These observations in human disease are paralleled by experimental data in the rat where—independent of alterations in blood pressure, volume overload, plasma renin and angiotensin II and BNP- ablation of the 50% of functioning renal mass (a model of mild renal dysfunction) initiates myocardial gene responses involving a major inflammatory pathway conducive to TGF-β activation and fibrosis [41]. Here, NPPB is linked to Abnormal renal physiology.