Declining into failure: The age-dependent loss of the L-type calcium channel within the sinoatrial node

Sandra A. Jones, Mark R. Boyett, Matthew K. Lancaster

    Research output: Contribution to journalArticlepeer-review

    Abstract

    BACKGROUND - The spontaneous activity of pacemaker cells in the sinoatrial (SA) node controls heart rate under normal physiological conditions. Clinical studies have shown the incidence of SA node dysfunction increases with age and occurs with peak prevalence in the elderly population. The present study investigated whether aging affected the expression of Cav1.2 channels and whether these changes could affect pacemaker activity, in turn leading to age-related SA node degeneration. METHODS AND RESULTS - The SA node region was isolated from the right atrium of guinea pigs between birth and 38 months of age. Immunofluorescence studies showed Cav1.2 protein was present as punctate labeling around the outer membrane of atrial cells but was absent from the center of the SA node. The area lacking Cav1.2-labeled protein progressively increased from 2.06±0.1 (mean±SEM) mm at 1 month to 18.72±2.2 mm at 38 months (P
    Original languageEnglish
    Pages (from-to)1183-1190
    Number of pages7
    JournalCirculation
    Volume115
    Issue number10
    DOIs
    Publication statusPublished - Mar 2007

    Keywords

    • Aging
    • Calcium
    • Electrophysiology
    • Ion channels
    • Pacemakers
    • Proteins
    • Sinoatrial node

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