@techreport{oai:kindai.repo.nii.ac.jp:00003060,
 author = {東野,  英明 and 丹羽,  淳子 and 田渕,  正樹 and 大島,  佳奈},
 month = {Jan},
 note = {0.2％のM-SHRSP 低塩群で、脳卒中の発症や致死率と脳病変変化が高食塩群よりも抑制されていた。3％トリクロロメチアジド（TCM）のM-SHRSP への投与は、脳卒中発症抑制、eNOS, nNOS mRNA発現上昇、Nox1, p22phox mRNA 発現低下、白血球でのsuperoxide 産生低下、腎内動脈線維化抑制作用を示した。4.0％食塩負荷で増加した遺伝子にKS, Sgne1, Hspa9a, Srpr が、低下したものにgi in PPARsignaling passway, complete cds.[AY539885]があり、何れもシグナル伝達に必須の遺伝子で、総じて食塩過剰摂取は血管機能に悪影響を与えることを示した。（英文） M-SHRSP given the food containing 0.2％ sodium chloride　showed lower incidences of brain stroke, lower fatal rates, lighter pathological changes in cerebral vessel than those of the rats feed foods containing much salt. M-SHRSP given 3.0％ trichloro-methiazide (TCM) were inhibited the incidence of brain stroke. The expressions of eNOS, and nNOS mRNAs were elevated, and NOx1 and p22phox RNAs, superoxide production and fibrous changes in the kidney were inhibited by dosing of TCM. KS, Sgne1 mRNAs were increased at the cortex of kidney in 6- and 9-week-old WKY and SHRSP given 4.0％ sodium chloride for 2 days. New knowledge regarding unfavorable salt effects was obtained as above., 研究種目：基盤研究（C）研究期間：2007～2009課題番号：19500699研究分野：総合領域科研費の分科・細目：生活科学・食生活学, application/pdf},
 title = {塩分過剰摂取による脳血管脆弱化の機序解明},
 year = {2009},
 yomi = {ヒガシノ, ヒデアキ and ニワ, アツコ and タブチ, マサキ and オオシマ, カナ}
}