作者: Jessica M. Osmond , Anne M. Dorrance
DOI: 10.1210/EN.2008-0808
关键词:
摘要: Direct mineralocorticoid receptor (MR) activation with deoxycorticosterone acetate has deleterious effects on the cerebral vasculature. Inhibition of 11beta-hydroxysteroid dehydrogenase type II (11betaHSD2) mimics detrimental elevated mineralocorticoids in heart, but effect enzyme inactivation vasculature is unknown. Therefore, we hypothesized that systemic 11betaHSD2 inhibition carbenoxolone (CBX) would cause remodeling middle artery (MCA) and increase damage caused by ischemia. Six-week-old male Sprague Dawley rats were divided into control CBX (2.5 mg/d) + 0.9% NaCl treated. After 4 wk treatment, used to assess either structure reactivity MCA or response ischemia using occlusion technique. Cerebral was assessed 2,3,5-triphenyltetrazolium chloride staining expressed as a percentage hemisphere infarcted. treatment increased systolic blood pressure (153.2 +/- 7.3 vs. 122.1 4.4 mm Hg; P < 0.05) compared rats. MCAs from treated smaller stiffer than over range intralumenal pressures, indicating inward vessel. significantly ischemic infarct size (27.1 5.4% 14.8 4.2%; 0.05). These data indicate 11betaHSD2, and, thus, disproportionate glucocorticoid MR, results worsens outcome ischemia, further underscoring importance understanding mechanism which MR leads cerebrovascular disease.