through stimulation of guanylate cyclase.
These three factors—leukocyte adhesion, proliferation, and subsequent platelet aggregation—are of great significance in the initial phase of arteriosclerosis. The weakening of the Arg-NO system seems a likely pathogenetic factor in vascular lesions. Several variables are discussed as triggering factors for defects in NOS activity (C): reduced receptor coupling of the agonists, marginal substrate (Arg) or cofactor availability, or inactivation of EDRF (NO) on its way to the site of its intended activity. The latter is blamed mainly on oxidized LDL and/or peroxide anions. In arteriosclerotic vessels, an abnormal vasoconstrictor (endothelin 1) might also form, compensating for the relaxing effect of NO.
Regulatory Functions I
A. NO Synthesis
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