The main results showed that the chronic BK excess in the kidneys causes cardiac hypertrophy, changes in the regulation of the local, and systemic renin angiotensin systems, increased heart rate and cardiac output, decreased heart rate variability, maintenance of GFR despite of reduced blood flow in the renal artery, and changes in gene expression in kidney, mainly increasing angiotensinogen and decreasing vasopressin V1A receptor mRNA levels. Here, AGT is linked to cardiac hypertrophy.