Abstract

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 Ca 2+ in the interstitial compartment [Ca 2+ ISF]. We tested the hypothesis that high Na + intake alters renal [Ca 2+ 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 [Ca 2+ 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 Ca 2+ excretion in W or DS and significantly increased urinary Ca 2+ excretion in DR. When fed 0.45% NaCl, renal [Ca 2+ ISF] was lower in W and DR compared with DS. Feeding 8% NaCl significantly increased [Ca 2+ ISF] in W, had no effect on this parameter in DR, and significantly decreased [Ca 2+ ISF] in DS ([Ca 2+ 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 [Ca 2+ 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 [Ca 2+ ISF].

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.