(Hypertension. 2006;48:804.)
© 2006 American Heart Association, Inc.
Brief Reviews |
From the Unidad de Regulación Neurohumoral (X.F.F.), Departamento de Ciencias Fisiológicas, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile; and the Department of Molecular Physiology and Biological Physics (B.E.I., B.R.D.), The Robert M. Berne Cardiovascular Research Center, University of Virginia, Charlottesville, Va.
Correspondence to Brian R. Duling, University of Virginia Cardiovascular Research Center, University of Virginia, PO Box 801394, Charlottesville, VA 22908. E-mail brd@virginia.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
| Introduction |
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Augmented vasomotor tone typically plays a key role in the development of hypertension, and tone depends on cellcell communication established by paracrine molecules and, in addition, gap junctions. Paracrine-based linkages between cells of the vasculature are well known, and the possible roles of such linkages in the genesis of hypertension have been extensively explored. Much less is known of the roles of gap junctional communication in establishing vasomotor tone and of the effects of modification of gap junctions on hypertension.
| Structure and Regulation of Gap Junctions |
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