The underlying mechanisms of myocardial preconditioning after a brief period of renal ischemia-reperfusion are unknown. The phenomenon itself and the involvement of AT(1) angiotensin receptors was therefore investigated using an in vivo rat model of acute myocardial infarction. Anesthetized rats underwent a left thoracotomy and pericardiotomy. A laparotomy was performed to expose the left renal artery. Animals were then preconditioned with four episodes, each consisting of 5 min of renal artery occlusion followed by 10 min of reperfusion, or underwent a 60 min sham period of anesthesia. Subsequently, the left coronary artery was occluded for 30 min and reperfused for 2 h. Area at risk and infarct size was estimated along with hemodynamic and temperature data recording. The infarct-to-risk ratio was limited from 56.36 +/- 2.36 and 50.65 +/- 4.71 in control to 12.0 +/- 0.48 and 12.57 +/- 0.44 in preconditioned hearts, by volume and weight methods. The protective effect of renal preconditioning on the myocardium was not abolished by losartan 1 mg/kg (10.11 +/- 0.12 and 11.2 +/- 1.4) pretreatment whereas it was completely attenuated by losartan 5 mg/kg (46.5 +/- 1.0 and 47.8 +/- 1.4) administration. Thus we can infer that angiotensin AT(1) receptors participate in renal preconditioning of the myocardium in in vivo rat hearts.
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Singh et al. (2004) studied this question.