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(Received for publication, April 22, 1997, and in revised form, July 24, 1997)
From the 20-Hydroxyeicosatetraenoic acid (20-HETE), a
cytochrome P450 metabolite of arachidonic acid, is a potent
vasoconstrictor, and has been implicated in the myogenic activation of
renal and cerebral arteries. We examined the role of protein kinase C
(PKC) in the signal transduction pathway by which 20-HETE induces
vasoconstriction and inhibition of whole-cell K+
current in cat cerebral vascular smooth muscle. 20-HETE induced a
concentration-dependent constriction in isolated
pressurized cat middle cerebral arteries (
Volume 272, Number 43,
Issue of October 24, 1997
pp. 27345-27352
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.
20-Hydroxyeicosatetraenoic Acid-induced Vasoconstriction and
Inhibition of Potassium Current in Cerebral Vascular Smooth Muscle Is
Dependent on Activation of Protein Kinase C
§
,§
,
and§
Cardiovascular Research Center and
§ Department of Physiology, Medical College of Wisconsin,
Milwaukee, Wisconsin 53226 and 
The Clement J. Zablocki Veterans
Affairs Medical Center, Milwaukee, Wisconsin 53295
29 ± 8% at 1 µM). However, in the presence of an
N-myristoylated PKC pseudosubstrate inhibitor peptide (Myr
PKC-I(19-27)), 20-HETE induced a
concentration-dependent vasodilation (26 ± 4% at 1 µM). In whole-cell voltage clamp studies, application of
20-HETE inhibited whole-cell K+ current recorded in cat
cerebral vascular smooth muscle cells, an effect that was attenuated by
MyrPKC-I(19-27). Further evidence for the role of PKC
activation in response to 20-HETE is the finding that 20-HETE increased
the phosphorylation of myristoylated, alanine-rich PKC substrate in
cultured cat cerebral vascular smooth muscle cells in a concentration-
and PKC-dependent manner. These data provide evidence that
PKC is an integral part of the signal transduction pathway by which
20-HETE elicits vasoconstriction of cerebral arteries and inhibition of
whole-cell K+ current in cat cerebral vascular smooth
muscle.
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