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(Arteriosclerosis, Thrombosis, and Vascular Biology. 1997;17:3164-3173.)
© 1997 American Heart Association, Inc.

Articles

Dopamine as a Novel Antimigration and Antiproliferative Factor of Vascular Smooth Muscle Cells Through Dopamine D1-Like Receptors

Kenichi Yasunari; Masakazu Kohno; Tadayoshi Hasuma; Takeshi Horio; Hiroaki Kano; Koji Yokokawa; Mieko Minami; ; Junichi Yoshikawa

From the The First Department of Internal Medicine (K.Y., M.K., T.Ho., H.K., K.Y., M.M., J.Y.) and The Second Department of Biochemistry (T.Ha.), Osaka City University Medical School, Asahi-machi, Abeno-ku, Osaka, Japan.

Correspondence to Kenichi Yasunari, MD, The First Department of Internal Medicine, Osaka City University Medical School, 1-5-7 Asahi-machi, Abeno-ku, Osaka 545, Japan.

Abstract Vascular smooth muscle cell (VSMC) migration and proliferation are believed to play key roles in atherosclerosis. To elucidate the role of vascular dopamine D1-like receptors in atherosclerosis, the effects of dopamine and specific D1-like agonists SKF 38393 and YM 435 on platelet-derived growth factor (PDGF) BB-mediated VSMC migration and proliferation were studied. We observed that cells stimulated by PDGF-BB (5 ng/mL), showed increased migration and proliferation. These effects were prevented by coincubation with dopamine, SKF 38393, or YM 435 (1 to 10 µmol/L), and this prevention was reversed by Sch 23390 (1 to 10 µmol/l), a specific D1-like antagonist. These actions are mimicked by forskolin (1 to 10 µmol/L), a direct activator of adenylate cyclase and 8-bromo-cAMP at 0.1 to 1 mmol/L and are blocked by a specific protein kinase A inhibitor, N-[2-(p-bromocinnamylamino)ethyl]-5-isoquinoline-sulfonamide (H 89), but not blocked by its negative control, N-[2-(N-formyl)-p-chlorociannamylamino)ethyl]-5-isoquinoline sulfonamide (H 85). PDGF-BB (5 ng/mL)-mediated activation of phospholipase D, protein kinase C, and mitogen activated protein kinase activity were significantly suppressed by coincubation with dopamine. These results suggest that vascular D1-like receptor agonists inhibit migration and proliferation of VSMC, possibly through protein kinase A activation and suppression of activated phospholipase D, protein kinase C, and mitogen-activated protein kinase activity.

Key Words: dopamine • vascular smooth muscle • migration • proliferation

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