Telemetric blood pressure studies in NKCC1‐deficient mice

Blood pressure measurements by tail‐cuff have shown reduced levels in NKCC1‐deficient mice (NKCC1−/−). By radiotelemetry 24h mean arterial blood pressure (MAP) was not different in NKCC1−/− and WT mice (108 ± 2 vs. 110 ± 2 mm Hg; n=19 vs. n=7). MAP was not altered by either 1 week low (0.03%) or high Na intake (8%) in WT mice. In NKCC1−/− MAP decreased in the day time during low Na and increased by about 10 mm Hg at night time during high Na. MAP reductions in response to hydralazine (1 mg/kg), isoproterenol (10 μg/mouse), candesartan (50 μg/mouse) and quinaprilate (50 μg/mouse) were consistently and significantly greater in NKCC1−/− than WT mice. PRC (ng Ang I/ml hr) and aldosterone (pg/ml) were higher in NKCC1−/− than WT (PRC: 5566 ± 825 vs.1458 ± 165; aldo: 974 ± 100 vs. 456 ± 108). High Na suppressed PRC and aldosterone in both NKCC1−/− and WT (PRC: 1202 ± 181 vs. 287 ± 96; aldo: 178 ± 25 vs.162 ± 56) while a low Na diet increased PRC and aldosterone in WT but not NKCC1−/−. In summary: 24h MAP is the same in NKCC1−/− and WT on standard diets, MAP of NKCC1−/− mice is more sensitive to increases and decreases of Na intake than MAP of WT, plasma renin and aldosterone are elevated in NKCC1−/− mice. We conclude that NKCC1 stabilizes MAP in response to changes in Na intake and peripheral vasodilation, and that this may be related to a more responsive renin system.