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Am J Physiol Heart Circ Physiol 280: H2144-H2152, 2001;
0363-6135/01 $5.00
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Vol. 280, Issue 5, H2144-H2152, May 2001

Importance of PKC and PI3Ks in ethanol-induced contraction of cerebral arterial smooth muscle

Zhi-Wei Yang1, Jun Wang2, Tao Zheng1, Bella T. Altura1,4, and Burton M. Altura1,3,4

Departments of 1 Physiology and Pharmacology, 2 Anesthesiology, and 3 Medicine and 4 Center for Cardiovascular and Muscle Research, Health Science Center at Brooklyn, State University of New York, Brooklyn, New York 11203

We investigated the relationships of two potential intracellular signaling pathways, protein kinase C (PKC) and phosphatidylinositol 3-kinases (PI3Ks), to ethanol-induced contractions in cerebral arteries. Ethanol (20-200 mM) induces concentration-dependent constriction in isolated canine basilar arteries that is inhibited in a concentration-dependent manner by pretreatment of these vessels with 10-9-10-3 M Gö-6976 (an antagonist selective for PKC-alpha and PKC-beta I), 10-10-10-4 M bisindolylmaleimide I (a specific antagonist of PKC), and 10-10-10-4 M wortmannin or 10-8-10-2 M LY-294002 (selective antagonists of PI3Ks). Ethanol-induced increases in intracellular Ca2+ concentration (from ~100 to ~500 nM) in canine basilar smooth muscle cells are also suppressed markedly (~20-70%) in the presence of a similar concentration range of Gö-6976, bisindolymaleimide I, wortmannin, or LY-294002. This study suggests that activation of PKC isoforms and PI3Ks appears to be an important signaling pathway in ethanol-induced vasoconstriction of cerebral blood vessels.

canine basilar arteries; cerebrovasospasm; ethanol; stroke; protein kinase C; phosphatidylinositol 3-kinases


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