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Vol. 287, Issue 1, 435-439, October 1998
Department of Biochemistry, University of Minnesota, St. Paul,
Minnesota (K.D.M., A.D.J.M., B.M.C.-F.) and
Department of Pharmacology,
University of Minnesota, Minneapolis, Minnesota (B.M.C.-F.);
Department
of Pharmacology and Experimental Therapeutics, University of Maryland
School of Medicine, Baltimore, Maryland (E.F.R.P, E.X.A.)
ACh receptors sensitive to nicotine (nAChR) are present in human skin
keratinocytes and in bronchial epithelial cells. They are stimulated by
ACh secreted by the same cells that express them, and they modulate
cell motility and shape. A variety of non-neuronal tissues, including
endothelial cells, synthesize ACh, which raises the possibility that
they are sensitive to nicotine. We demonstrate here that endothelial
cells that line blood vessels express functional nAChRs. Their
structure and ion-gating properties are similar to those of the nAChRs
expressed by ganglionic neurons and by skin keratinocytes and bronchial
epithelial cells. In situ hybridization experiments using
primary cultures of endothelial cells from human aorta demonstrated the
presence in these cells of the subunits believed to contribute to
ganglionic ACh receptors (AChRs) of the 
3 subtype: 3, 5, 
2
and 4. Binding of radiolabeled epibatidine
a high-affinity specific
ligand of certain neuronal AChRs, including the 3 subtypesrevealed
the presence of approximately 900 specific binding sites per cell. We
assessed the presence of functional AChRs by patch-clamp experiments.
Cultured human endothelial cells express ion channels that are opened
by (+)-anatoxin-a and are blocked by dihydro--erythroidine. These
are specific agonist and antagonist, respectively, of neuronal AChRs of
the 3 subtype. The ion-gating properties of the endothelial AChRs were similar to those of neuronal ganglionic AChRs. The presence of
AChRs sensitive to nicotine in endothelial cells may be related to the
toxic effects of nicotine on the vascular system.
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