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. Author manuscript; available in PMC: 2010 May 1.
Published in final edited form as: Pflugers Arch. 2008 Sep 16;458(1):77–88. doi: 10.1007/s00424-008-0589-z

Figure 2.

Figure 2

Transport systems involved in the generation of the driving force for paracellular divalent cation resorption in the TAL. Left: Two components are contributing to the lumen positive, transepithelial potential. Component “a” consists of NKCC2 (Na+-K+-2Cl−-symport, affected in Bartter type I), ROMK (apical potassium channel, affected in Bartter type II), ClC-Kb (basolateral Cl− channel, affected in Bartter type III) with its subunit barttin (affected in Bartter type IV). Component “b” is a Na+ diffusion potential due to a paracellular back-leak of Na+. Right: Mechanisms by which CaSR (Ca2+-sensing receptor), may modulate paracellular divalent cation transport either by affecting the transepithelial potential (inhibition of NKCC2, ROMK and Na+/K+-ATPase through a Ca2+ and PLA2-dependent increase in 20-HETE) and/or through a cAMP-dependent PKA-effect on claudin-16 as proposed by Ikari et al. [41].