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      Myocardial postconditioning is lost in vascular nitrate tolerance.

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          Abstract

          Organic nitrates play an important role in the therapy of ischemic heart disease; however, their clinical application is limited by the development of vascular nitrate tolerance. We have previously shown attenuation of the cardioprotective effect of preconditioning in vascular nitrate tolerance. Here, we studied whether the development of vascular nitrate tolerance affects the infarct size, limiting effect of ischemic postconditioning (IPost) in the myocardium, and whether the activation of survival kinases plays a role in the molecular mechanism of postconditioning in the presence or absence of vascular nitrate tolerance. Male Wistar rats were treated with nitroglycerin/vehicle for 3 days to induce vascular nitrate tolerance. On the fourth day, isolated hearts were subjected to 30-minute coronary occlusion followed by 120-minute reperfusion with or without IPost. In nontolerant hearts, postconditioning significantly decreased infarct size as compared with ischemia/reperfusion; however, postconditioning failed to decrease infarct size in hearts of nitrate tolerant rats. Phosphorylation of ERK 1/2, Akt, or endothelial nitric oxide synthetase showed no significant differences between the groups at the 10th minute of reperfusion. Vascular nitrate tolerance interferes with the infarct size limiting effect of IPost. Activation of survival kinases is not crucial in the molecular mechanism of postconditioning, which remains unaffected in nitrate tolerance.

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          Author and article information

          Journal
          J. Cardiovasc. Pharmacol.
          Journal of cardiovascular pharmacology
          Ovid Technologies (Wolters Kluwer Health)
          1533-4023
          0160-2446
          Sep 2013
          : 62
          : 3
          Affiliations
          [1 ] *Cardiovascular Research Group, Department of Biochemistry, University of Szeged, Hungary; and †Pharmahungary Group, Szeged, Hungary; and Departments of ‡Pathophysiology and §Pharmacology and Pharmacotherapy, Semmelweis University, Budapest, Hungary.
          Article
          10.1097/FJC.0b013e3182993ae0
          23669719

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