Different α-adrenoceptors mediate migration of vascular smooth muscle cells and adventitial fibroblasts in vitro

Author:

Zhang Hua1,Facemire Carie S.1,Banes Albert J.2,Faber James E.1

Affiliation:

1. Departments of Cell and Molecular Physiology and

2. Orthopedics, School of Medicine, University of North Carolina, Chapel Hill, North Carolina 27599

Abstract

Norepinephrine directly induces growth of the vascular wall, which may involve not only proliferation of smooth muscle cells (SMCs) and adventitial fibroblasts (AFBs) but also augmentation of their migration. To test this hypothesis, growth-arrested SMCs and AFBs from rat aorta were exposed to norepinephrine. Norepinephrine caused dose-dependent migration of both cell types that was dependent on chemotaxis. In contrast, platelet-derived growth factor (PDGF)-BB, used as a positive control, stimulated both chemotaxis and chemokinesis. Only α1D-adrenoceptors (AR) and α2-AR antagonists inhibited norepinephrine migration of SMCs, whereas norepinephrine migration of AFBs was only inhibited by α1A-AR and α1B-AR antagonists; β-AR blockade was without effect. Norepinephrine and PDGF-BB were additive for AFB, but not SMC, migration. Stimulation of migration was reversed at high norepinephrine concentrations (10 μM); this inhibition was mediated by α2- and β-ARs in AFBs but not in SMCs. Thus norepinephrine induces migration of SMCs and AFBs via different α-ARs. This action may participate in wall remodeling and norepinephrine potentiation of injury-induced intimal lesion growth.

Publisher

American Physiological Society

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology

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