A large body of the evidence is available to the causative relationship between the elevated blood plasma concentrations of LDL and the atherogenesis. The oxid-LDL (modified LDL) is internalized more rapidly by the macrophages, and there is now substantial evidence that the modified LDL is actually present in atherosclerotic lesions. Recently it has been proved that the endothel cells and monocyta/macrophages generate nitric oxide (NO) from arginine, and that the LDL inhibits the formation of NO in endothel cells. The authors found that the human LDL in vitro exerts an inhibitory effect on the formation of NO in murine PED (peritoneal exudate cells) and synchronously severalfold increasing of the arginase activity in the culture media. Both effects of LDL proved to be dose dependent and the oxid-LDL has been found to be more effective. The increased activity of arginase provides a very likely explanation for the reducing of NO production in macrophage treated by LDL. The reducing or blocking of NO-formation causes a local vasocontraction which induces clinical symptoms.
|Number of pages||4|
|Publication status||Published - May 31 1992|
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