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Altered TRPV5 Expression in Dahl Salt‐sensitive Rats (LB728)
Author(s) -
Burns Rebecca,
Wells Candace,
Pointer MIldred
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.lb728
Subject(s) - reabsorption , medicine , endocrinology , calcium , chemistry , medullary cavity , excretion , kidney , distal convoluted tubule , urinary system , calcium channel , urinary calcium , renal physiology
We have previously shown that urinary calcium excretion is increased in Dahl salt‐sensitive (DS) rats following a high salt diet and this higher urinary calcium excretion is associated with the elevated blood pressure observed in DS following a high salt diet. The mechanism of the calcium loss following a high salt diet is undefined. In this report we investigate whether the transient receptor potential cation channel subfamily V member 5 (TRPV5), a calcium channel protein expressed on the luminal surface of the thick ascending loop and distal tubule and involved in transcellular calcium reabsorption, expression is altered in DS rats. Dahl DS and salt‐resistant (DR) rats were placed on a high (8%) salt diet for one week. At the end of the treatment period kidneys were collected for performing western analysis for TRPV5 protein expression in renal cortical and medullary tissue. Renal medullary TRPV5 protein levels were higher in DS rats (n=3) compared to DR rats (n=3) (1.4 ± 0.3 vs. 0.03 ± 0.03 arbitrary units; p<0.05). There was no difference in renal cortical TRPV5 expression between DS and DR rats. Higher medullary TRPV5 expression in DS rats on a high salt diet suggests that there is a compensatory attempt to increase calcium reabsorption. However, the compensatory increase in TRPV5 does not appear to prevent the increased urinary calcium excretion in DS rats following a high salt diet. Further studies are needed to investigate other renal calcium transporters involved in calcium reabsorption to explain the urinary calcium loss in hypertensive DS rats. Grant Funding Source : Supported by 2P20MD000175 and APS Frontiers in Physiology