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

2. 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  , DOI: ( /ki )
Copyright © 2010 International Society of Nephrology Terms and Conditions

3. 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  , DOI: ( /ki )
Copyright © 2010 International Society of Nephrology Terms and Conditions

4. 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  , DOI: ( /ki )
Copyright © 2010 International Society of Nephrology Terms and Conditions