Changes are observed in the renal kallikrein-kinin system in hypertensive disease, which are displayed by compensatory increase in its activity in patients with labile hypertension and decrease in the activity of this system in patients with a stable stage of the disease. An inadequate reaction to a load experienced from walking or from a reduced volume of extracellular fluid and sodium balance in the body was noted in all stages. The absence of a reaction or the inhibition of the activity of the renal kallikrein-kinin system in response to the intake of furosemid may be a manifestation of its altered sensitivity to the electrolyte shifts in the organism and the decrease in the volume of extracellular fluid. The kallikrein-kinin system is concerned with the noted shifts in renal function linked with the transport of sodium and water in patients with the labile stage of the disease, to which the correlative connection between kallikrein excretion and natriuresis and urine excretion attests. It is suggested that the renal kallikrein-kinin system in patients with the initial stage of hypertensive disease contributes to the adaptation of renal function to the altered conditions of hemodynamics and the increased activity of the renin-angiotensin-aldosterone system.