INCREASED KALLIKREIN ACTIVITY IN THE RABBIT RENAL VASCULATURE DURING LOW-SODIUM INTAKE

1. Vascular tissue has been shown to possess a kallikrein-kinin system that may participate in the kinin-mediated increase in renal sodium e xcretion. As sodium deprivation has been demonstrated to increase kall ikrein 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 netwo rk (IAN) from the rabbit kidney. Kininogenase activity was determined in rabbits on a normal sodium (n = 14) or sodium-restricted (n = 9) di et. 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 r abbits on a sodium-restricted diet (90.7 +/- 16.5 pg kinin/mg per 30 m in). Specific tissue kallikrein activity was measured by comparing the difference in kininogenase activity in homogenates treated with soybe an-trypsin inhibitor (SBTI) compared with homogenates treated with SBT I and aprotinin. This difference was much larger in the sodium-restric ted 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 res ponse to sodium restriction. Increased kinins during sodium restrictio n may modulate the presser and anti-natriuretic systems activated duri ng negative sodium balance.