BK channels and a new form of hypertension P Richard Grimm, Steven C. Sansom  Kidney International  Volume 78, Issue 10, Pages 956-962 (November 2010) DOI: 10.1038/ki.2010.272 Copyright © 2010 International Society of Nephrology Terms and Conditions

Figure 1 Compromised extracellular volume regulation in BKβ1-KO. Volume status was determined by hematocrits (a) and weight change (b) of Ca-activated K channel knockout (BKβ1-KO) and wild type (WT) on either control (normal K: 0.32% Na and 0.6% K) or high K (0.32% Na and 5.0% K) diets. *Denotes significant difference (P<0.05) compared with using the unpaired t-test. ∓Denotes significant difference compared with normal K (control) using analysis of variance plus the Student–Newman–Keuls test. ¶Denotes significant difference compared with high K using analysis of variance plus the Student–Newman–Keuls test. Kidney International 2010 78, 956-962DOI: (10.1038/ki.2010.272) Copyright © 2010 International Society of Nephrology Terms and Conditions

Figure 2 Effect of K diet on MAP of BKβ1-KO and BKβ4-KO. (a) MAPs of BKβ1-KO versus wild type (WT). (b) BKβ4-KO versus WT. Low K contains 0.32% Na and 0.1% K. All other symbols are the same as in Figure 1. Kidney International 2010 78, 956-962DOI: (10.1038/ki.2010.272) Copyright © 2010 International Society of Nephrology Terms and Conditions

Figure 3 Illustration of how high K-fed Ca-activated K channel knockout (BKβ1-KO) mice can develop Na, Cl, and fluid retention. On high dietary K intake, the absence of BKβ1 in the connecting tubule (CNT) results in relative basolateral K recycling instead of its secretory role. The elevated K stimulates aldosterone (Aldo) 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. Kidney International 2010 78, 956-962DOI: (10.1038/ki.2010.272) Copyright © 2010 International Society of Nephrology Terms and Conditions