Affiliations: Department of Internal Medicine, School of Medicine, Keio University, Tokyo, 160 Japan | Department of Biochemistry, School of Medicine, Keio University, Tokyo, 160 Japan | Department of Bioengineering and Whitaker Institute for Biomedical Engineering, University of California, San Diego, La Jolla, CA 92093‐0412, USA
Note: [] Correspondence: Dr Geert W. Schmid‐Schönbein, Department of Bioengineering and Whitaker Institute for Biomedical Engineering, University of California, San Diego, La Jolla, CA 92093‐0412, USA. Tel.: +1 858 534 3852; Fax: +1 858 534 6896; E‐mail: gschmidt@ucsd.
Abstract: The mechanisms that lead to organ injury in hypertension are incompletely understood. In particular, there is a lack of evidence that serves to link the elevation of arterial blood pressure with end organ damage. Experimental models of hypertension have a range of microvascular abnormalities in addition to a shift in blood pressure. There is evidence for an oxidative stress in microvascular endothelium derived from xanthine and NADPH oxidase. Furthermore, there exists an immune suppression accompanied by abnormally elevated circulating leukocyte counts, depression of selectin membrane adhesion to the endothelium and enhanced cell apoptosis. Many of the deficiencies in the spontaneously hypertensive rats can be corrected by adrenalectomy, suggesting a contribution of glucocorticoids to the abnormalities in this model. These observations suggest a significantly enhanced vascular oxidative stress which is accompanied by a frustrated inflammatory response due to a glucocorticoid dependent deficiency of leukocyte adhesion to vascular endothelium.
