EFFECT OF METABOLIC ALKALOSIS AND METABOLIC-ACIDOSIS ON URINARY KALLIKREIN EXCRETION OF ANESTHETIZED RATS - EVIDENCE FOR A ROLE OF BLOOD-PHAS REGULATOR OF RENAL KALLIKREIN SECRETION

The effect of altering the acid-base status on urinary kallikrein excr etion of barbiturate-anaesthetized rats was investigated. Alkalosis wa s induced in a group of rats by intravenous (i.v.) infusion of NaOH at 0.45 mmol . h(-1) for 30 min. Acidosis was induced in two groups of r ats by i.v. infusion of HCl at 1.5 mmol . h(-1) for 30 min (uncompensa ted acidosis) or 0.15 mmol . h(-1) for 3 h (compensated acidosis), res pectively. Time controls received 0.45 mmol . h(-1) NaCl. Rats with al kalosis excreted less kallikrein than their controls (P < 0.05). Rats with uncompensated acidosis excreted more active kallikrein (P < 0.05) , whereas rats with compensated acidosis excreted similar amounts when compared with their respective controls. In rats with uncompensated a cid-base derangements, the urinary kallikrein excreted per millilitre of glomerular filtrate was correlated with blood H+ activity (r = 0.99 , P < 0.01). Arterial blood pressure, haematocrit, glomerular filtrati on rate, urine flow rate and Na+ and K+ excretions of experimental and control animals did not differ. Thus, renal kallikrein secretion into the tubular fluid appears to be regulated by blood proton activity. T his, along with our previous demonstration that kallikrein inhibits HC O3- secretion into the tubular lumen (Renal Physiol 17:301-306, 1994; J Physiol(Lend) 488:163-170, 1995), indicates that this enzyme is part of a feedback loop regulating acid-base balance.