Abstract
The kidney macula densa (MD) controls the tubuloglomerular feedback system and stimulates renin release from the granular cells through sensing the change of luminal NaCl concentration ([NaCl]) in proportion to changes in glomerular filtration rate. Although moderate/low water permeability of luminal membrane of MD cells has been reported, its molecular identity is still unknown. To identify molecular machineries of the transmembrane water permeability, we examined a functionally intact MD cell line (NE-MD: Yasuoka Y et al, Jpn J Physiol 2005) with RT-PCR, western blotting, Immunohistochemistry (IHC). Antibodies against neuronal nitric oxide synthase (nNOS) and a renal outer medullary potassium channel (ROMK) confirmed the authenticity of NE-MD cells. RT-PCR revealed AQP1 mRNA expression in NE-MD cells, but not AQP2, AQP3, and AQP4 mRNAs. Immunoblots with anti AQP1 antibody revealed a positive, but weak 28-kDa band corresponding to very much stronger bands of both red blood cells and AQP1-transfected HeLa cells. IHC of the mouse kidney cortex showed the strong staining in the proximal tubule and the much weaker staining in the macula densa. These data suggest that although the expression level of AQP1 protein is low, AQP1 may facilitate water transport of MD cells, if any, to promote the cell volume change upon changes in luminal [NaCl]. [J Physiol Sci. 2008;58 Suppl:S86]
