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Prolonged Vasoconstriction of Small Resistance Arteries Involves Actin Polymerization Causing Cytoskeletal Remodeling Within the Vascular Smooth Muscle Cells (VSMC)
Author(s) -
Galiñanes Edgar Luis,
MartinezLemus Luis
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.lb449
Subject(s) - vasoconstriction , cytoskeleton , actin , fluorescence microscope , vascular smooth muscle , chemistry , biophysics , medicine , biology , anatomy , microbiology and biotechnology , endocrinology , fluorescence , cell , biochemistry , smooth muscle , physics , quantum mechanics
Two groups of isolated, cannulated and pressurized rat cremasteric arterioles with myogenic tone, that were previously transfected with Actin Alexa Flour®488 using electroporation, were imaged hourly with a confocal microscope for 4 hours while incubated at 34C in the absence (control) or presence (treated) of norepinephrine (NE,10‐5.5M) plus angiotensin‐II (Ang,10‐7M). Fluorescence intensity was taken from individual VSMCs using 3D image reconstruction. Over the entire incubation period, treated arterioles (N=6) had a decrease in mean fluorescence of 40% compared to controls (N=4). With removal of the agonists, the mean florescence of our controls returned within 10% of that obtained at myogenic tone while the treated group remained reduced by 30%. Previous reports indicate polymerization of G‐Actin into F‐Actin can decrease fluorescence due to the phenomenon of quenching. Therefore the observation that overall fluorescence at the end of 4hours in the treatment group did not return to control levels implies that actin remained polymerized. Our results are consistent with our hypothesis that prolonged vasoconstriction induces VSMC cytoskeletal remodeling by causing actin polymerization.