Membrane function and vascular reactivity.
This communication examines the possibility that nitric oxide (NO) production by endothelial cells results from changes in cell membrane fluidity. Lysophosphatidylcholine (LPC) alters fluidity of the endothelial cell membranes causing vascular relaxation. Through membrane alterations LPC influences function of a number of membrane receptors and modulates enzyme activity. As a result of detergent action, lysophosphatidylcholine (LPC) causes activation of guanylate cyclase, stimulates sialyltransferase and regulates protein kinase C activity. It has already been demonstrated that ionic detergents, such as Triton X-100 also cause vascular relaxation, possibly induced by NO production from endothelial cells. It is postulated that production of nitric oxide results from changes in membrane viscosity; this may represent a mechanism for its regulation in biological systems.
Huntington Medical Research Institutes, Department of Experimental Cardiology, Pasadena, CA 91105.
R J
RJ
Bing
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Termin
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A
Conforto
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R
Dudek
M J
MJ
Hoffmann
D000818:Animals; D004730:Endothelium, Vascular / Q000502:physiology*; D006801:Humans; D008244:Lysophosphatidylcholines / Q000378:metabolism; D008560:Membrane Fluidity / Q000502:physiology*; D008954:Models, Biological; D009569:Nitric Oxide / Q000378:metabolism; D011956:Receptors, Cell Surface / Q000502:physiology; D014664:Vasodilation / Q000502:physiology
D008244:Lysophosphatidylcholines; D011956:Receptors, Cell Surface; D009569:Nitric Oxide