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CALCIUM SPARKLETS IN ARTERIAL SMOOTH MUSCLE
Author(s) -
Santana Luis F,
Navedo Manuel F,
Amberg Gregory C,
NievesCintrón Madeline,
Votaw V Scott,
UfretVincenty Carmen A
Publication year - 2008
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2007.04867.x
Subject(s) - myocyte , contraction (grammar) , calcium , biophysics , chemistry , perfusion , confocal , vascular smooth muscle , confocal microscopy , calcium signaling , medicine , anatomy , smooth muscle , microbiology and biotechnology , biology , physics , optics
SUMMARY1 Voltage‐dependent, L‐type Ca 2+ channels (LTCC) play an essential role in arterial smooth muscle contraction and, consequently, the regulation of arterial diameter, tissue perfusion and blood pressure. However, the spatial organization of functional LTCC in arterial myocytes is incompletely understood. 2 Total internal reflection fluorescence and swept‐field confocal microscopy revealed that the opening of a single or a cluster of LTCC produces local elevations in [Ca 2+ ] i called Ca 2+ sparklets. In arterial myocytes, Ca 2+ sparklets are produced by the opening of Cav1.2 channels. 3 The Ca 2+ sparklet activity is bimodal. In low activity mode, rare stochastic openings of solitary LTCC produce limited Ca 2+ influx (‘low activity Ca 2+ sparklets’). In contrast, discrete clusters of LTCC associated with protein kinase Ca (PKCa) operate in a sustained, high‐activity mode resulting in substantial Ca 2+ influx (‘persistent Ca 2+ sparklets’). 4 The Ca 2+ sparklet activity varies regionally within a myocyte depending on the relative activities of nearby PKCa and opposing protein phosphates 2A and 2B. 5 Low‐ and high‐activity persistent Ca 2+ sparklets modulate local and global [Ca 2+ ] i in arterial smooth muscle, suggesting that this Ca 2+ signal may play an important role in the regulation of vascular function.