Renin-angiotensin system. II. Renal angiotensinase activity

Abstract

It has been well known that the kidney is a rich source of angiotensinases. On the other hand, an increased plasma angiotensinase activity in the patients with uremia has been reported. However, the mechanism responsible for this increased plasma angiotensinase activity is obscure. Therefore, the present study was attempted (1) to examine the several properties of renal angiotensinases in normal rats, and (2) to investigate whether the experimental injuries of rat kidney can induce a release of angiotensinase into renal venous blood. Materials and Methods: Male white Wistar rats weighing between 200 and 250 g were used in all the experiments. Experimental groups were as follows: 1) Normal control group 2) Mercuric chloride intoxication group 3) Unilateral ureteral ligation group 4) Bilateral ureteral ligation group 5) Acute unilateral renal arterial constriction group 6) Aminonucleoside-nephrosis group The determination of angiotensinase activity was carried out using biological methods, based on the principle of incubating a known concentration of asparagine1-angiotensin (Hypertensin, Ciba) with the material under standardized conditions and then assaying for residual pressor activity. Angiotensinase activity of plasma was expressed as nanograms (ng)/ml of plasma/10 min and that of kidney as ng/mg of wet weight tissue/20 min, respectively. Results. 1. Kidney showed higher angiotensin-ase activity than small intestine, liver, lung, adrenals, plasma, brain and skeletal muscle. Red blood cell hemolysate showed the highest activity. 2. The angiotensinase activity of renal cortex Was greater than that of medulla. 3. The optimal pH of renal angiotensinase activity was observed at 7.4 before freezing and thawing. 4. The treatment of freezing and thawing resulted in a marked increase of the renal angiotensinase activity at pH 4.6 and, finally, it reached the level similar to that at pH 7.4.