Abstract
To assess the role of sodium metabolism and renin-angiotensin-aldosterone system in the regulation of the synthesis orr activation of renal kallikrein, we studied chronic effect of sodium loading with 1% NaCl and angiotensin II infusion (900μg/kg/day) on urinary active and inactive kallikrein excretion in rats. Angiotensin II infusion was done under normal sodium diet and sodium loading. Urinary inactive kallikrein was evaluated as the kallikrein activated by trypsin (200μg/ml urine). Chronic loading of sodium increased urine volume, urinary sodium excretion, and urinary total, active and inactive kallikrein without the change in the ratio of active to total kallikrein, whereas it decreased plasma angiotensin II and aldosterone concentration. Chronic infusion of angiotensin II on regular diets increased urinary total, active and inactive kallikrein excretion without the change in the ratio of active to total kallikrein, urine volume, and urinary sodium excretion. Additionally it elevated systolic blood pressure, plasma angiotensin II and aldosterone levels. On the contrary, chronic infusion of angiotensin II on sodium loading with 1% NaCl did not induce any changes in urinary total, active, and inactive kallikrein, the ratio of active to total kallikrein, urine volume, and urinary sodium excretion, whereas it increased slightly plasma angiotensin II and aldosterone concentration. These results indicate that chronic sodium loading and angiotensin II infusion might stimulate the synthesis of renal kallikrein. In addition, it is suggested that volume status may play some role in the regulation or the synthesis of renal kallikrein.
