Journal
STROKE
Volume 33, Issue 3, Pages 802-808Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/hs0302.104089
Keywords
calcium; cerebral arteries; muscle, smooth, vascular; potassium channels; ryanodine receptor calcium release channel
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Funding
- NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR016435] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL063722, R01HL044455] Funding Source: NIH RePORTER
- NCRR NIH HHS [P20 RR16435] Funding Source: Medline
- NHLBI NIH HHS [HL-63722, HL-44455] Funding Source: Medline
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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/F-0) of 2.02 +/- 0.04 and size of 8.2 +/- 0.5 mum(2) (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.
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