NPR1 and cardiac hypertrophy: In mice with an exclusive deletion of NPR-A, administration of antihypertensives such as 6-hydroxydopamine resulted in blood pressure values that were comparable to those of mice with a blockade of the AT1A receptor (through either gene deletion or pharmacological inhibition), but did not result in any effects relating to limiting fibrosis and myocardial hypertrophy as NPR-A, as mentioned above, directly regulates hypertrophy and fibrosis independently of blood pressure [121].