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Reduced coronary vasodilatation to diadenosine tetraphosphate after ischemia‐reperfusion in isolated rat heart
Author(s) -
GarciaVillalon Angel Luis,
Fernandez Nuria,
Monge Luis,
Dieguez Godofredo
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.1025.1
Subject(s) - glibenclamide , vasodilation , purinergic receptor , medicine , ischemia , agonist , coronary vasodilator , chemistry , endocrinology , adenosine , receptor , diabetes mellitus
Diadenosine polyphosphates increase during coronary ischemia. To analyze their role in coronary ischemia‐reperfusion, the response to diadenosine tetrataphosphate (Ap4A, 10 −7 ‐ 10 −5 M) was recorded in isolated perfused rat hearts after precontraction of the coronary vasculature with 11‐dideoxy‐1a,9a‐epoxymethanoprostaglandin F 2α (U46619, 10 −8 ‐3×10 −8 ). In control hearts, Ap4A produced concentration‐dependent vasodilatation both at the basal coronary resting tone or after precontracting coronary vasculature with U46619, and this vasodilatation was reduced by the antagonist of purinergic P 2Y receptors reactive blue 2 (2×10 −6 M) and the blocker of ATP‐sensitive potassium channels (K ATP ) glibenclamide (10 −5 M). After ischemia‐reperfusion, the vasodilatation to Ap4A diminished, and in this case the relaxation to Ap4A was not modified by reactive blue 2 or glibenclamide. The agonist of P 2Y purinergic receptors UTP (10 −7 ‐ 10 −5 M) produced coronary vasodilatation which also was reduced after ischemia‐reperfusion. These results suggest that the coronary relaxation to Ap4A is reduced after ischemia‐reperfusion, and that this reduction may be due to impaired response of purinergic P 2Y receptors and of K ATP potassium channels. (Supported by FMMA grant Nº AP57242009 and FIS grant Nº PS09/00394)