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Renal interstitial Ca2+ during sodium loading of normotensive and Dahl-salt hypertensive rats

2003; Oxford University Press; Volume: 16; Issue: 9 Linguagem: Inglês

10.1016/s0895-7061(03)00914-2

1941-7225

C Palmer,

Ion Transport and Channel Regulation

It is now established that cells in many tissues including renal epithelial cells and perivascular sensory nerves have mechanisms that monitor and respond to the concentration of Ca2+ in the interstitial compartment [Ca2+ISF]. We tested the hypothesis that high Na+ intake alters renal [Ca2+ISF] and that the response is altered in salt-sensitive hypertensive versus normotensive rats. Male Wistar (W), Dahl salt-resistant (DR), and Dahl salt-sensitive (DS) rats were fed diets containing 0.45% or 8% NaCl for 7 days beginning at 8 to 10 weeks of age. Systolic blood pressure (BP) was measured before and at the end of the 7-day period. During the last 12 h the animals were placed in metabolic cages for urine collection. They were then anesthetized and renal [Ca2+ISF] was determined using in situ microdialysis. Feeding 8% NaCl caused a significant increase in systolic BP only in DS. The 8% NaCl also caused a significant increase in renal urinary Na+ excretion in all groups, had no effect on renal Ca2+ excretion in W or DS and significantly increased urinary Ca2+ excretion in DR. When fed 0.45% NaCl, renal [Ca2+ISF] was lower in W and DR compared with DS. Feeding 8% NaCl significantly increased [Ca2+ISF] in W, had no effect on this parameter in DR, and significantly decreased [Ca2+ISF] in DS ([Ca2+ISF] for DS on 0.45% NaCl = 1.89 ± 0.15 v 8% NaCl = 1.08 ± 0.07 mmol/L, n = 6 to 12, P < .05). These results indicate that Na+ loading significantly alters renal [Ca2+ISF]; that the response of DS is disturbed relative to controls, and are consistent with the hypothesis that Na+ loading can alter cell function by modulating [Ca2+ISF].