These data show that the response of the cardiomyocytes of NPR-A knockout mice to angiotensin II is enhanced, and results in hypertrophy and interstitial fibrosis, again confirming the role of NPR-A as an inhibitor of the pathological processes of myocardial hypertrophy and cardiac interstitial fibrosis. Here, NPR1 is linked to Interstitial cardiac fibrosis.