title: Angiotensin (1-7) facilitates cardioprotection of ischemic preconditioning on ischemia-reperfusion-challenged rat heart.
abstract: Ischemic preconditioning (IPC) is one of the most promising strategies used to protect the myocardium from ischemia-reperfusion injury. Ang (1-7) exhibits cardioprotective activity; however, its therapeutic potential on IPC-induced cardioprotection has not been reported in ischemia-reperfusion injury till date. Therefore, the first set of experiment was designed to evaluate the direct effect of Ang (1-7), in perfusion medium, on cardioprotective activity of IPC in rat heart challenged to ischemia-reperfusion injury. In addition, the acute and chronic effects of pretreated Ang (1-7) were investigated on cardioprotection of IPC in ischemia-reperfusion-challenged hearts in subsequent sets of experiments. The results showed that Ang (1-7) potentiated the IPC-induced increase in coronary flow and heart rate, decrease in lactate dehydrogenase and creatine kinase activity, ventricular fibrillation, and infarct size in ischemia-reperfusion-challenged animals in direct and chronic sets of experiments. Further, Ang (1-7) enhanced the IPC-induced attenuation in mitochondrial dysfunction, oxidative stress, and apoptosis in ischemia-reperfusion-challenged hearts in both sets of experiments. A-779, Mas receptor antagonist, abrogated potentiation effects of Ang (1-7) on IPC-induced cardioprotection in ischemia-reperfusion-challenged rats in the above set of experiments. These observations indicate that Ang (1-7)/Mas receptor activation could be a potential adjuvant to IPC during ischemia-reperfusion-induced cardiac injury.
authors.affiliation: Division of Pharmacology, Institute of Pharmaceutical Research, GLA University, Mathura, 281406, India.
authors.forename: Pradeepkant
authors.initials: P
authors.lastname: Pachauri
authors.affiliation: Division of Pharmacology, Institute of Pharmaceutical Research, GLA University, Mathura, 281406, India. debapriya.garabadu@gla.ac.in.
authors.forename: Debapriya
authors.identifier: http://orcid.org/0000-0002-4235-3926
authors.initials: D
authors.lastname: Garabadu
authors.affiliation: Division of Pharmacology, Institute of Pharmaceutical Research, GLA University, Mathura, 281406, India.
authors.forename: Ahsas
authors.initials: A
authors.lastname: Goyal
authors.affiliation: Division of Pharmacology, Institute of Pharmaceutical Research, GLA University, Mathura, 281406, India.
authors.forename: Prabhat Kumar
authors.initials: PK
authors.lastname: Upadhyay
mesh_terms: D000803:Angiotensin I / Q000494:pharmacology*; D000818:Animals; D002316:Cardiotonic Agents / Q000494:pharmacology*; D019194:Ischemic Preconditioning; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D010446:Peptide Fragments / Q000494:pharmacology*; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins / Q000819:agonists / Q000378:metabolism; D051381:Rats; D043562:Receptors, G-Protein-Coupled / Q000819:agonists / Q000378:metabolism
chemical_list: D002316:Cardiotonic Agents; D010446:Peptide Fragments; D000090063:Proto-Oncogene Mas; D011518:Proto-Oncogene Proteins; D043562:Receptors, G-Protein-Coupled; D000803:Angiotensin I; C118790:angiotensin I (1-7)
keywords: Apoptosis; Heart; Mitochondria; Oxidative stress; Renin–angiotensin system