{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,28]],"date-time":"2026-04-28T14:52:49Z","timestamp":1777387969736,"version":"3.51.4"},"reference-count":34,"publisher":"Wiley","issue":"13","license":[{"start":{"date-parts":[[2010,6,11]],"date-time":"2010-06-11T00:00:00Z","timestamp":1276214400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["J of Neuroscience Research"],"published-print":{"date-parts":[[2010,10]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Hypertension reduces endothelial nitric oxide synthase (eNOS) expression and leads to endothelial dysfunction. However, few studies have demonstrated the influences of hypertension on eNOS function in the cerebral cortex. The present study investigates the influences of hypertension on endothelial function in the cerebral cortex and the protective effects of antihypertensive agents against brain ischemia through the preservation of endothelial function. Five\u2010 and ten\u2010week\u2010old male Wistar rats and spontaneously hypertensive rats (SHR) were used for experiments. Five\u2010week\u2010old SHR received olmesartan, hydralazine, or vehicle for 5 weeks in drinking water. eNOS activation in the cerebral cortex was evaluated by analyzing levels of total and Ser<jats:sup>1177<\/jats:sup>\u2010phosphorylated eNOS protein by Western blot. Blood pressure of 10\u2010week\u2010old SHR without treatment was clearly high, and the ratio of phospho\u2010eNOS\/total eNOS protein was significantly low. Five\u2010week treatment with olmesartan or hydralazine suppressed the elevation of blood pressure and the reduction of phosphorylated eNOS\u2010Ser<jats:sup>1177<\/jats:sup> in SHR, and olmesartan was more effective in maintaining phosphorylation of eNOS\u2010Ser<jats:sup>1177<\/jats:sup> than hydralazine. To assess the contribution of eNOS to maintaining cerebral blood flow (CBF), we monitored CBF by laser\u2010Doppler flowmetry after L\u2010N<jats:sup>5<\/jats:sup>\u2010(1\u2010iminoethyl)ornithine (L\u2010NIO) infusion. CBF response to L\u2010NIO was preserved in olmesartan\u2010treated SHR but not in hydralazine\u2010treated SHR. Furthermore, infarct volume 48 hr after transient focal brain ischemia in olmesartan\u2010treated SHR was significantly reduced compared with vehicle\u2010treated SHR. These findings indicate that chronic prehypertensive treatment with olmesartan could attenuate brain ischemic injury through the maintenance of endothelial function in the cerebral cortex in SHR. \u00a9 2010 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/jnr.22441","type":"journal-article","created":{"date-parts":[[2010,6,11]],"date-time":"2010-06-11T20:32:08Z","timestamp":1276288328000},"page":"2889-2898","source":"Crossref","is-referenced-by-count":40,"title":["An angiotensin II type 1 receptor blocker can preserve endothelial function and attenuate brain ischemic damage in spontaneously hypertensive 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