Calcium-sensing Receptor Stimulates Luminal K+-dependent H+ Excretion in Medullary Thick Ascending Limbs of Henle's Loop of Mouse Kidney
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- Farajov Elnur Ilham
- Department of Medical Informatics, Tohoku University Graduate School of Medicine
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- Morimoto Tetsuji
- Department of Pediatrics, Tohoku University Graduate School of Medicine
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- Aslanova Ulviyya Fizuli
- Department of Pediatrics, Tohoku University Graduate School of Medicine
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- Kumagai Naonori
- Department of Pediatrics, Tohoku University Graduate School of Medicine
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- Sugawara Noriko
- Department of Pediatrics, Tohoku University Graduate School of Medicine
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- Kondo Yoshiaki
- Department of Medical Informatics, Tohoku University Graduate School of Medicine
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The calcium-sensing receptor (CaSR) is known well as a sensor of extracellular calcium for regulating parathyroid hormone secretion. CaSR is located along all nephron segments in the kidney. While hypercalcemia strongly enhances urinary acidification, the relationship between CaSR and acid-base metabolism in the kidney is still uncertain. In the present study, we examined whether CaSR activation caused acid secretion in the medullary thick ascending limb (mTAL), which is one of the major nephron segments involved in both mineral and acid-base regulation. The effects of a potent calcimimetic neomycin (Neo) on intracellular pH (pHi) were analyzed in the in vitro miroperfused mouse mTALs. The mTALs were incubated with 2,7-bis-(2-carboxyethyl)-5(6)-carboxyfluoresceine-acetoxymethylester (BCECF-AM) for microfluorescent pHi measurements. In HCO3−/CO2-buffered solution, the steady-state pHi was 7.17 ± 0.01 (n = 19). Basolateral Neo at 0.4 mM in basolateral side significantly alkalinized the mTAL cells to 7.28 ± 0.02 (n = 19), while Neo in the lumen had no effect on pHi. Neo in the basolateral side alkalinized the mTALs in the absence of ambient Na+ and the presence of H+-ATPase inhibitor bafilomycin in the lumen, indicating that the effect of Neo is unrelated to Na+-dependent acid-base transporters such as Na+-H+ exchangers and Na+-HCO3− cotransporter, or to luminal H+-ATPase. In contrast, the effect of Neo on pHi was inhibited by K+ removal or treatment with specific H+-K+-ATPase (HKa) inhibitors, ouabain and Sch-28080Sch-28080, in the lumen. Our results suggest that hypercalcemia induces urinary acidification partly by stimulating luminal K+-dependent H+-excretion via CaSR in mouse mTALs.
収録刊行物
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- The Tohoku Journal of Experimental Medicine
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The Tohoku Journal of Experimental Medicine 216 (1), 7-15, 2008
東北ジャーナル刊行会
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詳細情報 詳細情報について
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- CRID
- 1390282679218779008
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- NII論文ID
- 10021951516
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- NII書誌ID
- AA00863920
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- ISSN
- 13493329
- 00408727
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- Crossref
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可