Endothelin and angiotensin II are the strongest vasoconstrictors. Angiotenin II acts directly by being actively transported through the epithelium and into the abluminal space, where it reacts with multiple smooth muscle cell receptors (Pepine et al, 1997). Endothelin is derived within the endothelium. Along with direct reaction onto a smooth muscle cell receptor, endothelin is feed-forward stimulated by angiotensin II. On the reverse side, endothelium houses nitric oxide, the powerful vasorelaxer. To function, nitric oxide production is stimulated by receptors on the endothelium responding to physical stimuli, such as shear stress, or physiologic stimuli such as bradykinin and acetylcholine. Nitric oxide travels into the smooth muscle cells, where it elevates the level of cyclic GMP, which relaxes the muscle. Also within the endothelium, nitric oxide indirectly increases the function of both prostacyclin and endothelium-derived hyperpolarizing factor. Prostacyclin is transported into the smooth muscle cell and raises the level of cyclic AMP to relax the cell, while endothelium-derived hyperpolarizing factor opens more potassium channels in the smooth muscle cell membrane (Pepine et al, 1997).

The mechanism for atherogenesis is not surely known because of varying evidence of how superoxide anion affects the endothelium. In a simple view, atherogenesis is caused by the immune system response upon the endothelium to the various risk factors. To any degree, these factors all decrease nitric oxide activity. That effect will induce three types of endothelial cell adhesion molecules to be expressed, the most important being vascular cell adhesion molecule-1. A chemoattractant is released and recruits monocytes from the circulation. The monocytes adhere to the endothelium by adhesion cytokines. Low-density lipoproteins-present in practically all individuals' endothelium of the developed world-freely move in and out of the tunica intima. The endothelium and smooth muscle cells produce superoxide anions, or oxygen free radicals. The anions invoke the monocytes to migrate into the intima, as well as promote more monocyte adhesion to the endothelium (Sheppard & Davies, 1998). The monocytes in the intima convert into macrophages, and do nothing until the next critical step. A small portion of the lipids within the intima is oxidized by the superoxide anions. The macrophages' scavenger receptors take up some of this lipid. Because the receptors do not down-regulate, lipid uptake continues and transforms the macrophages into foam cells (Sheppard & Davies, 1998). The foam cells lie in the intima and form the lesion of the endothelium. When death of the foam cell occurs, the lipids inside move out and form the lipid core of an atheroma. Continual lipid deposition, smooth muscle proliferation, an

Some common words found in the essay are:
PAI-1 PAI-1, , Sheppard Davies, Angiotensin II, Angiotenin II, VIIIa Platelet, GMP L-arginine, PAI-1 Stimuli, nitric oxide, smooth muscle, et al, II PAI-1, al 1997, pepine et al, pepine et, et al 1997, smooth muscle cell, muscle cell, angiotensin ii, angiotensin-converting enzyme, smooth muscle cells, muscle cells, coronary artery, coronary artery disease,
Approximate Word count = 1905
Approximate Pages = 8 (250 words per page double spaced)