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論文

論文
林, 浩孝 ; 大野, 智 ; 橋本, 慎太郎 ; 新井, 隆成 ; 鈴木, 信孝
出版情報: 日本補完代替医療学会誌 = Japanese journal of complementary and alternative medicine.  5  pp.37-47,  2008-01-01.  日本補完代替医療学会 = The Japanese Society for Complementary and Alternative Medicine
URL: http://hdl.handle.net/2297/28432
概要: 「特定保健用食品」のうち,生活習慣病の 1 つである高血圧に関連して「血圧が高めの方に適する」表示をした食品については,現在のところ,再許可等特定保健用食品を含め約 90 種類の商品がある.そのうちのいくつかについて,安全性・有効性について 解説する. Of “foods for specified health use (FOSHU)”, approximately 90 kinds are presently indicated as “appropriate for hypertension”. In this review we describe their safety and effectiveness. 続きを見る
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論文

論文
大桑, 仁
出版情報: 金沢大学十全医学会雑誌.  100  pp.615-631,  1991-08-20.  金沢大学十全医学会
URL: http://hdl.handle.net/2297/8284
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論文

論文
Seok, Young Mi ; Azam, Mohammed Ali ; Okamoto, Yasuo ; Sato, Atsushi ; Yoshioka, Kazuaki ; Maeda, Masataka ; Kim, In Kyeom ; Takuwa, Yoh
出版情報: Hypertension.  56  pp.934-941,  2010-11-01.  American Heart Association
URL: http://hdl.handle.net/2297/25788
概要: 金沢大学医薬保健研究域医学系<br />Rho-mediated inhibition of myosin light chain (MLC) phosphatase (MLCP), together with Ca-depen dent MLC kinase activation, constitutes the major signaling mechanisms for vascular smooth muscle contraction. We recently unveiled the involvement of Ca-induced, phosphoinositide 3-kinase (PI3K) class IIα isoform (PI3K-C2α)-dependent Rho activation and resultant Rho kinase-dependent MLCP suppression in membrane depolarization- and receptor agonist-induced contraction. It is unknown whether Ca- and PI3K-C2α- dependent regulation of MLCP is altered in vascular smooth muscle of hypertensive animals and is involved in hypertension. Therefore, we studied the role of the Ca-PI3K-C2α-Rho-MLCP pathway in spontaneously hypertensive rats (SHRs). PI3K-C2α was readily detected in various vascular beds of Wistar-Kyoto rats and activated by high KCl. High KCl also stimulated vascular Rho activity and phosphorylation of the MLCP regulatory subunit MYPT1 at Thr in a PI3K inhibitor wortmannin-sensitive manner. In mesenteric and other vessels of SHRs at the hypertensive but not the prehypertensive stage, the activity of PI3K-C2α but not class I PI3K p110α was elevated with concomitant rises of Rho activity and Thr-phosphorylation of MYPT1, as compared with normotensive controls. Infusion of the Ca channel antagonist nicardipine reduced blood pressure with suppression of vascular activity of PI3K-C2α-Rho and phosphorylation of MYPT1 in hypertensive SHRs. Infusion of wortmannin lowered blood pressure with inhibition of PI3K-C2α-Rho activities and MYPT1 phosphorylation in hypertensive SHRs. These observations suggest that an increased activity of the Ca-PI3K-C2α-Rho signaling pathway with resultant augmented MLCP suppression contributes to hypertension in SHRs. The Ca- and PI3K-C2α-dependent Rho stimulation in vascular smooth muscle may be a novel, promising target for treating hypertension. © 2010 American Heart Association, Inc. 続きを見る
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論文

論文
米倉, 秀人 ; Yonekura, Hideto
出版情報: 平成11(1999)年度 科学研究費補助金 基盤研究(C) 研究成果報告書概要 = 1999 Fiscal Year Final Research Report Summary.  1998 – 1999  pp.4p.-,  2001-10-22. 
URL: http://hdl.handle.net/2297/00064046
概要: 金沢大学医学部<br />日本人の高血圧症の90%は未だ原因の明らかでない本態性高血圧症に分類される。本研究は、本態性高血圧症の発症・進展に関わる遺伝素因の実体を明らかにするためのアプローチとして、本症モデル動物の血管で発現異常 を示す遺伝子を分離し、その構造と機能を明らかにすることを目的とする。1.ヒト本態性高血圧症のモデル動物である自然発症高血圧ラット(spontaneously hypertensive rat、以下SHR)、その重症型であるSHR-SP(SHR-stroke prone)および正常親株(WKY)の大動脈よりRNAを分離し、蛍光ディファレンシャルディスプレイ法によりSHRおよびSHR-SPで発現増大もしくは低下を示すmRNA分子種の候補を複数種検出した。2.RT-PCR法により、それらに対応するcDNA断片を分離し、これらをプローブとして3種のラットの動脈より分離したRNAを用いてノーザン解析を行ない、1種のmRNAがSHRとSHR-SPの動脈で発現上昇をきたしていることを確認した。3.同定したmRNAに対する全長cDNAをrapid amplification of cDNA ends(RACE)法により分離し、塩基配列を決定した結果、当該mRNAはcyr61のラットホモログであることが明らかとなった。4.cyr61遺伝子の高血圧症発症過程での発現をNorthern法により解析した結果、cyr61 mRNAの大動脈での発現量比はWKY:SHR:SHRSP=1:2.7:3.7(4週齢)、1:2:1.8(6週齢)、1:1.2:1.6(12週齢)であり、cyr61 mRNAはWKYと血圧差の殆どない4週齢から既にSHR、SHRSP大動脈で発現が上昇することが明らかとなった。5.In situ hybridizationの結果、cyr61の発現上昇は大動脈平滑筋細胞での過剰発現のためであった。6.各組織由来のRNAを用いたNorthern blot解析の結果、cyr61 mRNAは大動脈でもっとも強い発現が認められ、心臓がそれに続いた。7.FISH法により、cyr61はラット第1番染色体長腕12-13領域にマップされ、これは従来報告されている高血圧関連QTL(quantitative trait loci)の何れにも属さなかった。<br />For the study of essential hypertension, spontaneously hypertensive rats (SHR) and stroke-prone spontaneously hypertensive rats (SHRSP) have proven to be valuable models. In the present study, we applied a fluorescent differential display method to mRNAs from aortae of SHR, SHRSP and their parental strain, Wistar Kyoto rats (WKY) towards identifying the genes involved in the development of the hypertension, and came across a gene which is consistently upregulated in the hypertensive rats. Nucleotide sequence determination of the corresponding cDNA revealed that the gene is the rat orthologue of cyr61. Northern blot analysis showed that cyr61 expression increases in SHR and SHRSP before the onset of hypertension, and is sustained thereafter at higher levels than in age-matched WKY. In situ hybridization analysis demonstrated that cyr61 is expressed strongly in smooth muscle cells in media, and faintly in fibroblasts in adventitia, of the hypertensive rat aorta, while in WKY the expression is only in fibroblasts. Fluorescent in situ hybridization mapped the cyr61 gene to rat chromosome 1p12-13, which has not been previously reported as a quantitative trait locus for blood pressure regulation. These results suggest that cyr61 is an additional factor which may be involved in the development of systemic hypertension.<br />研究課題/領域番号:10670010, 研究期間(年度):1998 – 1999 続きを見る