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Effects of vasoconstrictors on the biomechanical properties of single vascular smooth muscle cells
Author(s) -
Hong Zhongkui,
Sun Zhe,
Li Zhaohui,
Meininger Gerald
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.1115.25
Subject(s) - vascular smooth muscle , chemistry , angiotensin ii , vasodilation , fibronectin , cremaster muscle , extracellular matrix , contraction (grammar) , cell , biophysics , cytoskeleton , microbiology and biotechnology , medicine , anatomy , endocrinology , microcirculation , smooth muscle , biology , biochemistry , receptor
Vascular diameter is regulated by vasoconstrictors and vasodilators. Physical coupling of vascular smooth muscle cells (VSMC) to one another and to extracellular matrix (ECM) are necessary for a vessel to mechanically function. We hypothesized that VSMC adhesion to ECM may also be modulated by vasoactive agonists as one of the temporal events in the contractile process. Atomic force microscopy with fibronectin‐functionalized probes was employed to investigate biomechanics of rat cremaster arterioles VSMC. Cellular responses were recorded by real time measurement of cell membrane displacement and cell elasticity in absence and presence of endothelin‐1 (ET‐1) or angiotensin II (AII). The results show that ET‐1 (10 −8 M) or AII (10 −9 ‐10 −6 M) immediately cause vertical cell membrane displacement by 100–300 nm. An increase in cell elasticity followed at 20–30 min post ET‐1 or AII treatment. These findings suggest that activation of the contractile apparatus rapidly causes cell shape change but other cytoskeletal changes occur more slowly. Further studies are required to clarify the molecular mechanisms linking cell contraction and elasticity with adhesion. (1P01HL095486 to G.A.M. and AHA 0835676N to Z.S.)