High Salt Up‐Regulates Ca2+‐Sensing Receptor and Na+/Ca2+ Exchanger Expression in Kidneys of Dahl Salt‐Sensitive Rats

Abstract

The G protein‐coupled Ca2+‐sensing receptor (CaSR) provides the primary mechanism for Ca2+e‐mediated regulation of the release of parathyroid hormone (PTH) as a result of parathyroid cells sensing small changes in the [Ca2+]e. However, the CaSR is also involved in the fine regulation of serum Ca2+ levels and renal Ca2+ excretion, independent of PTH secretion. The mechanisms underlying these latter effects are not clear. We studied the effect of high salt on urinary ion excretion, blood pressure and expression of the CaSR and NCX1in kidneys of Dahl SR and SS rats. Our results show that four weeks of feeding a high salt diet increased BP in SS, increased urinary Na+/Ca2+ excretion in SR and SS but reduced K+ excretion. The high salt diet caused minimal structural changes in the kidneys, as determined by haematoxylin/eosin (H&E) and periodic acid‐Schiff (PAS) staining. Immunohistochemical analysis of tissue sections showed localization of the CaSR and NCX1 in the thick ascending limb of the loop of Henle, collecting ducts, cortical distal tubules, which was up‐regulated by the high salt in SS animals. NCX1 expression and localization in this study tracks closely with the CaSR. Thus, expression levels and localization patterns of these protein suggest that CaSR modulation of ion transporter and channel proteins could account for the difference in ion excretion observed between SS and SR rats as well as their responses to the high salt diet.Support or Funding InformationNIH Grant SC1 HL136278This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.