Efficacy of Angiotensin II Type 1 Receptor Blockade on Reperfusion-Induced Arrhythmias and Mortality Early After Myocardial Infarction Is Increased in Transgenic Rats With Cardiac Angiotensin II Type 1 Overexpression

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Abstract
Angiotensin II induces ischemia/reperfusion (I/R)-induced arrhythmias and blockade of the angiotensin II type 1 receptor (AT1R) may therefore be beneficial in preventing arrhythmias and decreasing mortality after myocardial infarction (MI). Because the AT1R is upregulated after myocardial ischemia, it was hypothesized that the level of AT1R expression would mediate the response to AT1R blockade. Transgenic (TGR) rats that overexpress the human AT1R and Sprague–Dawley rats were used as controls. Total duration of arrhythmia (seconds) after I/R injury was similar in TGR and SD rats (433 ± 109 vs. 376 ± 117, p = n.s.). AT1R blockade with losartan decreased total duration of arrhythmia in the TGR rats (433 ± 110 s–164 ± 48 s; p

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