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Abstract
Endothelin-1 (ET-1) is a potent vasoconstrictor peptide that induces characteristically
long-lasting contractions. We used rat aortic rings to investigate the role of protein
kinase C (PKC) in ET-1-induced contractions and prostacyclin (PGI2) release. ET-1 (10−9 M) produced a gradual and sustained contraction in rat aortic rings. Pretreatment
of aortic rings with different doses (10−9 M and 10−6 M) of diltiazem (voltage-sensitive L-type calcium channel blocker) produced significant
inhibition of ET-1- and PDBu-induced contractions and PGI2 release. Inhibition was first noted at 10−9 M and was complete at 10−6 M. Conversely, pretreatment of aortic rings with different doses (10−9 M and 10−6 M) of calcium channel blockers (thapsigargin, an intracellular calcium channel blocker,
or conotoxin, a voltage-sensitive N-type calcium channel blocker) produced no changes
on ET-1- or PDBu-induced contraction or PGI2 release. These results provide further support for the concept that PKC mediates
ET-induced contractions and PGI2 release in rat aortic rings via an increase in intracellular calcium and this increase
is due to the influx of extracellular calcium and not to the release of calcium from
the sarcoplasmic reticulum.
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Article info
Publication history
Accepted:
May 14,
1996
Received:
March 11,
1996
Identification
Copyright
© 1996 Published by Elsevier Inc.
