Effects of Thiazide on the Expression of TRPV5, Calbindin-D28K, and Sodium Transporters in Hypercalciuric Rats.
10.3346/jkms.2009.24.S1.S161
- Author:
Hye Ryoun JANG
1
;
Sejoong KIM
;
Nam Ju HEO
;
Jeong Hwan LEE
;
Hyo Sang KIM
;
Soren NIELSEN
;
Un Sil JEON
;
Yun Kyu OH
;
Ki Young NA
;
Kwon Wook JOO
;
Jin Suk HAN
Author Information
1. Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea. jshan@snu.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
Hypercalciuria;
Thiazides;
Transporters
- MeSH:
Animals;
Biological Transport;
Calcium/urine;
Calcium Channels/chemistry;
Calcium-Binding Protein, Vitamin D-Dependent/*biosynthesis;
Hydrochlorothiazide/pharmacology;
Hypercalciuria/*therapy;
Male;
Models, Biological;
Rats;
Rats, Sprague-Dawley;
Sodium/*metabolism;
Sodium-Hydrogen Antiporter/chemistry;
Sodium-Potassium-Chloride Symporters/metabolism;
TRPV Cation Channels/*biosynthesis/chemistry;
Thiazides/*pharmacology
- From:Journal of Korean Medical Science
2009;24(Suppl 1):S161-S169
- CountryRepublic of Korea
- Language:English
-
Abstract:
TRPV5 is believed to play an important role in the regulation of urinary calcium excretion. We assessed the effects of hydrochlorothiazide (HCTZ) on the expression of TRPV5, calbindin-D28K, and several sodium transporters in hypercalciuric rats. Sprague- Dawley rats were divided into 4 groups; control, HCTZ, high salt, and high salt with HCTZ group in experiment 1; control, HCTZ, high calcium (Ca), and high Ca with HCTZ group in experiment 2. To quantitate the expression of TRPV5, calbindin- D28K, and sodium transporters, western blotting was performed. In both experiments, HCTZ significantly decreased urinary calcium excretion. TRPV5 protein abundance decreased in all hypercalciuric rats, and restored by HCTZ in both high salt with HCTZ and high Ca with HCTZ group. Calbindin-D28K protein abundance increased in the high salt and high salt with HCTZ groups, but did not differ among groups in experiment 2. Protein abundance of NHE3 and NKCC2 decreased in all hypercalciuric rats, and were restored by HCTZ in only high Ca-induced hypercalciuric rats. In summary, protein abundance of TRPV5, NHE3, and NKCC2 decreased in all hypercalciuric rats. The hypocalciuric effect of HCTZ is associated with increased protein abundance of TRPV5 in high salt or calcium diet-induced hypercalciuric rats.
