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J Physiol Volume 583, Number 3, 847-854, September 15, 2007 DOI: 10.1113/jphysiol.2007.135525
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SYMPOSIUM REPORT

Exercise hyperaemia in the heart: the search for the dilator mechanism

Dirk J. Duncker1 and Daphne Merkus1

1 Division of Experimental Cardiology, Department of Cardiology, Thoraxcentre, Cardiovascular Research School (COEUR) Erasmus MC, University Medical Center Rotterdam, Rotterdam, The Netherlands

Coronary blood flow is tightly coupled to myocardial oxygen consumption to maintain a consistently high level of myocardial oxygen extraction over a wide range of physical acitivity. This tight coupling has been proposed to depend on periarteriolar oxygen tension, signals released from cardiomyocytes (adenosine acting on KATP channels) and the endothelium (prostanoids, nitric oxide, endothelin) as well as neurohumoral influences (catecholamines, endothelin), but the contribution of each of these regulatory pathways, and their interactions, to exercise hyperaemia in the human heart are still incompletely understood. Thus, in the human heart, nitric oxide, prostanoids, adenosine and KATP channels each contribute to resting tone, but evidence for a critical contribution to exercise hyperaemia is lacking. In dogs KATP channel activation together with adenosine and nitric oxide contribute to exercise hyperaemia in a non-linear redundant fashion. In contrast, in swine nitric oxide, adenosine and KATP channels contribute to resting coronary resistance vessel tone control in a linear additive manner, but are not mandatory for exercise hyperaemia in the heart. Rather, exercise hyperaemia in swine appears to involve KCa channel opening that is mediated, at least in part, by exercise-induced beta-adrenergic activation, possibly in conjunction with exercise-induced blunting of an endothelin-mediated vasoconstrictor influence. In view of these remarkable species differences in coronary vasomotor control during exercise, future studies are required to determine whether exercise hyperaemia in humans follows a canine or porcine control design.

(Received 29 April 2007; accepted after revision 31 May 2007; first published online 7 June 2007)
Corresponding author D. J. Duncker: Experimental Cardiology, Thoraxcentre, Erasmus MC, University Medical Center Rotterdam, Box 2040, 3000 CA Rotterdam, The Netherlands. Email: d.duncker{at}erasmusmc.nl


This report was presented at The Journal of Physiology Symposium on Exercise hyperemia, Washington, DC, USA, 2 May 2007. It was commissioned by the Editorial Board and reflects the views of the author.




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