Sarcoplasmic Reticulum and Membrane Currents

  1. Derek J. Chadwick Organizer and
  2. Jamie A. Goode
  1. Gerald M. Herrera and
  2. Mark T. Nelson

Published Online: 7 OCT 2008

DOI: 10.1002/0470853050.ch14

Role Of The Sarcoplasmic Reticulum In Smooth Muscle: Novartis Foundation Symposium 246

Role Of The Sarcoplasmic Reticulum In Smooth Muscle: Novartis Foundation Symposium 246

How to Cite

Herrera, G. M. and Nelson, M. T. (2002) Sarcoplasmic Reticulum and Membrane Currents, in Role Of The Sarcoplasmic Reticulum In Smooth Muscle: Novartis Foundation Symposium 246 (eds D. J. Chadwick and J. A. Goode), John Wiley & Sons, Ltd, Chichester, UK. doi: 10.1002/0470853050.ch14

Author Information

  1. Department of Pharmacology, University of Vermont, Given Medical Building, 89 Beaumont Avenue, Burlington, VT 05405-0068, USA

  1. This paper was presented at the symposium by Mark T. Nelson, to whom correspondence should be addressed.

Publication History

  1. Published Online: 7 OCT 2008
  2. Published Print: 15 JUN 2002

Book Series:

  1. Novartis Foundation Symposia

Book Series Editors:

  1. Novartis Foundation

ISBN Information

Print ISBN: 9780470844793

Online ISBN: 9780470853054

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Summary

Local and global Ca2+ signals from voltage-dependent Ca2+ channels (VDCCs) and ryanodine-sensitive Ca2+ release (RyRs) channels in the sarcoplasmic reticulum (SR) encode information to different Ca2+-sensitive targets including the large- (BK) and small-conductance (SK) Ca2+-activated K+ channels in the surface membrane. In smooth muscle, unlike cardiac muscle, Ca2+ signalling to RyRs is not local, exhibiting a significant lag between VDCC activation and subsequent RyR stimulation, measured as Ca2+ sparks and associated BK currents. However, Ca2+ signalling from RyRs (Ca2+ sparks) to BK channels appears to be local in arterial (ASM) and urinary bladder smooth muscle (UBSM), consistent with a close proximity of SR RyRs to BK channels. The response of BK channels in ASM and UBSM depends on the tuning of the Ca2+/voltage sensitivity of the BK channel by its accessory subunit, the β1 subunit. UBSM, in contrast to ASM, has both BK and SK channels. SK channels in UBSM are solely activated by Ca2+ signals from VDCCs, whereas BK channels are activated by Ca2+ from both VDCCs and RyRs. The differential regulation of BK and SK channels by Ca2+ signals underlies their roles in regulating action potential duration and membrane potential (BK channels) and after-hyperpolarizations (SK channels) in smooth muscle.