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. Author manuscript; available in PMC: 2013 Jul 31.
Published in final edited form as: Kidney Int. 2011 Jan;79(1):5–8. doi: 10.1038/ki.2010.400

Figure 1.

Figure 1

Simplified scheme of regulation of thiazide-sensitive Na-Cl cotransporter (NCC) regulation. NCC is synthesized and then glycosylated (green fork) within the golgi apparatus (not shown, for clarity). The NCC then moves to and into the apical membrane, where it exists as a dimer. To be full active, NCC undergoes phosphorylation along its amino terminal cytoplasmic domain, mediated largely by SPAK, thereby permitting NaCl transport. Little is know about mechanisms of removal from the membrane. Arginine vasopressin (AVP), aldosterone (Aldo), and angiotensin II (Ang II) all stimulate NCC activity. Trafficking may be a rapid effect, modulated predominantly by AVP and Ang II. Phosphorylation may occur within the membrane, and is enhanced by all three factors.