A working hypothesis for the development of hypertension associated with excess accumulation of sodium salt. Sodium retention stimulates production of endogenous digitalis, which elevates vascular tone and cardiac output. This increases blood pressure and directly inhibits the renal tubular Na+,K+-ATPase, resulting in reduced sodium reabsorption. Sodium balance is then achieved concurrently with the development of hypertension. A full color version of this figure is available at the Hypertension Research journal online.