URINARY KALLIKREIN - A MARKER OF BLOOD-PRESSURE SENSITIVITY TO SALT

We evaluated if a rat strain inbred for low urinary kallikrein excreti on differs from normal-kallikrein Wistar rats regarding blood pressure levels in basal conditions and during alterations in sodium balance. Blood pressure was measured in unanesthetized rats on normal sodium in take. Then, blood pressure sensitivity to salt was evaluated over a pe riod of 20 days of high sodium diet (0.84 mmol per g chow). Low-kallik rein rats showed greater systolic blood pressure levels (125 +/- 3 us. 114 +/- 2 mm Hg in controls, P < 0.01) at nine weeks of age. Systolic blood pressure was increased after sodium loading in the low-kallikre in group and remained unchanged in controls (150 +/- 6 vs. 112 +/- 2 m m Hg, P < 0.01). This effect was associated with a reduced cumulative urinary excretion of sodium in the low-kallikrein rats. No group diffe rence was found in the clearance of endogenous creatinine in basal con ditions. Urinary creatinine excretion decreased during sodium loading, particularly in the low-kallikrein group. The group-difference in uri nary kallikrein excretion found in basal conditions (6.85 +/- 0.31 vs. 20.74 +/- 1.71 nkat/24 hr in controls, P < 0.01) was enhanced by high salt diet (2.96 +/- 0.67 vs. 22.07 +/- 2.47 nkat/24 hr in controls, P < 0.01). In addition, renal kallikrein activity and content were redu ced in low-kallikrein rats. The latter group showed a greater ratio of heart weight to body wt both in basal conditions and after sodium loa ding. The ratio of kidney weight to body wt was reduced after sodium l oading. These results indicate that a genetically-determined defect in urinary kallikrein excretion is associated with a greater blood press ure sensitivity to salt, possibly due to altered renal sodium handling .