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Cardiovascular Research Advance Access originally published online on November 24, 2008
Cardiovascular Research 2009 81(2):336-343; 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 ischaemia–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, Arzobispo Morcillo 2, 28029 Madrid, Spain

* Corresponding author. Tel: +34 91 497 5412; fax: +34 91 497 5478. E-mail address: 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 ischaemia–reperfusion. The objective of this study was to analyse their effects in such conditions.

Methods and results: Rat hearts were perfused in a Langendorff preparation and the response to diadenosine pentaphosphate (Ap5A, 10–7–10–5 M) was recorded. 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 pre-contracting coronary arteries with 9,11-dideoxy-11{alpha}, 9{alpha}-epoxymethanoprostaglandin F2{alpha} (U46619 [GenBank] ). After ischaemia–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, 3 x 10–6 M), inhibited this vasoconstriction, while the antagonist of purinergic P2Y receptors, Reactive Blue 2 (2 x 10–6 M), inhibited the vasodilatation, both before and after ischaemia–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 (2 x 10–6 M), reduced contraction and increased the relaxation in response to Ap5A after ischaemia–reperfusion but not under control conditions.

Conclusion: Ischaemia–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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