NSAIDs acutely inhibit TRPC channels in freshly isolated rat glomeruli

Biochem Biophys Res Commun. 2011 May 6;408(2):242-7. doi: 10.1016/j.bbrc.2011.04.005. Epub 2011 Apr 5.

Abstract

Using a novel approach for analysis of TRPC channel activity, we report here that NSAIDs are involved into regulation of TRPC channels in the podocytes of the freshly isolated decapsulated glomeruli. Fluorescence and electron microscopy techniques confirmed the integrity of podocytes in the glomeruli. Western blotting showed that TRPC1, 3 and 6 are highly expressed in the glomeruli. Single-channel patch clamp analysis revealed cation currents with distinct TRPC properties. This is the first report describing single TRPC-like currents in glomerular podocytes. Furthermore, our data provide a novel mechanism of NSAIDs regulation of TRPC channels, which might be implicated in maintaining the glomerular filtration barrier.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology*
  • Diclofenac / pharmacology
  • Glomerulosclerosis, Focal Segmental / drug therapy
  • Glomerulosclerosis, Focal Segmental / metabolism
  • Ibuprofen / pharmacology
  • Kidney Glomerulus / drug effects*
  • Male
  • Rats
  • Rats, Sprague-Dawley
  • TRPC Cation Channels / antagonists & inhibitors*
  • TRPC Cation Channels / metabolism

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • TRPC Cation Channels
  • Diclofenac
  • Ibuprofen