This communication examines the possibility that nitric oxide (NO) pro
duction by endothelial cells results from changes in cell membrane flu
idity. Lysophosphatidylcholine (LPC) alters fluidity of the endothelia
l cell membranes causing vascular relaxation. Through membrane alterat
ions LPC influences function of a number of membrane receptors and mod
ulates enzyme activity. As a result of detergent action, lysophosphati
dylcholine (LPC) causes activation of guanylate cyclase, stimulates sy
alytransferase and regulates protein kinase C activity. It has already
been demonstrated that ionic detergents, such as Triton X-100 also ca
use vascular relaxation, possibly induced by NO production from endoth
elial 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.