Abstract
BackgroundUrinary Ca2+ excretion increases with dietary NaCl. NaCl-induced calciuria may be associated with hypertension, urinary stone formation and osteoporosis, but its mechanism and long-term effects are not fully understood. This study examined alterations in the expressions of renal Ca2+ transporters, channels and claudins upon salt loading to better understand the mechanism of salt-induced urinary Ca2+ loss.MethodsEight-week old Wistar-Kyoto rats were fed either 0.3% or 8% NaCl diet for 8 weeks. Renal cortical expressions of Na+/Ca2+ exchanger 1 (NCX1), Ca2+ pump (PCMA1b), Ca2+ channel (TRPV5), calbindin-D28k, and claudins (CLDN-2, -7, -8, -16 and −19) were analyzed by quantitative PCR, western blot and/or immunohistochemistry.ResultsFractional excretion of Ca2+ increased 6.0 fold with high-salt diet. Renal cortical claudin-2 protein decreased by approximately 20% with decreased immunological staining on tissue sections. Claudin-16 and −19 expressions were not altered. Renal cortical TRPV5, calbindin-D28k and NCX1 expressions increased 1.6, 1.5 and 1.2 fold, respectively.ConclusionsChronic high-salt diet decreased claudin-2 protein and increased renal TRPV5, calbindin-D28k, and NCX1. Salt loading is known to reduce the proximal tubular reabsorption of both Na+ and Ca2+. The reduction in claudin-2 protein expression may be partly responsible for the reduced Ca2+ reabsorption in this segment. The concerted upregulation of more distal Ca2+-transporting molecules may be a physiological response to curtail the loss of Ca2+, although the magnitude of compensation does not seem adequate to bring the urinary Ca2+ excretion down to that of the normal-diet group.
Highlights
Urinary Ca2+ excretion increases with dietary NaCl
Urinary Ca2+ excretion increases with sodium chloride (NaCl) ingestion [1]. This dietary NaCl-induced calciuria may lead to osteoporosis at low calcium intake [2,3] and is associated with urinary stone formation [1] and hypertension [4]
Claudins and other tight junction proteins are known to be important in determining the permeability characteristics of various epithelia [7]
Summary
Urinary Ca2+ excretion increases with dietary NaCl. NaCl-induced calciuria may be associated with hypertension, urinary stone formation and osteoporosis, but its mechanism and long-term effects are not fully understood. Urinary Ca2+ excretion increases with sodium chloride (NaCl) ingestion [1] This dietary NaCl-induced calciuria may lead to osteoporosis at low calcium intake [2,3] and is associated with urinary stone formation [1] and hypertension [4]. The increase in urinary Ca2+ excretion is postulated to be due to salt-induced It is not clear if long-term salt loading has any effects on Ca2+-transporting molecule expressions in the kidney. Claudins and other tight junction proteins are known to be important in determining the permeability characteristics of various epithelia [7]. The distributions and functions of these tight junction proteins are becoming known, but information on their regulation, especially in the kidney, is just emerging
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