Blood pressure sensitivity to salt in rats with low urinary kallikrein excretion.

We evaluated if a rat strain inbred for reduced urinary kallikrein excretion differs from normal-kallikrein Wistar rats regarding blood pressure in basal conditions and during alterations in sodium balance. Low-kallikrein rats showed greater systolic blood pressure values (125 +/- 3 vs. 114 +/- 2 mmHg in controls, P < 0.01) at 9 weeks of age. Systolic blood pressure was increased after 20 days of dietary sodium loading in the low-kallikrein group and remained unchanged in controls (150 +/- 6 vs. 112 +/- 2 mmHg, P < 0.01) and this effect was associated with a reduced cumulative excretion of sodium (23% less in the low-kallikrein group compared with controls, P < 0.01). Urinary creatinine excretion was decreased by sodium loading in both groups, and this effect was more pronounced in the low-kallikrein group. The group-difference in urinary kallikrein excretion found in basal conditions (2.49 +/- 0.10 vs. 7.78 +/- 0.53 Pkat/100 g body weight, P < 0.01) was enhanced by high salt diet (1.05 +/- 0.21 vs. 8.31 +/- 0.70 Pkat/100 g body weight, P < 0.01). The ratio of heart weight to body weight was significantly greater in low-kallikrein rats (331 +/- 7 vs. 275 +/- 4 mg/100 g body weight, P < 0.01), whereas the ratio of kidney weight to body weight was lower (329 +/- 5 vs. 370 +/- 8 mg/100 body weight, P < 0.01). Our results indicate that a genetically-determined defect in urinary kallikrein excretion is associated with a greater blood pressure sensitivity to salt, possibly due to altered renal sodium handling.