In:
American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 294, No. 6 ( 2008-06), p. H2761-H2768
Abstract:
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 α-adrenergic receptor induces vasoconstriction, whereas the activation of dopamine receptor induces vasorelaxation. We hypothesize that the D 1 -like receptor and/or D 3 receptor also inhibit α 1 -adrenergic receptor-mediated proliferation in vascular smooth muscle cells (VSMCs). In this study, VSMC proliferation was determined by measuring [ 3 H]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 [ 3 H]thymidine incorporation via the α 1 -adrenergic receptor in aortic VSMCs from Sprague-Dawley rats. The proliferative effects of norepinephrine were attenuated by the activation of D 1 -like receptors or D 3 receptors, although a D 1 -like receptor agonist, fenoldopam, and a D 3 receptor agonist, PD-128907, by themselves, at low concentrations, had no effect on VSMC proliferation. Simultaneous stimulation of both D 1 -like and D 3 receptors had an additive inhibitory effect. The inhibitory effect of D 3 receptor was via protein kinase A, whereas the D 1 -like receptor effect was via protein kinase C-ζ. The interaction between α 1 -adrenergic and dopamine receptors, especially D 1 -like and D 3 receptors in VSMCs, could be involved in the pathogenesis of hypertension.
Type of Medium:
Online Resource
ISSN:
0363-6135
,
1522-1539
DOI:
10.1152/ajpheart.01344.2007
Language:
English
Publisher:
American Physiological Society
Publication Date:
2008
detail.hit.zdb_id:
1477308-9
SSG:
12
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