and exercise trained (HF-TR) aortic-banded miniature swine displaying LV hypertrophy. Six months postsurgery, in vivo coronary vascular responses to endothelin-1 (ET-1) and adenosine were measured in the left anterior descending coronary artery. Baseline and maximal coronary vascular conductance were similar between all groups. ET-1-induced reductions in coronary vascular conductance (P < 0.05) were greater in HF vs. sedentary control and HF-TR groups. Pretreatment with the ET type A (ET(A)) receptor blocker BQ-123 prevented ET-1 hypersensitivity in HF animals. Whole cell voltage clamp was used to characterize composite K(+) currents (I(K(+))) in coronary smooth muscle cells. Raising internal Ca(2+) from 200 to 500 nM increased Ca(2+)-sensitive K(+) current in HF-TR and control, but not HF animals. In conclusion, an ET(A)-receptor-mediated hypersensitivity to ET-1, elevated resting LV wall tension, and decreased coronary smooth muscle cell Ca(2+)-sensitive I(K(+)) was found in sedentary animals with LV hypertrophy. Low-intensity interval exercise training preserved normal coronary vascular function and smooth muscle cell Ca(2+)-sensitive I(K(+)), illustrating a potential mechanism underlying coronary vascular dysfunction in a large-animal model of LV hypertrophy. Our results demonstrate the potential clinical impact of exercise on coronary vascular function in HF patients displaying pathological LV hypertrophy.
Craig A Emter; Darla L Tharp; Jan R Ivey; Venkataseshu K Ganjam; Douglas K Bowles
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, N.I.H., Extramural     Date:  2011-08-12
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  301     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2011 Oct 
Date Detail:
Created Date:  2011-09-29     Completed Date:  2011-11-22     Revised Date:  2013-06-28    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1687-94     Citation Subset:  IM    
Dept. of Biomedical Science, Univ. of Missouri-Columbia, 1600 E. Rollins, E117 Veterinary Medicine, Columbia, MO 65211, USA.
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MeSH Terms
Blood Pressure / physiology
Capillaries / physiology
Cardiotonic Agents / pharmacology
Coronary Circulation / physiology
Coronary Disease / pathology,  physiopathology*
Coronary Vessels / physiology
Dobutamine / pharmacology
Endothelin-1 / metabolism
Heart Rate / physiology
Hypertrophy, Left Ventricular / pathology,  physiopathology*
Muscle, Smooth, Vascular / physiology
Myocardial Contraction / physiology
Peptides, Cyclic / pharmacology
Physical Conditioning, Animal / physiology*
Potassium Channels, Calcium-Activated / physiology*
Receptor, Endothelin A / antagonists & inhibitors,  physiology
Swine, Miniature
Grant Support
Reg. No./Substance:
0/Cardiotonic Agents; 0/Endothelin-1; 0/Peptides, Cyclic; 0/Potassium Channels, Calcium-Activated; 0/Receptor, Endothelin A; 136553-81-6/cyclo(Trp-Asp-Pro-Val-Leu); 34368-04-2/Dobutamine

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

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