Regulation of renal calcium transporter expressions and phosphate metabolism

Research Project

Project/Area Number	23790950
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	Kidney internal medicine
Research Institution	Fukushima Medical University
Principal Investigator	YATABE Midori 福島県立医科大学, 医学部薬理学講座, 助教 (30510325)
Project Period (FY)	2011 – 2012
Project Status	Completed (Fiscal Year 2012)
Budget Amount *help	¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000) Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000) Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Keywords	高血圧学 / カルシウム・リン代謝 / 腎臓 / 尿細管 / カルシウム輸送体 / リン / 発現調節 / 食塩 / カルシウム / 再吸収 / Na+/Ca2+交換輸送体
Research Abstract	Dietary NaCl intake increases the excretion of calcium into urine, which may lead to osteoporosis and urinary tract stone formation. In dietary NaCl-loaded rats, we have found that the expression of calcium reabsorbing molecules on the distal tubule increases while the protein expression of a molecule that enhances calcium reabsorption in the proximal tubule, claudin 2, is decreased. NaCl ingestion may lead to calcium loss in part via reduced expression of claudin 2. In the kidney, Na+/Ca2+exchanger 1 (NCX1) is mainly expressed in the distal tubule and the vascular smooth muscle. In vivo renal cortical administration of NCX1 inhibitor in rats lead to a decrease in serum phosphate without altering calcium dynamics, and it also decreased urinary protein and glomerular size. These observations suggest a role of renal NCX1 in phosphate metabolism and control of urinary protein and intraglomerular pressure, which are important aspects of chronic kidney disease.