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

Author

Listed:
  • 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
    Stanford University School of Medicine)

  • 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)

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.

Suggested Citation

  • Robert Brenner & Guillermo J. Peréz & Adrian D. Bonev & Delrae M. Eckman & Jon C. Kosek & Steven W. Wiler & Andrew J. Patterson & Mark T. Nelson & Richard W. Aldrich, 2000. "Vasoregulation by the β1 subunit of the calcium-activated potassium channel," Nature, Nature, vol. 407(6806), pages 870-876, October.
    • Handle: RePEc:nat:nature:v:407:y:2000:i:6806:d:10.1038_35038011
    DOI: 10.1038/35038011
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