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Smooth Muscle Actin Polymerization and Vasoconstriction‐Induced Inward Remodeling of Resistance Arteries
Author(s) -
Staiculescu Marius Catalin,
Galinanes E. L.,
Zhao G.,
Li M.,
Ulloa U.,
Jin M.,
Martinez-Lemus L.A.
Publication year - 2012
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.26.1_supplement.lb639
Subject(s) - vasoconstriction , actin , chemistry , actin remodeling , microbiology and biotechnology , angiotensin ii , biophysics , actin cytoskeleton , cytoskeleton , endocrinology , biology , biochemistry , receptor , cell
In hypertension, the most common structural change in arterioles is inward eutrophic remodeling, a reduction in passive luminal diameter without variations in wall cross‐sectional area. As prolonged vasoconstriction causes inward eutrophic remodeling and is associated with vascular smooth muscle (VSM) actin polymerization, we hypothesize that prolonged exposure to norepinephrine (NE) + angiotensin II (Ang‐II) requires actin polymerization to induce inward remodeling. Actin‐Alexa 488 was electroporated into VSM within isolated rat‐cremaster arterioles. Exposure to NE+Ang‐II for 4 hours induced inward remodeling and reduced the fluorescence from actin‐Alexa by 42%. Cytochalasin D blunted the decreased fluorescence caused by NE+Ang‐II by 28%, and prevented the maintenance of vasoconstriction. In vitro, actin polymerization decreased the fluorescence of actin‐Alexa suggesting that in arterioles the NE+Ang‐II‐induced inward remodeling requires actin polymerization. Rho kinase inhibition also prevented NE+Ang‐II from maintaining vasoconstriction, while direct activation of Rho/Rac/Cdc42 resulted in inward remodeling. This suggests that actin polymerization mediated by Rho, Rac, and/or Cdc42 was needed for NE+Ang‐II to induce inward remodeling. These mechanisms may contribute to the structural narrowing of resistance vessels encountered in hypertension. Supported by NIH HL‐088105.