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Am J Physiol Heart Circ Physiol (June 2, 2006). doi:10.1152/ajpheart.01109.2005
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01109.2005v1
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Submitted on October 20, 2005
Accepted on June 1, 2006

NO and prostanoids blunt the endothelin-mediated coronary vasoconstrictor influence in exercising swine

Daphne Merkus1*, Oana Sorop1, Birgit Houweling1, Frans Boomsma2, Anton H van den Meiracker2, and Dirk J. Duncker1

1 Experimental Cardiology, Thoraxcenter, Erasmus MC, Rotterdam, Netherlands
2 Internal Medicine, Erasmus MC, Rotterdam, Netherlands

* To whom correspondence should be addressed. E-mail: d.merkus{at}erasmusmc.nl.

Withdrawal of the endothelin (ET)- mediated vasoconstrictor influence contributes to metabolic coronary vasodilation during exercise. Since production of NO and prostanoids increases with increasing shear stress and NO and prostanoids are able to modify the release of ET, we hypothesized that the withdrawal of ET-mediated coronary vasoconstriction during exercise is mediated through NO and/or prostanoids. To test this hypothesis, 19 chronically instrumented swine were studied at rest and while running on a treadmill up to 85-90% of maximal heart rate. Blockade of ETA/ETB receptors with tezosentan resulted in an increase in coronary venous O2 levels (i.e. in coronary vasodilation) at rest, that waned at increasing levels of exercise intensity. Inhibition of either NO synthase (N{omega}-nitro-L-arginine; NLA) or cyclo-oxygenase (indomethacin) did not affect the response to tezosentan under resting conditions, but unmasked a vasodilator response to tezosentan during exercise. The vasodilator response to tezosentan during exercise increased progressively after combined administration of NLA and indomethacin. These findings suggest that NO and prostanoids act synergistically to inhibit the vasoconstrictor influence of ET on the coronary circulation during exercise, thereby facilitating the exercise-induced vasodilation of coronary resistance vessels.




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