title: Inhibition of Angiotensin-II Production Increases Susceptibility to Acute Ischemia/Reperfusion Arrhythmia.
abstract: BACKGROUND Myocardial ischemia and reperfusion lead to impairment of electrolyte balance and, eventually, lethal arrhythmias. The aim of this study was to investigate the effects of pharmacological inhibition of angiotensin-II (Ang-II) production on heart tissue with ischemia-reperfusion damage, arrhythmia, and oxidative stress. MATERIAL AND METHODS Rats were divided into 4 groups: only ischemia/reperfusion (MI/R), captopril (CAP), aliskiren (AL), and CAP+AL. The drugs were given by gavage 30 min before anesthesia. Blood pressure and electrocardiography (ECG) were recorded during MI/R procedures. The heart tissue and plasma was kept so as to evaluate the total oxidant (TOS), antioxidant status (TAS), and creatine kinase-MB (CK-MB). RESULTS Creatine kinase-MB was not different among the groups. Although TAS was not affected by inhibition of Ang-II production, TOS was significantly lower in the CAP and/or AL groups than in the MI/R group. Furthermore, oxidative stress index was significantly attenuated in the CAP and/or AL groups. Captopril significantly increased the duration of VT during ischemia; however, it did not have any effect on the incidence of arrhythmias. During reperfusion periods, aliskiren and its combinations with captopril significantly reduced the incidence of other types of arrhythmias. Captopril alone had no effect on the incidence of arrhythmias, but significantly increased arrhythmias score and durations of arrhythmias during reperfusion. MAP and heart rate did not show changes in any groups during ischemic and reperfusion periods. CONCLUSIONS Angiotensin-II production appears to be associated with elevated levels of reactive oxygen species, but Ang-II inhibitions increases arrhythmia, mainly by initiating ventricular ectopic beats.
authors.affiliation: Department of Physiotherapy and Rehabilitation, School of Health Sciences, Istanbul Bilim University, Istanbul, Turkey.
authors.forename: Eylem
authors.initials: E
authors.lastname: Taskin
authors.affiliation: Department of Physiology, Faculty of Medicine, University of Erciyes, Kayseri, Turkey.
authors.forename: Kadir Ali
authors.initials: KA
authors.lastname: Tuncer
authors.affiliation: Department of Biophysics, Faculty of Medicine, University of Adiyaman, Adiyaman, Turkey.
authors.forename: Celal
authors.initials: C
authors.lastname: Guven
authors.affiliation: Department of Biology, Faculty of Science and Arts, Düzce University, Düzce, Turkey.
authors.forename: Salih Tunc
authors.initials: ST
authors.lastname: Kaya
authors.affiliation: Department of Physiology, Faculty of Medicine, University of Erciyes, Kayseri, Turkey.
authors.forename: Nurcan
authors.initials: N
authors.lastname: Dursun
mesh_terms: D000577:Amides / Q000494:pharmacology; D000804:Angiotensin II / Q000096:biosynthesis* / Q000378:metabolism; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D001794:Blood Pressure / Q000187:drug effects; D002216:Captopril / Q000494:pharmacology; D052279:Creatine Kinase, MB Form / Q000378:metabolism; D005650:Fumarates / Q000494:pharmacology; D006321:Heart / Q000187:drug effects* / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000503:physiopathology; D018384:Oxidative Stress / Q000187:drug effects; D051381:Rats
chemical_list: D000577:Amides; D000806:Angiotensin-Converting Enzyme Inhibitors; D000959:Antihypertensive Agents; D005650:Fumarates; D000804:Angiotensin II; C446481:aliskiren; D002216:Captopril; D052279:Creatine Kinase, MB Form