Abstract
In this study we examined the expression of (pro)renin receptor (PRR) and renin in hearts of transgenic mice that express rat tonin with acute myocardial infarction (AMI). We used male 10 to 12 week‐old wild type controls (CT, C57 black six) and mice expressing rat tonin (TGM(rTon)). All animal were genotyped and divided into 2 subgroups: TGM(rTon) Sham and TGM(rTon) AMI; CT Sham and CT AMI. Expression levels of RPR and renin mRNAs were determined using quantitative RT‐PCR. In TGM(rTon) AMI, RPR mRNA were significantly decreased in all structures compared to CT AMI (AT:0.52±0.009 vs. 1.02±0.119; LV:0.108±0.036 vs. 1.044±0,160 and RV:0.523±0.05 vs. 0.613±0.146, respectively). The TGM(rTon) AIM showed significantly decreased RPR mRNA levels in the LV compared to TGM(rTon) Sham (0.571±0.081 vs. 1.067±0.117, respectively). In TGM(rTon) AIM, renin mRNA levels was significantly lower for all structures analyzed compared to CT AMI (AT: 0.012±0.005 vs.1.103±0.295; LV: 0.063±0,03 vs. 0.558±0,206; RV: 0.055±0,007 vs. 1.670±0.56, respectively. In TGM(rTon) AIM, renin mRNA levels was significantly lower for AT and RV compared to TGM(rTon) Sham (AT: 0,153 ± 0,01 vs. 0,277±0,018, VD: 0,194±0,025 vs. 0,523±0,05, respectively. The results suggest that tonin can influenciate in the synthesis of RPR and renin mRNA leves in the heart. Supported by Fapesp (10/19989–4).
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