Corticosteroid receptors macrophages and cardiovascular disease

Cells of the zona fasciculata and zona reticularis lack aldosterone synthase (CYP11B2) that converts corticosterone to aldosterone, and thus these tissues produce only the weak mineralocorticoid corticosterone. However, both these zones do contain the CYP17A1 missing in zona glomerulosa and thus produce the major glucocorticoid, cortisol. Zona fasciculata and zona reticularis cells also contain CYP17A1, whose 17,20-lyase activity is responsible for producing the androgens, dehydroepiandosterone (DHEA) and androstenedione. Thus, fasciculata and reticularis cells can make corticosteroids and the adrenal androgens, but not aldosterone.

Fortunately, effective stress-management strategies can diminish the ill effects of stress. The presence of intact, strong, supportive social support networks among friends, family, educational and religious or other group affiliations can help reduce the subjective experience of stress during the teen years. Recognition of the problem and helping teens develop stress-management skills can also be valuable preventive measures. In severe cases, a physician or other health-care professional can recommend counseling or other treatments that can reduce the long-term risks of teen stress.

steroid ster·oid (stěr'oid', stēr'-)
n.
Any of numerous naturally occurring or synthetic fat-soluble organic compounds having as a basis 17 carbon atoms arranged in four rings and including the sterols and bile acids, adrenocortical and sex hormones, certain natural drugs such as digitalis compounds, and the precursors of certain vitamins. Also called steroid hormone . adj. ste·roid·al (stĭ-roid', stě-)
Relating to or characteristic of steroids or steroid hormones.

Glucocorticoids are potent anti-inflammatories, regardless of the inflammation's cause; their primary anti-inflammatory mechanism is lipocortin-1 (annexin-1) synthesis. Lipocortin-1 both suppresses phospholipase A2 , thereby blocking eicosanoid production, and inhibits various leukocyte inflammatory events ( epithelial adhesion , emigration , chemotaxis , phagocytosis , respiratory burst , etc.). In other words, glucocorticoids not only suppress immune response, but also inhibit the two main products of inflammation, prostaglandins and leukotrienes . They inhibit prostaglandin synthesis at the level of phospholipase A2 as well as at the level of cyclooxygenase /PGE isomerase (COX-1 and COX-2), [29] the latter effect being much like that of NSAIDs , potentiating the anti-inflammatory effect.

Corticosteroid receptors macrophages and cardiovascular disease

corticosteroid receptors macrophages and cardiovascular disease

Glucocorticoids are potent anti-inflammatories, regardless of the inflammation's cause; their primary anti-inflammatory mechanism is lipocortin-1 (annexin-1) synthesis. Lipocortin-1 both suppresses phospholipase A2 , thereby blocking eicosanoid production, and inhibits various leukocyte inflammatory events ( epithelial adhesion , emigration , chemotaxis , phagocytosis , respiratory burst , etc.). In other words, glucocorticoids not only suppress immune response, but also inhibit the two main products of inflammation, prostaglandins and leukotrienes . They inhibit prostaglandin synthesis at the level of phospholipase A2 as well as at the level of cyclooxygenase /PGE isomerase (COX-1 and COX-2), [29] the latter effect being much like that of NSAIDs , potentiating the anti-inflammatory effect.

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