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Arteriolar Vasodilation Involves Actin Depolymerization
Author(s) -
Clifford Philip S.,
Ferguson Brian S.,
Jasperse Jeffrey L.,
Hill Michael A.
Publication year - 2017
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.31.1_supplement.684.4
Subject(s) - chemistry , vasodilation , cremaster muscle , actin , depolymerization , anatomy , biophysics , biochemistry , medicine , microcirculation , biology , organic chemistry
It is generally assumed that relaxation of arteriolar vascular smooth muscle occurs through hyperpolarization of the cell membrane, reduction in intracellular calcium concentration, and activation of myosin light chain phosphatase/inactivation of myosin light chain kinase. We hypothesized that vasodilation is related to depolymerization of F‐actin. Cremaster muscles were dissected from rats under sodium pentobarbital anesthesia (50mg/kg). Cremaster 1A arterioles (n=20) were dissected free of surrounding skeletal muscle and cannulated with glass micropipettes after which they were pressurized and warmed to 34°C. Internal diameter was monitored with an electronic video caliper. The concentration of G‐actin was determined in flash frozen whole arterioles by ultracentrifugation and western blot. Arterioles dilated by > 40% of initial diameter in response to pinacidil (10 −5 mM) and sodium nitroprusside (5×10 −5 mM). The G‐actin/sm22α ratio was 1.43±0.18 at 10mmHg in arterioles with no tone and 0.67±0.09 at 70mmHg with myogenic tone. The G‐actin/sm22α ratio increased to 1.32±0.34 when arterioles were dilated with pinacidil and 1.14±0.18 with sodium nitroprusside. Since F and G‐actin are reciprocally related, the increase in G‐actin/sm22α indicates F‐actin depolymerization. These findings suggest that actin depolymerization is an important mechanism for vasodilation to external agonists.