Open AccessEffects of Thiazide on the Expression of TRPV5, Calbindin-D28K, and Sodium Transporters in Hypercalciuric Rats
Author(s) -
Hye Ryoun Jang,
Sejoong Kim,
Nam Ju Heo,
Jeonghwan Lee,
Hyosang Kim,
Søren Nielsen,
Un Sil Jeon,
Yun Kyu Oh,
Ki Young Na,
Kwon Wook Joo,
Jin Suk Han
Publication year - 2009
Publication title -
journal of korean medical science/journal of korean medical science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.743
H-Index - 66
eISSN - 1598-6357
pISSN - 1011-8934
DOI - 10.3346/jkms.2009.24.s1.s161
Subject(s) - endocrinology , medicine , hydrochlorothiazide , thiazide , chemistry , calcium , excretion , hypercalciuria , calbindin , urinary calcium , diuretic , biology , blood pressure
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-D(28K), 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-D(28K), 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-D(28K) 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.