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Vol. 285, Issue 2, 759-766, May 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 test whether the elevated
intracellular Ca++ level
([Ca++]i) resulting from store-operated
Ca++ entry was associated with vascular smooth muscle
contraction. Cyclopiazonic acid (CPA), a selective inhibitor of
sarcoplasmic reticulum Ca++-ATPase,
concentration-dependently (1-10 µM) elevated
[Ca++]i in rat aorta, as indicated by an
increase in the fura-2 340/380 ratio. Simultaneous measurement of
contraction demonstrated that 1 and 10 µM CPA induced insignificant
and variable amounts of contraction, respectively. Verapamil (10 µM)
had relatively little effect on the 1 and 10 µM CPA-elevated
[Ca++]i. In contrast, Ni++ (0.1 mM), in the presence of verapamil, abolished the 1 µM CPA-elevated [Ca++]i. Ni++ (0.1 mM) also
partially decreased the 10 µM CPA-elevated
[Ca++]i and, furthermore, abolished the
associated contraction. A higher Ni++ concentration (1 mM)
abolished the 10 µM CPA-elevated [Ca++]i
that remained after verapamil and 0.1 mM Ni++. Phorbol
dibutyrate (10 nM), a protein kinase C activator, potentiated contractions to 1 and 10 µM CPA in the presence of verapamil. Ni++ (0.1 mM) abolished the enhanced contractions, and
decreased the elevated [Ca++]i. These results
suggest that 1) elevated [Ca++]i due to
store-operated Ca++ entry is dissociated from contraction;
2) the elevated [Ca++]i is restricted to at
least two noncontractile compartments that can be differentiated by
their relative sensitivities to blockade by low (0.1 mM) and higher (1 mM) Ni++ concentrations, and 3)
[Ca++]i elevation within the compartment
sensitive to blockade by 0.1 mM Ni++ can be coupled to
contraction via protein kinase C activation.
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