Objectives: Angiotensin II-dependent induction of TGF-b induces b-adrenoceptor-dependent hypertrophy by induction of ornithine decarboxylase (ODC). We have evidence from transgene TGF-b1 expressing mice that the level of ODC expression is associated with heart failure. Following this we hypothesized that adverse effects of hypertrophy cannot be seen in transgenic renin expressing rats that are known to display a defect in b-adrenoceptor coupling. Methods: 20 TG(mRen2)27 rats and their non- transgenic littermates (NTG) were used in these experiments at the age of 3 months and analyzed eight weeks later. Half of them received captopril (30 mg/kg) with tap-water to distinguish between angiotensin II and direct renin effects. Results: Myocytes isolated from TG (mRen2)27 rats were longer but not thicker than myocytes from NTG, irrespectively of captopril. Left ventricular developed pressure was higher in TG rats compared to NTG (125.2 mmHg vs. 76.2 mmHg) and in TG rats receiving captopril compared to NTG receiving captopril (98.7 mmHg vs. 64.3 mmHg). This indicates a specific effect of remodelling evoked by renin but not by angiotensin II. TG rats not receiving captopril developed hypertension (MAP: 156.5 mmHg vs. 100.9 mmHg) and hypertrophy (left ventricular weight-to-tibia length 29.1 g/mm vs. 24.8 mmHg; ANP expression +5.29-fold). However, ODC was not significantly induced nor any of fibrotic (TGF- b1, collagen-1), apoptotic (bax, bcl-2), or calcium handling proteins (SERCA2a, NCX, phopholamban). Myocytes isolated from TG rats displayed a disturbed responsiveness to isoprenaline stimulation irrespectively of captopril. Conclusion: A specific physiological ventricular remodelling of the left ventricle is evoked by renin that does not lead to a transition to adverse remodelling even in the presence of hypertension. Based on our previous studies the lack of ISO-responsiveness seems to be responsible for this type of hypertrophy.