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Endothelin and Ion Channels

  • Tracy L. Keith
  • Robert F. Highsmith

Abstract

Endothelin was initially characterized as a peptidergic vasoconstricting factor in 1985,1 and its amino acid sequence was reported in 1988.2 Three isoforms have since been identified and specific receptors localized in various organ systems (for reviews see refs. 3–5). In the vasculature ET-1 is known to interact with at least two receptors, ETA on smooth muscle mediating constriction, and ETB on endothelial cells mediating vasodilation.6 These actions have been noted in the coronary and cerebral circulations as well as in the pulmonary, renal and mesenteric vascular beds.3,4 In addition to its vasoactive properties ET has been reported to contract nonvascular smooth muscle in bronchial airways, the gastrointestinal tract and in the uterus.7 It has also been shown to regulate secretion from neuroendocrine cells8 and it is known to be a growth factor, stimulating proliferation of smooth muscle cells.9 While numerous reports have described these actions of ET-1, the signaling mechanisms in these respective cell types are incompletely resolved. Some common themes involve receptor activation and mobilization of calcium as well as recruitment of a variety of second messengers. The focus of this chapter is on the role of ion channels in the signaling processes triggered by ET-1 in a variety of cell types.

Keywords

Smooth Muscle Cell Vascular Smooth Muscle Nonselective Cation Channel Endothelium Derive Relaxing Factor Porcine Coronary Artery 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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© Springer-Verlag Berlin Heidelberg 1998

Authors and Affiliations

  • Tracy L. Keith
  • Robert F. Highsmith

There are no affiliations available

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