Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Sarcoplasmic reticulum and membrane currents.

Gerald M Herrera1, Mark T Nelson

  • 1Department of Pharmacology, University of Vermont, Burlington 05405-0068, USA.

Novartis Foundation Symposium
|August 8, 2002
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Endothelial Arf6 sustains electrical signaling and cerebral blood flow in mice through PIP<sub>2</sub>-dependent activation of Kir2.1 channels.

Proceedings of the National Academy of Sciences of the United States of America·2026
Same author

Electromechanical Dynamics and Myogenic Responses in Cerebral Smooth Muscle Cells and Capillary Pericytes.

bioRxiv : the preprint server for biology·2026
Same author

Electro-Calcium uncoupling precedes neurodegeneration in Alzheimer's disease.

bioRxiv : the preprint server for biology·2026
Same author

Publisher Correction: Overactive bladder phenotype induced by chronic activation of hypothalamic neuroendocrine stress pathways in rats with no extrinsic behavioral stress applied.

Scientific reports·2026
Same author

Endothelial Arf6 sustains capillary electrical signaling and cerebral blood flow through PIP<sub>2</sub> regeneration and activation of Kir2.1 channels.

bioRxiv : the preprint server for biology·2026
Same author

Overactive bladder phenotype induced by chronic activation of hypothalamic neuroendocrine stress pathways in rats with no extrinsic behavioral stress applied.

Scientific reports·2025
Same journal

Genetic and therapeutic control of diabetogenic CD8+ T cells.

Novartis Foundation symposium·2009
Same journal

Translating mucosal antigen based prevention of autoimmune diabetes to human.

Novartis Foundation symposium·2009
Same journal

Re-establishing immune tolerance in type 1 diabetes via regulatory T cells.

Novartis Foundation symposium·2009
Same journal

Immune markers of disease and therapeutic intervention in type 1 diabetes.

Novartis Foundation symposium·2009
Same journal

Towards a curative therapy in type 1 diabetes: remission of autoimmunity, maintenance and augmentation of beta cell mass.

Novartis Foundation symposium·2009
Same journal

CD8 and cytotoxic T cells in type 1 diabetes.

Novartis Foundation symposium·2009
See all related articles

Calcium (Ca2+) signals from voltage-dependent Ca2+ channels and ryanodine receptors regulate ion channels in smooth muscle. Differential Ca2+ signaling pathways activate large- (BK) and small-conductance (SK) channels, impacting muscle function.

Area of Science:

  • Physiology
  • Molecular Biology
  • Cellular Signaling

Background:

  • Smooth muscle Ca2+ signaling involves voltage-dependent Ca2+ channels (VDCCs) and sarcoplasmic reticulum ryanodine receptors (RyRs).
  • Ca2+-activated K+ channels, including large- (BK) and small-conductance (SK) channels, are key targets of Ca2+ signals.
  • Differential localization and kinetics of Ca2+ signals influence channel activation.

Purpose of the Study:

  • To investigate the distinct roles of VDCCs and RyRs in smooth muscle Ca2+ signaling.
  • To elucidate the differential activation of BK and SK channels by various Ca2+ sources.
  • To understand how Ca2+ signaling pathways regulate ion channel function in arterial and urinary bladder smooth muscle.

Main Methods:

  • Electrophysiological recordings of Ca2+ currents and channel activity.

Related Experiment Videos

  • Measurement of Ca2+ sparks and Ca2+ transients.
  • Analysis of BK and SK channel regulation by Ca2+ and voltage.

    • Main Results:

    • Ca2+ signaling to RyRs in smooth muscle exhibits a lag compared to cardiac muscle.
    • RyR-mediated Ca2+ signaling to BK channels is local in arterial (ASM) and urinary bladder smooth muscle (UBSM).
    • BK channels are regulated by the beta1 subunit, while UBSM possesses both BK and SK channels with distinct Ca2+ activation profiles.

    Conclusions:

    • BK and SK channels are differentially regulated by local and global Ca2+ signals in smooth muscle.
    • These distinct signaling pathways contribute to the regulation of membrane potential and action potentials.
    • Understanding these mechanisms is crucial for smooth muscle physiology and pathophysiology.