Disruption of K2P6.1 Produces Vascular Dysfunction and Hypertension in Mice

K2P6.1, a member of the 2-pore domain K channel family, is highly expressed in the vascular system; however, its function is unknown. We tested the following hypotheses. K2P6.1 regulates the following(1) systemic blood pressure; (2) the contractile state of arteries; (3) vascular smooth muscle cell...

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Bibliographic Details
Published in:Hypertension (Dallas, Tex. 1979) Tex. 1979), 2011-10, Vol.58 (4), p.672-678
Main Authors: Lloyd, Eric E, Crossland, Randy F, Phillips, Sharon C, Marrelli, Sean P, Reddy, Anilkumar K, Taffet, George E, Hartley, Craig J, Bryan, Robert M
Format: Article
Language:English
Subjects:
Arterial hypertension. Arterial hypotension
Biological and medical sciences
Blood and lymphatic vessels
Cardiology. Vascular system
Clinical manifestations. Epidemiology. Investigative techniques. Etiology
Medical sciences
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Summary:K2P6.1, a member of the 2-pore domain K channel family, is highly expressed in the vascular system; however, its function is unknown. We tested the following hypotheses. K2P6.1 regulates the following(1) systemic blood pressure; (2) the contractile state of arteries; (3) vascular smooth muscle cell migration; (4) proliferation; and/or (5) volume regulation. Mice lacking K2P6.1 (KO) were generated by deleting exon 1 of Kcnk6. Mean arterial blood pressure in both anesthetized and awake KO mice was increased by 17±2 and 26±3 mm Hg, respectively (P
ISSN:0194-911X
1524-4563
DOI:10.1161/HYPERTENSIONAHA.111.175349