Microvascular oxidative stress, immune reaction and apoptosis in hypertensives

摘要: The mechanisms that lead to organ injury in hypertension are incompletely understood. In particular, there is a lack of evidence serves link the elevation arterial blood pressure with end damage. Experimental models have range microvascular abnormalities addition shift pressure. There for an oxidative stress endothelium derived from xanthine and NADPH oxidase. Furthermore, exists immune suppression accompanied by abnormally elevated circulating leukocyte counts, depression selectin membrane adhesion enhanced cell apoptosis. Many deficiencies spontaneously hypertensive rats can be corrected adrenalectomy, suggesting contribution glucocorticoids this model. These observations suggest significantly vascular which frustrated inflammatory response due glucocorticoid dependent deficiency endothelium.