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This Article Full Text Full Text (PDF) All Versions of this Article: 294/6/H2761    most recent 01344.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Li, Z. Articles by Jose, P. A. Search for Related Content PubMed PubMed Citation Articles by Li, Z. Articles by Jose, P. A.

Inhibitory effect of D₁-like and D₃ dopamine receptors on norepinephrine-induced proliferation in vascular smooth muscle cells

¹Department of Cardiology, Daping Hospital, and ²Xinqiao Hospital, The Third Military Medical University, Chongqing, People's Republic of China; and Departments of ³Pediatrics, ⁴Physiology and Biophysics, Georgetown University Medical Center, Washington, District of Columbia

Submitted 16 November 2007 ; accepted in final form 14 April 2008

The sympathetic nervous system plays an important role in the regulation of blood pressure. There is increasing evidence for positive and negative interactions between dopamine and adrenergic receptors; the activation of the -adrenergic receptor induces vasoconstriction, whereas the activation of dopamine receptor induces vasorelaxation. We hypothesize that the D₁-like receptor and/or D₃ receptor also inhibit ₁-adrenergic receptor-mediated proliferation in vascular smooth muscle cells (VSMCs). In this study, VSMC proliferation was determined by measuring [³H]thymidine incorporation, cell number, and uptake of 3-(4,5-dimethylthiazol-2-yl)-diphenyltetrazolium bromide (MTT). Norepinephrine increased VSMC number and MTT uptake, as well as [³H]thymidine incorporation via the ₁-adrenergic receptor in aortic VSMCs from Sprague-Dawley rats. The proliferative effects of norepinephrine were attenuated by the activation of D₁-like receptors or D₃ receptors, although a D₁-like receptor agonist, fenoldopam, and a D₃ receptor agonist, PD-128907, by themselves, at low concentrations, had no effect on VSMC proliferation. Simultaneous stimulation of both D₁-like and D₃ receptors had an additive inhibitory effect. The inhibitory effect of D₃ receptor was via protein kinase A, whereas the D₁-like receptor effect was via protein kinase C-. The interaction between ₁-adrenergic and dopamine receptors, especially D₁-like and D₃ receptors in VSMCs, could be involved in the pathogenesis of hypertension.

₁-adrenergic receptor; hypertension