Membrane function and vascular reactivity

Author:

Bing R. J.1,Termin A.2,Conforto A.1,Dudek R.1,Hoffmann M. J.2

Affiliation:

1. Huntington Medical Research Institutes, Department of Experimental Cardiology, 734 Fairmount Avenue, Pasadena, CA 91105

2. California Institute of Technology, Department of Environmental Engineering, Pasadena, CA 91105

Abstract

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 syalytransferase 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.

Publisher

Portland Press Ltd.

Subject

Cell Biology,Molecular Biology,Biochemistry,Biophysics

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3. Moncada, S., Palmer, R. M. J. and Higgs, E. A. (1991) Nitric oxide: physiology, pathophysiology and pharmacology.Pharmacological Reviews 2:109?142.

4. Bing, R. J. and Saeed, M. (1987) The role of lysolecithin in the relaxation of vascular smooth muscle.Biosci. Rep. 10:783?789.

5. Bing, R. J., Saito, T., Wolf, A. and Menon, N. K. (1988) The effect of phospholipid (lysophosphatidylcholine) on arterial relaxationin vitro andin situ.Trans. Assoc. Am. Phys.,C1:70?78.

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