Chronic stress and probably the accompanying changes in personal behaviours can influence life expectancy. The role of adrenocorticotropic hormone (ACTH) and cortisol in atherosclerosis is not widely accepted and incompletely characterized. Several reports support a role of these hormones in atherogenesis by modulating the function of vascular endothelium, the recruitment of circulating monocytes to the artery wall and their differentiation into macrophages- foam cells, by controlling the expression of pro- and anti-inflammatory interleukins. Previous reports suggested an important role of ACTH and cortisol in the modulation of atherosclerotic plaque progression by removal of excess free cholesterol from macrophages. Studies suggested a crucial role of these hormones on the development of acute coronary syndromes [(ACS); unstable angina, and acute myocardial infarction] and stroke, by modulating platelet aggregation and thrombus formation. This review focuses on the identified mechanisms and roles of ACTH and cortisol in atherogenesis, progression of atherosclerosis and the development of ACS. Finally, it proposes experimental studies to evaluate the therapeutic potential of new glucocorticoid antagonists, the effects that may derive from the inhibition cortisol synthesis and the role of 11beta-hydroxysteroid dehydrogenase type 1 inhibitors in atherogenesis, progression of atherosclerosis and the development of ACS. These hormones may be a possible additional target for the prevention and treatment of atherosclerosis.

Patients with 'inappropriately' normal morning cortisol production had high IL-6 levels. 'Inappropriately' normal cortisol, detected in 75% of UA and 50% of SA patients, may be insufficient for limiting inflammation. These findings have novel clinical implications and suggest new therapeutic approaches in the treatment of these patients.

No abstract

Intracellular cAMP is an ubiquitous intracellular second messenger that regulates important cellular functions. Intracellular cAMP levels are regulated by the enzymes adenylyl cyclase and phosphodiesterases. The role of cAMP in atherosclerosis is not widely accepted and incompletely characterized. Several reports support a role of cAMP in atherogenesis by modulating the function of vascular endothelium, the production of reactive oxygen species, the recruitment of circulating monocytes to the artery wall and their differentiation into macrophages- foam cells, by controlling the expression of pro- and anti-inflammatory interleukins, and regulating serum levels of triglycerides and cholesterol. Previous reports suggested an important role of cAMP in the modulation of atherosclerotic plaque progression by removal of excess free cholesterol from macrophages by inducing the ABCA1 secretory pathway and reducing circulating levels of cholesterol. Studies suggested a crucial role of cAMP on the development of acute coronary syndromes [(ACS); unstable angina, and acute myocardial infarction] and stroke, by modulating platelet aggregation and thrombus formation and the expression of metalloproteinases. This review focuses on the identified mechanisms and roles of cAMP in the prevention of atherosclerosis, atherogenesis, and progression of atherosclerosis and the development of ACS. Finally, it provides evidence that showed the beneficial effects that may derive from the inhibition of phosphodiesterase III and activation of adenylyl cyclase and subsequent elevation of cAMP levels. Thus, cAMP may be a possible target for the prevention and treatment of atherosclerosis.