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Vol. 284, Issue 3, 921-928, March 1998
Departments of
Pharmacology and Cell Biophysics (M.T., R.J.P.,
R.M.R.),
Molecular and Cellular Physiology (R.J.P.), and
Veterans
Affairs (R.M.R.), University of Cincinnati, Cincinnati, Ohio
The purpose of this study was to investigate the role of extracellular
Ca++ influx via L-type and non-L-type
Ca++ channels in thromboxane A2
receptor-mediated contraction. In intact rat aorta, U46619, a selective
thromboxane A2 receptor agonist, induced
concentration-dependent increases in intracellular Ca++
([Ca++]i) and contraction (EC50
values of 5.5 and 6.1 nM, respectively). U46619 (10 nM) induced ~60
to 70% of maximal [Ca++]i elevation and
contraction. Treatment with verapamil, an L-type Ca++
channel blocker, before 10 nM U46619 challenge, or during the plateau
[Ca++]i elevation and contraction, decreased
these parameters by ~50%. Ni++, a nonselective blocker
of cation channels, or SKF96365, a purported blocker of
receptor-operated Ca++ channels, further decreased the
contraction and abolished the [Ca++]i
elevation that remained after verapamil treatment of 10 nM U46619-challenged vessels. Pretreatment with verapamil and
Ni++ to prevent Ca++ influx and with
cyclopiazonic acid to deplete [Ca++]i stores
also partially prevented U46619-induced contraction, whereas
[Ca++]i elevation was abolished. These
results suggest that thromboxane A2 receptor-mediated
contraction of vascular smooth muscle partly depends on the influx of
extracellular Ca++ via both L-type and
non-L-type Ca++ channels, as well as a mechanism
independent of [Ca++]i elevation.
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