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 p(kat)/100 g body weight, P <0.01) was enhanced by high salt diet (1.05 ± 0.21 vs. 8.31 ± 0.70 p(kat)/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.
- blood pressure
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