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Title: Visualizing the temporal effects of vasoconstrictors on PKC translocation and Ca2+ signaling in single resistance arterial smooth muscle cells
Authors: Nelson, Carl P.
Willets, Jonathon M.
Davies, Noel W.
Challiss, R. A. John
Standen, Nicholas B.
First Published: Dec-2008
Publisher: American Physiological Society
Citation: American Journal of Physiology: Cell Physiology, 2008, 295 (6), pp. C1590-C1601.
Abstract: Arterial smooth muscle (ASM) contraction plays a critical role in regulating blood distribution and blood pressure. Vasoconstrictors activate cell surface receptors to initiate signaling cascades involving increased intracellular Ca2+ concentration ([Ca2+]i) and recruitment of protein kinase C (PKC), leading to ASM contraction, though the PKC isoenzymes involved vary between different vasoconstrictors and their actions. Here, we have used confocal microscopy of enhanced green fluorescence protein (eGFP)-labeled PKC isoenzymes to visualize PKC translocation in primary rat mesenteric ASM cells in response to physiological vasoconstrictors, with simultaneous imaging of Ca2+ signaling. Endothelin-1, angiotensin II, and uridine triphosphate all caused translocation of each of the PKC isoenzymes , , and ; however, the kinetics of translocation varied between agonists and PKC isoenzymes. Translocation of eGFP-PKC mirrored the rise in [Ca2+]i, while that of eGFP-PKC or - occurred more slowly. Endothelin-induced translocation of eGFP-PKC was often sustained for several minutes, while responses to angiotensin II were always transient. In addition, preventing [Ca2+]i increases using 1,2-bis-(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetra-(acetoxymethyl) ester prevented eGFP-PKC translocation, while eGFP-PKC translocated more rapidly. Our results suggest that PKC isoenzyme specificity of vasoconstrictor actions occurs downstream of PKC recruitment and demonstrate the varied kinetics and complex interplay between Ca2+ and PKC responses to different vasoconstrictors in ASM.
ISSN: 0002-9513
Type: Article
Description: This paper was published as American Journal of Physiology: Cell Physiology, 2008, 295 (6), pp. C1590-C1601. It is available from Doi: 10.1152/ajpcell.00365.2008
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Appears in Collections:Published Articles, Dept. of Cell Physiology and Pharmacology

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