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Vascular tone is regulated through actin polymerization mechanism in uterine artery
Author(s) -
Xiao DaLiao,
Buchholz John N.,
Zhang Lubo
Publication year - 2006
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.20.4.a229-b
Subject(s) - vascular smooth muscle , cytochalasin d , uterine artery , artery , anatomy , actin , blood vessel , medicine , constriction , chemistry , cardiology , biophysics , microbiology and biotechnology , biology , cytoskeleton , biochemistry , smooth muscle , pregnancy , gestation , genetics , cell
Little is known about the regulatory mechanisms of uterine artery smooth muscle vascular tone. The present study tested the hypothesis that vascular tone is regulated, at least partly, through actin polymerization mechanism in uterine artery. In pressurized resistance sized uterine arteries from pregnant sheep, we measured vascular diameter (μm) and [Ca 2+ ] i as a function of intravascular pressure. Increased pressure from 20 to 100 mmHg caused an increase in [Ca 2+ ] i and vessel diameters following by a significant decrease in vessel diameters, i.e., myogenic constriction. When pretreatment with cytochalasin B (10 μM), an inhibitor of actin polymerization, cytochalasin B completely blocked the myogenic constriction induced by increased intravascular pressure without significant changes of Ca 2+ signal in the uterine artery. The results suggest that vascular tone of uterine artery is regulated through both Ca 2+ mobilization and Ca 2+ sensitivity. Ca 2+ mobilization is necessary for initial of myogenic tone, but Ca 2+ sensitivity plays a key role in maintenance of myogenic tone in uterine artery. Furthermore, the thin filament mechanism, actin polymerization may be a novel mechanism in control of vascular tone under blood pressure.