1. Polymorphisms in endothelial nitric oxide synthase and atherogenesis
Aroon D Hingorani 
Atherosclerosis 
Volume 154, Issue 3, Pages (February 2001)
DOI: /S (00)

2. Fig. 1
Model summarising the mechanism by which common polymorphisms influence the susceptibility to complex disorder such as atherosclerosis. In single gene disorders (left panel) rare mutations in genes result in a major disturbance in the function of the encoded protein that is both necessary and sufficient to result in disease. In contrast in complex disorders (right panel), common polymorphisms cause a subtle alteration in the expression or activity of the encoded protein that is compatible with health but which, in the presence of additional adverse environmental or genetic influences leads to the development of the disease.
Atherosclerosis  , DOI: ( /S (00) )

3. Fig. 2
Nitric oxide is synthesised from l-arginine by eNOS. NO is not stored and therefore regulation of its availability is through changes in the expression or activity of eNOS or through changes in the concentration of endogenous inhibitors or activators.
Atherosclerosis  , DOI: ( /S (00) )

4. Fig. 3
Actions of endothelium-derived NO. NO is highly diffusible and influences the biology of a wide variety of cell types (see text). Most of the actions of NO on target cells are mediated through an elevation in cGMP. GTP, guanosine triphosphate; GC, souble guanylate cyclase; cGMP, cyclic guanosine monophosphate.
Atherosclerosis  , DOI: ( /S (00) )

5. Fig. 4
Comprehensive polymorphism map of human eNOS. (A) Gene organisation (B) Detail of the promotor.
Atherosclerosis  , DOI: ( /S (00) )

6. Fig. 5
Enzymatic studies of recombinant eNOS Glu298 and Asp 298. No discernable differences were detected between these two forms of eNOS with respect to substrate or co-factor/activity relationships or the effects of inhibitors.
Atherosclerosis  , DOI: ( /S (00) )