Document Detail


BK channels and a new form of hypertension.
MedLine Citation:
PMID:  20720523     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Large, Ca-activated K channels (BK) are comprised of an α pore (BKα) and one of four β subunits (BKβ1-4). When the gene for BKβ1 is knocked out (BKβ1-KO), the result is increased myogenic tone of vascular smooth muscle and hypertension. We reexamined whether the hypertension is entirely due to increased vascular tone, because most monogenic forms of hypertension have renal origins and BKβ1 resides in renal connecting tubule (CNT) cells. Moreover, BKβ1 is localized in the adrenal glands, where it may control production of aldosterone. This review will summarize our report that a majority of the hypertension of BKβ1-KO is the result of insufficient handling of dietary K, resulting in increased plasma K and hyperaldosteronism, the latter promoting Na and fluid retention. The fluid retention and hypertension are exacerbated by a high-K diet and reduced by eplerenone, an aldosterone receptor inhibitor. Genetic knockout of BKβ4 (BKβ4-KO), which resides in intercalated cells, also exhibits deficient K excretion, fluid retention, and mild hypertension that is not exacerbated when animals are treated with a high-K diet. These results show that the hypertension associated with BKβ1-KO occurs because of enhanced fluid retention, as well as because of the previously described vascular dysfunction.
Authors:
P Richard Grimm; Steven C Sansom
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2010-08-18
Journal Detail:
Title:  Kidney international     Volume:  78     ISSN:  1523-1755     ISO Abbreviation:  Kidney Int.     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-10-29     Completed Date:  2011-04-08     Revised Date:  2013-05-28    
Medline Journal Info:
Nlm Unique ID:  0323470     Medline TA:  Kidney Int     Country:  United States    
Other Details:
Languages:  eng     Pagination:  956-62     Citation Subset:  IM    
Affiliation:
Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland, USA.
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MeSH Terms
Descriptor/Qualifier:
Adrenal Medulla / physiopathology
Animals
Disease Models, Animal
Humans
Hyperaldosteronism / physiopathology*
Hypertension / genetics,  physiopathology*
Kidney / physiopathology
Large-Conductance Calcium-Activated Potassium Channels / genetics,  physiology*
Mice
Mice, Knockout
Muscle, Smooth, Vascular / physiopathology
Potassium / metabolism
Grant Support
ID/Acronym/Agency:
R01 DK071014-01A2/DK/NIDDK NIH HHS; R01 DK071014-02/DK/NIDDK NIH HHS; R01 DK071014-03/DK/NIDDK NIH HHS; R01 DK071014-04/DK/NIDDK NIH HHS; R01 DK071014-05/DK/NIDDK NIH HHS; R01 DK71014/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Large-Conductance Calcium-Activated Potassium Channels; 7440-09-7/Potassium
Comments/Corrections

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