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Am J Physiol Heart Circ Physiol (January 6, 2005). doi:10.1152/ajpheart.00522.2003
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Submitted on June 5, 2003
Accepted on December 22, 2004

Cardiac myocytes control release of endothelin-1 in the coronary vasculature

Daphne Merkus1*, Anna K Brzezinska2, Cuihua Zhang2, Suichi Saito2, and William M Chilian2

1 Experimental Cardiology, Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands
2 Department of Physiology, Louisiana State University Health Sciences Center, New Orleans, LA, USA

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

{alpha}-Adrenergic vasoconstriction in the coronary circulation is mediated through {alpha}-adrenoceptors on the cardiac myocytes and subsequent release of endothelin, a very potent, long-lasting vasoconstrictor. Recent studies have found that adult cardiac myocytes do not express the preproendothelin gene. Thus, we hypothesized that {alpha}-adrenoceptor stimulation on the cardiac myocytes results in the production of an endothelin releasing factor, which stimulates the coronary vasculature to produce endothelin. We tested this hypothesis by using an in vitro model in which isolated adult rat cardiac myocytes can be stimulated with an {alpha}-adrenoceptor agonist (phenylephrine). Their bathing fluid is then transferred to isolated coronary arterioles and vasoactive responses are measured. To identify the source of endothelin, the endothelin converting enzyme (ECE) inhibitor phosphoramidon is added to either the myocytes or the isolated arterioles. Phenylephrine enhanced the vasoconstrictor properties of the myocyte bathing fluid. Administration of phosphoramidon (either in the presence or absence of phenylephrine) to the myocytes had no effect on the vasoactive properties of the bathing fluid. In contrast, administration of phosphoramidon to the isolated arteriole prior to administration of the bathing fluid converted vasoconstriction to vasodilation, similar to the effect of the endothelin A receptor antagonist JKC-301, indicating that the endothelin is indeed produced by the coronary vasculature. In conclusion during {alpha}-adrenergic activation cardiac myocytes release a factor, probably Angiotensin II, that stimulates the vascular production of endothelin. Although the physiological implications of this mechanism are not obvious, this may represent a protective mechanisms that integrates neuronal vasoconstrictor mechanisms with myocardial metabolism, which minimizes periods of both coronary underperfusion and overperfusion.




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