Literature DB >> 25220869

Adaptations of the endothelin system after exercise training in a porcine model of ischemic heart disease.

Juan Carlos Robles1, Cristine L Heaps.   

Abstract

OBJECTIVE: To the test the hypothesis that exercise training would increase endothelin-mediated vasoconstriction in collateral-dependent arteries via enhanced contribution of ET(A).
METHODS: An ameroid constrictor was surgically placed around the proximal LCX artery to induce gradual occlusion in Yucatan miniature swine. Eight weeks postoperatively, pigs were randomized into sedentary or exercise-training (treadmill; 5 days/week; 14 weeks) groups. Subsequently, arteries (~150 μm diameter) were isolated from collateral-dependent and nonoccluded myocardial regions and studied.
RESULTS: Following exercise training, ET-1-mediated contraction was significantly enhanced in collateral-dependent arteries. Exercise training induced a disproportionate increase in the ET(A) contribution to the ET-1 contractile response in collateral-dependent arteries, with negligible contributions by ET(B). In collateral-dependent arteries of sedentary pigs, inhibition of ET(A) or ET(B) did not significantly alter ET-1 contractile responses in collateral-dependent arteries, suggesting compensation by the functionally active receptor. These adaptations occurred without significant changes in ET(A), ET(B), or ECE mRNA levels but with significant exercise-training-induced elevations in endothelin levels in both nonoccluded and collateral-dependent myocardial regions.
CONCLUSIONS: Taken together, these data reveal differential adaptive responses in collateral-dependent arteries based upon physical activity level. ET(A) and ET(B) appear to compensate for one another to maintain contraction in sedentary pigs, whereas exercise-training favors enhanced contribution of ET(A).
© 2014 John Wiley & Sons Ltd.

Entities:  

Keywords:  coronary artery disease; coronary artery occlusion; near-resistance arteries; stenosis

Mesh:

Substances:

Year:  2015        PMID: 25220869      PMCID: PMC4286434          DOI: 10.1111/micc.12174

Source DB:  PubMed          Journal:  Microcirculation        ISSN: 1073-9688            Impact factor:   2.628


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