Effects of restriction of sodium or administration of fludrocortisone on parotid salivary kallikrein in man.

Urinary kallikrein is increased by restriction of dietary sodium and by administration of fludrocortisone, a sodium-retaining steroid. In order to determine whether salivary kallikrein responds similarly, we studied 16 normal volunteers after 1-week periods of daily intake of 9, 109, and 259 mEQ of sodium; 10 subjects were studied after addition of 0.6 mg/day fludrocortisone for a week to a regimen of 109 mEq/day sodium. During sodium restriction, parotid saliva had a significantly higher mean concentration of kallikrein ad potassium and a significantly lower concentration of sodium than during periods of intake of 109 or 259 mEq/day sodium. Sodium restriction also caused significantly higher urinary excretion of kallikrein and aldosterone. Salivary amylase remained unchanged during the three sodium periods. Administration of fludrocortisone significantly increased the mean concentration of parotid kallikrein and excretion of urinary kallikrein in comparison with control levels, however the concentrations of parotid sodium and potassium did not change significantly. Four patients studied before and after removal of aldosterone-producing adenomas each showed decreased concentrations of parotid kallikrein and potassium and increased concentrations of parotid sodium after surgery. It is concluded that both salivary and urinary kallikrein increased in response to restriction of sodium and that these increases were mediated by levels of sodium-retaining steroid. Increased output of kallikrein in response to increased levels of sodium-retaining steroid may be a generalized response of organs that contain glandular kallikrein and can conserve sodium.

Characterization and localization of human renal kininogen.

Kininogen was isolated from human urine by batch adsorption with immobilized antibody to the immunologically identical heavy (H) chains of both high molecular weight (HMW) and low molecular weight (LMW) human plasma kininogens. All releasable kinin in the guanidinium chloride eluate was associated with kininogen antigen in gel filtration fractions. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis of the eluate gave major stained and antigenic bands corresponding to the major form of plasma LMW kininogen. Also, the staining patterns and antigenic profiles obtained upon alkaline disc gel electrophoresis of the urinary and plasma LMW kininogens were strikingly similar. When antibody to H chain was used in an indirect immunofluorescence technique, cytoplasmic staining was observed in cells of distal tubules and c cortical and medullary collecting ducts of human kidneys. No fluorescence was observed using antibody to the unique light (L) chain of plasma HMW kininogen and no intact HMW kininogen was found in urine by radioimmunoassay. We conclude that the kidney is a source of urinary kininogen, while the L chain antigen in urine probably represents filtered degradation products of plasma HMW kininogen.