CaltechAUTHORS
Published April 1, 1993 | Version public
Journal Article Metadata-only

Membrane function and vascular reactivity

Creators

  • 1. ROR icon Huntington Medical Research Institutes
  • 2. ROR icon California Institute of Technology

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.

Additional Information

© 1993 Plenum Publishing Corporation. Received January 4, 1993. This work was supported by grants from The Council for Tobacco Research, NY; The Herbert J. and Margaret W. Hoover Foundation, Pasadena, CA; The Patron Saint Foundation, Pasadena, CA and Miles Corporation, West Haven, CT. We wish to acknowledge A. Alegria and M. Vanasco for their technical assistance as well as L. DeChaine for her secretarial help.

Additional details

Identifiers

Eprint ID
62906
DOI
10.1007/BF01145958
Resolver ID
CaltechAUTHORS:20151214-155602204

Funding

Council for Tobacco Research
Herbert J. and Margaret W. Hoover Foundation
Patron Saint Foundation
Miles Corporation

Dates

Created
2015-12-15
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Updated
2021-11-10
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