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Ca2+ sparks and their function in human cerebral arteries.
George C Wellman1, David J Nathan, Christine M Saundry
1Department of Pharmacology, University of Vermont College of Medicine, Burlington, VT 05405-0068, USA. gwellman@zoo.uvm.edu.
Stroke
|March 2, 2002
Summary
Local calcium release events (Ca2+ sparks) activate BK channels, opposing cerebral artery constriction. This study identifies these sparks and currents in human cerebral artery cells, revealing their role in regulating artery diameter.
Area of Science:
- Cardiovascular Physiology
- Cellular Signaling
- Smooth Muscle Biology
Background:
- Ryanodine-sensitive Ca2+ channels in sarcoplasmic reticulum release local Ca2+ (Ca2+ sparks).
- Ca2+ sparks are hypothesized to oppose cerebral artery constriction via large-conductance Ca2+-activated K+ (BK) channels.
Purpose of the Study:
- To identify and characterize Ca2+ sparks and associated BK channel currents.
- To investigate the role of these events in human cerebral artery smooth muscle cells.
Main Methods:
- Patch-clamp technique for measuring membrane currents.
- Laser scanning confocal microscopy for intracellular Ca2+ imaging.
- Isolation of smooth muscle cells from human cerebral arteries.
Main Results:
- Ca2+ sparks (peak F/F0 2.02±0.04, size 8.2±0.5 µm²) occurred at ~1 Hz in human cerebral artery myocytes.
- 61% of Ca2+ sparks were associated with transient BK currents at -40 mV.
- Ryanodine (Ca2+ spark blocker) and iberiotoxin (BK channel blocker) induced contraction in human cerebral arteries.
Conclusions:
- Provides evidence for local Ca2+ signaling in human arterial myocytes.
- Suggests Ca2+ sparks and BK channel activity play a significant role in controlling human cerebral artery diameter.