Ca2+ sparks and their function in human cerebral arteries

George C. Wellman, David J. Nathan, Christine M. Saundry, Guillermo Perez, Adrian D. Bonev, Paul L. Penar, Bruce I. Tranmer, Mark T. Nelson

    Research output: Contribution to journalArticlepeer-review

    Abstract

    Background and Purpose - Local Ca2+ release events (Ca2+ sparks) caused by the opening of ryanodine-sensitive Ca2+ channels in the sarcoplasmic reticulum have been suggested to oppose constriction in cerebral arteries through the activation of large-conductance Ca2+-activated K+ (BK) channels. We report the first identification and characterization of Ca2+ sparks and associated BK channel currents in smooth muscle cells isolated from human cerebral arteries. Methods - Membrane currents and intracellular Ca2+ were measured with the use of the patch-clamp technique and laser scanning confocal microscopy. Results - Ca2+ sparks with a peak fractional fluorescence change (F/F0) of 2.02±0.04 and size of 8.2±0.5 μm2 (n = 108) occurred at a frequency of approximately 1 Hz in freshly isolated, cerebral artery myocytes from humans. At a holding potential of -40 mV, the majority of, but not all, Ca2+ sparks (61 of 85 sparks) were associated with transient BK currents. Consistent with a role for Ca2+ sparks in the control of cerebral artery diameter, agents that block Ca2+ sparks (ryanodine) or BK channels (iberiotoxin) were found to contract human cerebral arteries. Conclusions - This study provides evidence for local Ca2+ signaling in human arterial myocytes and suggests that these events may play an important role in control of cerebral artery diameter in humans.
    Original languageEnglish
    Pages (from-to)802-808
    Number of pages6
    JournalStroke
    Volume33
    Issue number3
    DOIs
    Publication statusPublished - 2002

    Keywords

    • Calcium
    • Cerebral arteries
    • Muscle, smooth, vascular
    • Potassium channels
    • Ryanodine receptor calcium release channel

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