Journal
AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY
Volume 281, Issue 6, Pages F1021-F1027Publisher
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajprenal.0085.2001
Keywords
mouse kidney morphology; amiloride-sensitive epithelial sodium channel; thiazide-sensitive sodium-chloride cotransporter; epithelial calcium channel; calcium-binding proteins
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The organization of Na+ and Ca2+ transport pathways along the mouse distal nephron is incompletely known. We revealed by immunohistochemistry a set of Ca2+ and Na+ transport proteins along the mouse distal convolution. The thiazide-sensitive Na+-Cl- cotransporter (NCC) characterized the distal convoluted tubule (DCT). The amiloride-sensitive epithelial Na+ channel (ENaC) colocalized with NCC in late DCT (DCT2) and extended to the downstream connecting tubule (CNT) and collecting duct (CD). In early DCT (DCT1), the basolateral Ca2+-extruding proteins [Na+/Ca2+ exchanger (NCX), plasma membrane Ca2+-ATPase (PCMA)] and the cytoplasmic Ca2+-binding protein calbindin D-28K (CB) were found at very low levels, whereas the cytoplasmic Ca2+/Mg2+-binding protein parvalbumin was highly abundant. NCX, PMCA, and CB prevailed in DCT2 and CNT, where we located the apical epithelial Ca2+ channel (ECaC1). Its subcellular localization changed from apical in DCT2 to exclusively cytoplasmic at the end of CNT. NCX and PMCA decreased in parallel with the fading of ECaC1 in the apical membrane. All three of them were undetectable in CD. These findings disclose DCT2 and CNT as major sites for transcellular Ca2+ transport in the mouse distal nephron. Cellular colocalization of Ca2+ and Na+ transport pathways suggests their mutual interactions in transport regulation.
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