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(Circulation. 2000;101:2302.)
© 2000 American Heart Association, Inc.

Basic Science Reports

Dopamine as a Novel Antioxidative Agent for Rat Vascular Smooth Muscle Cells Through Dopamine D₁-Like Receptors

Kenichi Yasunari, MD; Masakazu Kohno, MD; Hiroaki Kano, MD; Mieko Minami, MD; Junichi Yoshikawa, MD

From the First Department of Internal Medicine, Osaka City University Medical School, Osaka, Japan.

Background—To elucidate the roles of vascular D₁-like receptors in atherosclerosis, the effects of the specific D₁-like agonists on platelet-derived growth factor (PDGF)-BB–mediated oxidative stress in vascular smooth muscle cells (VSMCs) were studied.

Methods and Results—Immunohistochemical studies demonstrated the coexistence of D_1A and D_1B dopamine receptors in VSMCs. Western blotting revealed a band of 70 kDa for D_1A and D_1B dopamine receptors. VSMCs stimulated by PDGF-BB exhibited increased oxidative stress directly measured by flow cytometry. These effects were prevented by dopamine, SKF 38393, or YM 435, and this prevention was reversed by Sch 23390. These effects were blocked by a specific protein kinase A (PKA) inhibitor, N-(2-[p-bromocinnamylamino]ethyl)-5-isoquinolinesulfonamide (H 89). The PDGF-BB–mediated increase in oxidative stress of VSMCs was significantly suppressed by the indirect phospholipase D (PLD) inhibitor suramin or the specific protein kinase C (PKC) inhibitor calphostin C. Both antisense but neither sense nor scrambled oligonucleotides to D_1A and D_1B receptors inhibited dopamine-induced suppression of increase in oxidative stress of VSMCs induced by PDGF-BB.

Conclusions—These findings suggest that vascular D₁-like receptors (D_1A and D_1B receptors) inhibit any increase in oxidative stress of VSMCs, possibly through activation of PKA and suppression of PLD and PKC.

Key Words: catecholamines • muscle, smooth • atherosclerosis • receptors • hypertension • kidney

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