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Vasoregulation by the β1 subunit of the calcium-activated potassium channel

Robert Brenner, Guillermo J. Peréz, Adrian D. Bonev, Delrae M. Eckman, Jon C. Kosek, Steven W. Wiler, Andrew J. Patterson, Mark T. Nelson and Richard W. Aldrich ()
Additional contact information
Robert Brenner: Stanford University
Guillermo J. Peréz: College of Medicine, The University of Vermont
Adrian D. Bonev: College of Medicine, The University of Vermont
Delrae M. Eckman: College of Medicine, The University of Vermont
Jon C. Kosek: Palo Alto Veterans Administration Healthcare System
Steven W. Wiler: Stanford University
Andrew J. Patterson: Stanford University School of Medicine
Mark T. Nelson: College of Medicine, The University of Vermont
Richard W. Aldrich: Stanford University

Nature, 2000, vol. 407, issue 6806, 870-876

Abstract: Abstract Small arteries exhibit tone, a partially contracted state that is an important determinant of blood pressure. In arterial smooth muscle cells, intracellular calcium paradoxically controls both contraction and relaxation. The mechanisms by which calcium can differentially regulate diverse physiological responses within a single cell remain unresolved. Calcium-dependent relaxation is mediated by local calcium release from the sarcoplasmic reticulum. These ‘calcium sparks’ activate calcium-dependent potassium (BK) channels comprised of α and β1 subunits. Here we show that targeted deletion of the gene for the β1 subunit leads to a decrease in the calcium sensitivity of BK channels, a reduction in functional coupling of calcium sparks to BK channel activation, and increases in arterial tone and blood pressure. The β1 subunit of the BK channel, by tuning the channel's calcium sensitivity, is a key molecular component in translating calcium signals to the central physiological function of vasoregulation.

Date: 2000
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DOI: 10.1038/35038011

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