Expression of Calcium Transporters According to Dietary Sodium in the Distal Tubule of Rat Kidneys.
- Author:
Nam Ju HEO
1
;
Hyo Sang KIM
;
Jung Hwan LEE
;
Hye Ryoun JANG
;
Se Joong KIM
;
Yun Kyu OH
;
Ki Young NA
;
Kwon Wook JOO
;
Jin Suk HAN
Author Information
1. Department of Internal Medicine, College of Medicine, Seoul National University, Clinical Research Institute, Seoul National University Hospital, Seoul, Korea. jshan@snu.ac.kr
- Publication Type:Original Article
- Keywords:
Dietary sodium chloride;
TRPV cation channels;
Calcium-binding proteins;
Hypercalciuria
- MeSH:
Animals;
Blotting, Western;
Body Weight;
Calbindin 1;
Calcium*;
Calcium-Binding Proteins;
Diet;
Hematocrit;
Hypercalciuria;
Kidney*;
Polymerase Chain Reaction;
Rats*;
Rats, Sprague-Dawley;
Risk Factors;
RNA, Messenger;
Sodium;
Sodium Chloride, Dietary;
Sodium, Dietary*;
TRPV Cation Channels
- From:Korean Journal of Nephrology
2007;26(4):390-397
- CountryRepublic of Korea
- Language:English
-
Abstract:
PURPOSE: Hypercalciuria is a risk factor of renal calcium stone and proper initial management is dietary salt restriction. But the molecular mechanism responsible for this sodium calcium relationship remains unclear. The present study investigates the relationship between different amount of sodium intake and the expression level of transporters involved in the active calcium transport. METHODS: Sprague-Dawley rats were randomized into three groups: a normal salt group, a low salt group, and a high salt group. Expression of mRNA and protein of transient receptor potential vanilloid (TRPV) 5 and calbindin-D28K was determined by real-time quantitative PCR and western blots, respectively. RESULTS: Hematocrit and body weight showed no difference among the three groups. High salt diet led to significant increase in the amount of urinary calcium excretion and decreased mRNA expression of calbindin-D28K and TRPV5. Protein abundance of calbindin-D28K and TRPV5 was decreased but the result was statistically insignificant. Low salt diet decreased the amount of urinary calcium excretion without significant difference. Messenger RNA expression and protein abundance of calbindin-D28K and TRPV5 showed no difference, compared to those of normal salt group. CONCLUSION: These data suggest that high sodium intake increases urinary calcium excretion, which is accompanied by a decreased expression of calbindin-D28K mRNA.
