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 U infusion (900 Êg/kg/day) on urinary active and inactive kallikrein excretion in rats. Angiotensin u infusion was done under normal sodium diet and sodium loading. Urinary inactive kallikrein was evaluated as the kallikrein activated by trypsin (200 Êg/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 u and aldosterone concentration. Chronic infusion of angiotensin u 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 u and aldosterone levels. On the contrary, chronic infusion of angiotensin u 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 u and aldosterone concentration. These results indicate that chronic sodium loading and angiotensin u 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.
- active kallikrein
- inactive kallikrein
- renal kallikrein-kinin system
- renin-angiotensinaldosterone system
- sodium loading
ASJC Scopus subject areas