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INCREASED KALLIKREIN ACTIVITY IN THE RABBIT RENAL VASCULATURE DURING LOW SODIUM INTAKE
Author(s) -
Kuo Jay J.,
Zimmerman Ben G.
Publication year - 1997
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1997.tb01799.x
Subject(s) - kinin , endocrinology , kallikrein , medicine , sodium , chemistry , aprotinin , kidney , prekallikrein , natriuresis , kunitz sti protease inhibitor , trypsin , bradykinin , enzyme , biology , biochemistry , receptor , organic chemistry
SUMMARY 1. Vascular tissue has been shown to possess a kallikrein ‐kinin system that may participate in the kinin‐mediated increase in renal sodium excretion. As sodium deprivation has been demonstrated to increase kallikrein content in the kidney and urine we hypothesized that during low sodium intake, kallikrein should increase in the renal vasculature. 2. Kininogenase activity, reflecting kallikrein enzymatic content, was measured in a homogenate of a microdissected intrarenal arterial network (IAN) from the rabbit kidney. Kininogenase activity was determined in rabbits on a normal sodium ( n = 14) or sodium‐restricted ( n —9) diet. 3. Total kininogenase activity in rabbits on a normal sodium diet was 15.0 ± 2.7 pg kinin/mg per 30 min, while it was much higher in rabbits on a sodium‐restricted diet (90.7 ± 16.5 pg kinin/mg per 30 min). Specific tissue kallikrein activity was measured by comparing the difference in kininogenase activity in homogenates treated with soybean‐trypsin inhibitor (SBTI) compared with homogenates treated with SBTI and aprotinin. This difference was much larger in the sodium‐restricted rabbits than in rabbits on a normal sodium diet (29.5 ±3.8 vs 5.1 ± 1.7 pg kinin/mg per 30 min, respectively). 4. We conclude that the rabbit IAN produces kallikrein, which is markedly increased in response to sodium restriction. Increased kinins during sodium restriction may modulate the pressor and anti‐natriuretic systems activated during negative sodium balance.