Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2010 Jan;135(1):3–13. doi: 10.1085/jgp.200910265

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2009 Yang and Delay

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.jgp.org/misc/terms.shtml). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

PMC Copyright notice

Figure 6. — The chloride homeostasis in mouse VSNs was regulated by NKCC1, but not KCC. (A and B) The expression of transcript and protein for NKCC1 using RT-PCR and immunocytochemistry. (C) The dose dependence of an NKCC inhibitor, bumetanide, on the urine response. At 10 µM, bumetanide blocked ∼40% of the urine response, whereas at 50 µM, bumetanide blocked ∼85% of the response (n = 3). (D) In a representative VSN, urine responses were recorded before and after a 5-min incubation of 100 µM furosemide (KCC inhibitor) and 10 µM bumetanide. Furosemide did not influence the urine response, whereas bumetanide decreased about half of the amplitude for the urine response. The response recovered after the blockers were washed off. (E) In all six cells tested, urine-induced inward currents were not influenced by furosemide but decreased ∼50% in the presence of 10 µM bumetanide. **, P < 0.01; *, P < 0.05; NS, not significant difference, as determined with repeated measures one-way ANOVA with Bonferroni test. DU, 1:500 dilute urine.