Active and total (trypsin-activated) kallikrein were measured in urine and the discrete segments of the nephron of rabbits fed low and normal sodium diets. Kallikrein was measured by its kininogenase activity, and kinins generated were measured by radioimmunoassay. The amount of inactive kallikrein was calculated as the difference between total and active kallikrein. The nephrons were microdissected and divided into eight segments: (1) glomerulus; (2) proximal convoluted tubule; (3) cortical thick ascending limb; (4) bright portion of distal convoluted tubule; (5) granular portion of distal convoluted tubule; (6) granular portion of cortical collecting tubule; (7) light portion of cortical collecting tubule; and (8) medullary collecting tubule. As we have previously described, active and inactive kallikrein were localized mainly in the granular portion of the distal convoluted and cortical collecting tubules (connecting tubule). Both active and inactive kallikrein in the granular portion of the distal convoluted and cortical collecting tubule increased markedly during low sodium intake without altering the distribution profile. Urinary excretion of active and inactive kallikrein also increased significantly in the low sodium diet. More than 50% of total kallikrein was found in the inactive form in the nephron and urine. The ratio of active to total kallikrein in the nephron and urine was not changed by sodium restriction. These results suggest that sodium restriction stimulates the biosynthesis and excretion of both active and inactive kallikrein.
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