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Mecamylamine Suppresses Basal and Nicotine-Stimulated Choroidal Neovascularization
Author(s) -
Katsuji Kiuchi,
Masato Matsuoka,
Jenny Wu,
Raquel Lima e Silva,
Muralitharan Kengatharan,
Verghese Mary,
Shinji Ueno,
Katsutoshi Yokoi,
Naw Htee Khu,
John P. Cooke,
Peter A. Campochiaro
Publication year - 2008
Publication title -
investigative ophthalmology and visual science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.935
H-Index - 218
eISSN - 1552-5783
pISSN - 0146-0404
DOI - 10.1167/iovs.07-0089
Subject(s) - mecamylamine , choroidal neovascularization , nicotine , pharmacology , nicotinic agonist , nicotinic acetylcholine receptor , chemistry , medicine , macular degeneration , receptor , ophthalmology
Nicotinic acetylcholine receptors (nAChR) are best known for their role in neurotransmission, but they have recently been demonstrated on vascular endothelial cells. Acetylcholine is their endogenous ligand, but they are also stimulated by nicotine. By stimulating nAChR, nicotine promotes tumor angiogenesis as well as atherosclerotic plaque neovascularization. In this study, the authors investigated the role of nAChR in the pathogenesis of choroidal neovascularization (CNV).

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