The distal tubules of the kidney express the full set of the components of the kallikrein-kinin system, which works independently from the
plasma kallikrein-
kinin system. Studies on the role of the renal kallikrein-kinin system, using congenitally
kininogen-deficient Brown-Norway Katholiek rats and also
bradykinin B2 receptor knockout mice, revealed that this system starts to function and to induce natriuresis and diuresis when
sodium accumulates in the body as a result of excess
sodium intake or
aldosterone release, for example, by
angiotensin II. Thus, it can be hypothesized that the system works as a safety valve for
sodium accumulation. The large numbers of studies on hypertensive animal models and on essential hypertensive patients, particularly those with
salt sensitivity, indicate a tendency toward the reduced excretion of
urinary kallikrein, although this reduction is modified by
potassium intake and impaired renal function. We hypothesize that the reduced excretion of the renal
kallikrein may be attributable to a genetic defect of factor(s) in renal
kallikrein secretion process and may cause
salt-sensitive
hypertension after
salt intake.