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

Garcı́a-Villalón, Ángel Luis; Monge, Luis; Fernández, Núria; Salcedo, Adely; Narváez-Sánchez, Raúl; Diéguez, Godofredo

doi:10.1093/cvr/cvn321

Cited by 14 publications

(17 citation statements)

References 25 publications

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“…In control hearts, diadenosine pentaphosphate was observed to produce transient coronary vasoconstriction followed by marked vasodilatation, which are alterations modified by I/R [ 69 ]. Furthermore, the vasoconstriction response was inhibited by the blockade of P2X receptors by PPADS, whereas the vasodilatation was attenuated by the P2Y blocker, Reactive Blue in the I/R hearts [ 69 ]. The blockade of P2X receptors by PPADS was also found to attenuate the exercise-induced pressor reflex in heart failure [ 70 ] as well as after circulatory occlusion [ 71 ].…”

Section: Mechanisms Of Plp Action In the Ischemic Heart Diseasementioning

confidence: 96%

“…Purinergic P2Y antagonists, suramin and Reactive Blue, have also been reported to exert ischemic preconditioning in the rat heart [ 68 ]. In control hearts, diadenosine pentaphosphate was observed to produce transient coronary vasoconstriction followed by marked vasodilatation, which are alterations modified by I/R [ 69 ]. Furthermore, the vasoconstriction response was inhibited by the blockade of P2X receptors by PPADS, whereas the vasodilatation was attenuated by the P2Y blocker, Reactive Blue in the I/R hearts [ 69 ].…”

Section: Mechanisms Of Plp Action In the Ischemic Heart Diseasementioning

confidence: 99%

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Mechanisms of the beneficial effects of vitamin B6 and pyridoxal 5-phosphate on cardiac performance in ischemic heart disease

Dhalla

Takeda²,

Elimban

2013

Clinical Chemistry and Laboratory Medicine

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Although vitamin B6 and its metabolite, pyridoxal 5 ′ -phosphate (PLP), have been shown to exert bene ficial effects in ischemic heart disease, the mechanisms of their action are not fully understood. Some studies have shown that ventricular arrhythmias and mortality upon the occlusion of coronary artery were attenuated by pretreatment of animals with PLP. Furthermore, ischemia-reperfusion-induced abnormalities in cardiac performance and defects in sarcoplasmic reticular Ca 2 + -transport activities were decreased by PLP. The increase in cardiac contractile activity of isolated heart by ATP was reduced by PLP, unlike propranolol, whereas that by isoproterenol was not depressed by PLP. ATP-induced increase in [Ca ] i in cardiomyocytes was depressed by PLP. Both high-and low-affinity sites for ATP binding in sarcolemmal membranes were also decreased by PLP. These observations support the view that PLP may produce cardioprotective effects in ischemic heart disease by attenuating the occurrence of intracellular Ca 2 + overload due to the blockade of purinergic receptors.

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Section: Mechanisms Of Plp Action In the Ischemic Heart Diseasementioning

confidence: 96%

Section: Mechanisms Of Plp Action In the Ischemic Heart Diseasementioning

confidence: 99%

Mechanisms of the beneficial effects of vitamin B6 and pyridoxal 5-phosphate on cardiac performance in ischemic heart disease

Dhalla

Takeda²,

Elimban

2013

Clinical Chemistry and Laboratory Medicine

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“…However, Reactive Blue 2 did not modify the relaxation to acetylcholine before ischemia-reperfusion. An increase of vasodilating purinergic receptors after ischemia-reperfusion seems unlikely, as previous results from our laboratory show that vasodilatation to purinergic agonists is reduced, not increased, by ischemia-reperfusion in the coronary circulation [24,31,32]. Therefore, the change in the effect of Reactive Blue 2 may be because ATP release is reduced in control conditions and is stimulated after ischemia-reperfusion.…”

Section: Discussionmentioning

confidence: 84%

“…The response to acetylcholine was recorded after coronary precontraction with U46619. The duration of ischemia and reperfusion were chosen on the basis of previous studies demonstrating decreases in the endothelium-dependent coronary relaxation without alteration of endothelium-independent coronary relaxation [23,24]. To inhibit the synthesis of nitric oxide, the hearts were treated with the synthase inhibitor N-omega-nitro- L -arginine methyl ester ( L -NAME; 10 - 4 M ), added to the perfusion solution 15 min before and during the recording of the relaxation to acetylcholine.…”

Section: Methodsmentioning

confidence: 99%

Purinergic Component in the Coronary Vasodilatation to Acetylcholine after Ischemia-Reperfusion in Perfused Rat Hearts

Garcı́a-Villalón

Granado²,

Monge³

et al. 2014

J Vasc Res

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To determine the involvement of purinergic receptors in coronary endothelium-dependent relaxation, the response to acetylcholine (1 × 10^-8 to 3 × 10^-7M) was recorded in isolated rat hearts perfused according to the Langendorff procedure before and after 30 min of ischemia and 15 min of reperfusion and after the inhibition of nitric oxide synthesis with L-NAME (10^-4M), in the absence and presence of the antagonist of purinergic P2X receptors, PPADS (3 × 10^-6M), and of the antagonist of purinergic P2Y receptors, Reactive Blue 2 (3 × 10^-7M). In control conditions, the relaxation to acetylcholine was not altered by PPADS or Reactive Blue 2. The relaxation to acetylcholine was reduced after ischemia-reperfusion, and, in this condition, it was further reduced by treatment with PPADS or Reactive Blue 2. Likewise, the relaxation to acetylcholine was reduced by L-NAME, and reduced further by Reactive Blue 2 but not by PPADS. These results suggest that the relaxation to acetylcholine may be partly mediated by purinergic receptors after ischemia-reperfusion, due to the reduction of nitric oxide release in this condition.

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“…Then, the heart was quickly excised and transferred to a Langendorff apparatus while continuously perfused retrograde with Krebs-Henseleit buffer (NaCl 115 mM, KCl 4.6 mM, KH 2 PO 4 1.2 mM, MgSO 4 1.2 mM, CaCl 2 2.5 mM, NaHCO 3 25 mM, and glucose 11 mM) equilibrated with 95% O 2 + 5% CO 2 , pH of 7.3-7.4 at a constant pressure of 70 mmHg and a temperature of 37˚C. The cardiac function was monitored continuously by a power lab system (AD Instruments, Castle Hill, Australia) (22). All hearts were perfused for 20-25 minutes before the induction of ischemia to allow stabilization.…”

Section: Methodsmentioning

confidence: 99%

Protective Effects of Crocin on Ischemia-reperfusion Induced Oxidative Stress in Comparison With Vitamin E in Isolated Rat Hearts

Dianat

Esmaeilizadeh

Badavi

et al. 2014

Jundishapur J Nat Pharm Prod

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Background: Myocardial Injury caused by ischemia-reperfusion leads to cardiac dysfunction, tissue injury and metabolic changes. The production of reactive oxygen species (ROS) and lipid peroxidation are accompanied by ischemia-reperfusion injury. Objectives: The aim of this study was to assess the cardio protective potential effects of crocin in comparison with vitamin E on antioxidant capacity in ischemia-reperfusion of isolated rat hearts. Materials and Methods: Seventy male Sprague-Dawley rats were randomly divided into seven groups, including: sham, control and experimental groups treated with different doses of crocin (10, 20 and 40 mg/kg) or vitamin E (100 mg/kg) and a combination of crocin (40 mg/kg) with vitamin E (100 mg/kg) that were administrated orally for 21 days. The heart was quickly excised, transferred to a Langendorff apparatus at constant pressure and subjected to 30 minutes of global ischemia followed by 60 minutes of reperfusion. Cardiac damage markers and antioxidant enzymes were measured. Results:The results showed that superoxide dismutase and catalase enzyme activities increased and Mallon de aldehyde (MDA) decreased in animals pretreated by crocin (40 mg/kg) and vitamin E (100 mg/kg). Moreover, there was a significant improvement in post ischemic recovery of antioxidant capacity during reperfusion in rats receiving a combination of crocin (40 mg/kg) and vitamin E (100 mg/kg). Conclusions:The results demonstrated the protective role of crocin on antioxidant capacity, which may partially be related to stability or amplification of antioxidant systems. Like vitamin E, crocin may be beneficial for prevention or treatment of cardiac dysfunction and myocardial infarction in patients with ischemic heart disease.

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

Abstract: Ischaemia-reperfusion reduces the vasodilatory response to Ap5A and increases the vasoconstriction provoked due to a reduced influence of purinergic P(2Y) receptors and/or to the production of vasoconstrictor prostanoids.

Cited by 14 publications

References 25 publications

Mechanisms of the beneficial effects of vitamin B6 and pyridoxal 5-phosphate on cardiac performance in ischemic heart disease

Mechanisms of the beneficial effects of vitamin B6 and pyridoxal 5-phosphate on cardiac performance in ischemic heart disease

Purinergic Component in the Coronary Vasodilatation to Acetylcholine after Ischemia-Reperfusion in Perfused Rat Hearts

Protective Effects of Crocin on Ischemia-reperfusion Induced Oxidative Stress in Comparison With Vitamin E in Isolated Rat Hearts

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