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. Author manuscript; available in PMC: 2011 Jul 12.
Published in final edited form as: Kidney Int. 2010 Aug 18;78(10):956–962. doi: 10.1038/ki.2010.272

Figure 3.

Figure 3

Illustration of how high K fed BKβ1-KO can develop of Na, Cl and fluid retention. On high dietary K intake, the absence of BKβ1 in the CNT results in relative basolateral K recycling instead of its secretory role. The elevated K stimulates aldosterone production from the adrenals which have enhanced sensitivity to K in BKβ1-KO. The increased plasma aldosterone stimulates Na and Cl reabsorption instead of an exchange of K for Na.