Abstract
One of the substances important for homeostasis, released by vascular endothelial cells, is the Endothelium Derived Relaxing Factor (EDRF/NO) (1). It resembles the biological activity of PGI2, such as vasodilation, inhibition of platelet aggregation and adhesion, but the cellular “second messenger” for this mediator is c-GMP. Both PGI2 and EDRF/NO activity were found to be decreased in atherosclerosis (1). The EDRF/NO activity can be substituted by nitrovasodilators (so called “NO-donors”), such as SIN-I or sodium nitroprusside (NaNP).
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
Similar content being viewed by others
References
S. Moncada, R.M.J. Palmer, and E.A. Higgs, Nitric oxide: Physiology, pathophysiology, and pharmacology.Pharmacol. Rev. 43:109 (1991).
D.P. Hajjar, and B.B. Wexler, Metabolic activity of cholesterol esters in aortic smooth muscle cells is altered by prostaglandins I2 and E2, J. lip. Res. 24:1176 (1983).
D. P. Hajjar, and K.B. Pomerantz, Signal transduction in atherosclerosis: integration of cytokines and the eicosanoid network, FASEB J. 6:2933 (1992).
A. Dembinska-Kiec, A. Zmuda, J. Marcinkiewicz, H. Sinzinger, and R.J. Gryglewski, Influence of NO-donor (SIN-1) on functions of inflammatory cells, Agents Acions 1/2:32 (1991).
B.J. vanLenten, A.M. Fogelman, J. Seager, E. Ribi, M. Haberland, and P. Edwards, Bacterial endotoxin selectively prevents the expression of scavenger-receptor activity on human monocyte macrophages, J. ImmunoL 6:3718 (1985).
J.L. Goldstein, and M.S. Brown, The low-densoty lipoprotein pathway and its relation to atherosclerosis, A Ann Rev. Biochem. 46:897 (1977).
J.L. Goldstein, M.S. Brown, R.G.W. Anderson, D.W. Russel, and W.J. Schneider, Receptor-mediated endocytosis: concepts emerging from the LDL receptor system, Annu. Rev.Cell.BioL 1:1 (1985).
M.S. Brown, and J.L. Goldstein, A receptor-mediated pathway for cholesterol homeostasis, Science 232:34 (1986).
I. Gouni, K. Oka, J. Etienne, and L. Chan, Endotoxin-induced hypertriglyceridemia is mediated by suppression of lipoprotein lipase at a post-transcriptional level, J. Lip. Res. 34:139 (1993).
A. Wilson, R. Schaub, R. Goldstein, and P. Kuo, Suppression of aortic atherosclerosis in cholesterol fed rabbits by purified rabbit interferon, Arteriosclerosis 10:208 (1990).
W. Jessup, D. Mohr, S.P. Gieseg, R.T. Dean, and R. Stocker, The participation of nitric oxide in cell freeand its restriction of macrophage-mediated oxidation of low-density lipoprotein, Biochim. Biophys. Acta. 1180:73(1992).
M.F. Haberecht, D.A. Redburn, M. Nakane, and H.H.H.W. Schmidt, Immunocytochemical and histochemical localization of nitric oxide and soluble guanylyl cyclase in rabbit retina, Endot. 1:7 (1993).
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1995 Springer Science+Business Media New York
About this chapter
Cite this chapter
Dembinska-Kiec, A., Wybranska, I., Miszczuk-Jamska, B., Baczynska, E., Hartwich, J., Goldsztajn, P. (1995). Modulation of LDL and oxy-LDL Catabolism by No-Donors and PGE2 in Human Peripheral Blood Lymphocytes and Rat Macrophages. In: Weissman, B.A., Allon, N., Shapira, S. (eds) Biochemical, Pharmacological, and Clinical Aspects of Nitric Oxide. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1903-4_13
Download citation
DOI: https://doi.org/10.1007/978-1-4615-1903-4_13
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4613-5777-3
Online ISBN: 978-1-4615-1903-4
eBook Packages: Springer Book Archive