Volume regulation is defective in renal proximal tubule cells isolated from KCNE1 knockout mice

• Published in: Experimental physiology Vol. 89; no. 2; pp. 173 - 180
• Main Authors: Millar, I. D., Hartley, J. A., Haigh, C., Grace, A. A., White, S. J., Kibble, J. D., Robson, L.
• Format: Journal Article
• Language: English
• Published: 9600 Garsington Road , Oxford , OX4 2DQ , UK The Physiological Society 01-03-2004; Blackwell Science Ltd
• Subjects: Animals; Bicarbonates - pharmacology; Buffers; HEPES - pharmacology; Hypotonic Solutions - pharmacology; Ionophores - pharmacology; Ions; Kidney Tubules, Proximal - cytology; Kidney Tubules, Proximal - drug effects; Kidney Tubules, Proximal - metabolism; Mice; Mice, Knockout; Potassium - metabolism; Potassium Channels, Voltage-Gated - deficiency; Valinomycin - pharmacology
• ISSN: 0958-0670; 1469-445X
• DOI: 10.1113/expphysiol.2003.026674

The membrane protein KCNE1 has been implicated in cell volume regulation. Using a knockout mouse model, this study examined
the role of KCNE1 in regulatory volume decrease (RVD) in freshly isolated renal proximal tubule cells. Cell diameter was measured
using an optical technique in response to hypotonic shock and stimulation of Na + -alanine cotransport in cells isolated from wild-type and KCNE1 knockout mice. In HEPES buffered solutions 64% of wild-type
and 56% of knockout cells demonstrated RVD. In HCO − 3 buffered solutions 100% of the wild-type cells showed RVD, while in the knockout cells the proportion of cells displaying
RVD remained unchanged. RVD in the knockout cells was rescued by valinomycin, a K + ionophore. In wild-type HCO − 3 dependent cells the K + channel inhibitors barium and clofilium inhibited RVD. These data suggest that mouse renal proximal tubule is comprised of
two cell populations. One cell population is capable of RVD in the absence of HCO − 3 , whereas RVD in the other cell population has an absolute requirement for HCO − 3 . The HCO − 3 dependent RVD requires the normal expression of KCNE1.