Many of the functions it performs have been understood through animal experiments: mice with deletion of alleles of the NPR-A gene showed chronic salt-resistant hypertension, together with cardiac hypertrophy and fibrosis [87]; in humans, scientists found deletion of the NPR-A gene in nine Japanese subjects, eight of whom had essential hypertension, with the ninth individual showing myocardial hypertrophy although he was normotensive [88]. This evidence concerns the gene NPR1 and essential hypertension.