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).
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.
Objective
To the test the hypothesis that exercise training would increase endothelin-mediated vasoconstriction in collateral-dependent arteries via enhanced contribution of ET(A).
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).