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Cardiovascular Research Advance Access [Accepted Manuscript] published online on November 24, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn321
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org.

Coronary response to diadenosine pentaphosphate after ischemia-reperfusion in the isolated rat heart

Ángel Luis García-Villalón, Luis Monge, Nuria Fernández, Adely Salcedo, Raúl Narváez-Sánchez and Godofredo Diéguez

Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma de Madrid

Address for correspondence: Angel Luis García-Villalón, Departamento de Fisiología, Facultad de Medicina, Universidad Autónoma, Arzobispo Morcillo 2, 28029 Madrid, Spain. Phone number 34 91 4975412 Fax number 34 91 4975478 Email: angeluis.villalon{at}uam.es

Aims: Diadenosine polyphosphates are vasoactive mediators that may be released from platelet granules and which may be present at higher concentrations during coronary ischemia-reperfusion. The objective of this study was to analyze their effects in such conditions.

Methods: Rat hearts were perfused in a Langendorff preparation and the response to diadenosine polyphosphate (Ap5A, 10–7 - 10–5 M) was recorded.

Results: In control hearts, Ap5A produced a small, transient coronary vasoconstriction followed by marked vasodilatation, as well as a reduction in the left ventricular developed pressure dP/dt and heart rate, both at the basal coronary resting tone or after precontracting coronary arteries with 9,11-dideoxy-11{alpha}, 9{alpha}-epoxymethanoprostaglandin F2{alpha} (U46619 [GenBank] ). After ischemia-reperfusion, the vasoconstriction in response to Ap5A was augmented and vasodilatation diminished, both in hearts with basal or increased vascular tone. The pyridoxal derivative P2 purinoceptor antagonist, pyridoxalphosphate-6-azophenyl-2’,4’-disulfonic acid (PPADS, 3x10–6 M), inhibited this vasoconstriction, while the antagonist of purinergic P2Y receptors, Reactive Blue 2 (2x10–6 M), inhibited the vasodilatation, both before and after ischemia-reperfusion. The antagonist of nitric oxide synthesis N-{omega}-nitro-L- arginine methyl ester (L-NAME, 10–4 M) did not modify the response to Ap5A, whereas the cyclooxygenase inhibitor, meclofenamate (2x10–6 M), reduced contraction and increased the relaxation in response to Ap5A after ischemia-reperfusion but not under control conditions.

Conclusion: Ischemia-reperfusion reduces the vasodilatory response to Ap5A and increases the vasoconstriction provoked due to a reduced influence of purinergic P2Y receptors and/or to the production of vasoconstrictor prostanoids.

KEYWORDS perfused heart; purinergic P2x receptors; purinergic P2y receptors; coronary circulation

Time for primary review: 26 Days


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