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112 巻, 5 号
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安岐 康晴, 安部 陽一, 玉置 俊晃1998 年 112 巻 5 号 p. 287-297
発行日: 1998年
公開日: 2007/01/30
ジャーナル フリーThere has been an intense interest in multiple interacting paracrine systems that influence renal hemodynamics. The contractile responses at different sites along the renal vascular network exhibit distinct characteristics, depending on their receptor populations or activation mechanisms. These differences in effector mechanisms have also coupled with variations in paracrine signals from adjoining endothelial and epithelial cells. In this review, we have focused on the roles of nitric oxide (NO) and adenosine in the regulation of renal microvasculature and how they interact with other vasoactive factors. Vasopressin (VP) V2 receptors as well as V1 receptors exist in renal vasculature, especially in afferent arterioles, and V2-receptor stimulation induced vasodilation. V2-receptor-mediated vasodilation was attenuated by L-NNA. In addition, Ang II did not affect the diameter of isolated rabbit afferent arterioles, but after the treatment of L-NNA, Ang II exerted a dose-dependent vasoconstriction. Thus, NO modulated the renal vascular actions of VP and Ang II. Adenosine causes vasoconstriction via the A1 receptors, which are restricted primarily to the afferent arterioles. This selective action of adenosine suggests that adenosine exerts selective control of the renal vasculature. Adenosine augmented renal vasoconstriction by NE and Ang II via the adenosine A1 receptor, and the A1 receptor antagonist significantly reduced NE- or Ang II-induced renal vasoconstriction. The plurality of these interactions indicates that while it is very important to understand the specific direct cellular actions of each individual factor, it is equally important to understand how the various interactions are orchestrated under in vivo conditions.抄録全体を表示PDF形式でダウンロード (11946K) -
中西 真人, 水口 裕之1998 年 112 巻 5 号 p. 299-305
発行日: 1998年
公開日: 2007/01/30
ジャーナル フリーWe describe a method to prepare unilamellar fusogenic liposomes (FL) that can deliver their content directly into tissue cells and cancer cells of living animals as well as into cultured animal cells. The method consists of three important steps: 1) preparation of unilamellar liposomes encapsulating the molecules to be delivered: 2) preparation of the Sendai virus using fertilized chicken eggs; and 3) preparation of FLs by fusing UV-inactivated Sendai virus particles and naked liposomes. Purified FLs are stable at 4°C for 3 weeks and can be stored indefinitely below −70°C without loss of activity. The FL-mediated delivery is applicable to cells originating from various tissues, including those of humans, monkeys, cows, dogs, mice, rats, hamsters, and rabbits. However, human primary T cells primary B cells, and B cell lines are not susceptible to delivery. FLs are best suited to an examination of the biological activity of cytokines in the tissue cells of living animals. We also describe the possibility of developing FL-based hybrid vectors, which would mimic the functions of viruses and chromosomes.抄録全体を表示PDF形式でダウンロード (7658K) -
遠藤 康男1998 年 112 巻 5 号 p. 307-314
発行日: 1998年
公開日: 2007/01/30
ジャーナル フリーThe histamine-forming enzyme histidine decarboxylase (HDC) is induced in various tissues of mice in response to various physiological or inflammatory stimuli including stress, physical exercise, proinflammatory cytokines and hematopoietic cytokines. The induction of HDC also occurs in mast cell-deficient mice. The newly formed histamine produced through the induction of HDC diffuses away from its site of formation without being stored. Therefore, in addition to the release of histmine from mast cells or basophils, the induction of HDC is an important alternative mechanism for supplying histamine. Studies on the newly formed histamine may clarify new physiological or pathological roles of histamine. Here, we introduce a method that we devised for the simultaneous assay of HDC activity of many samples taken from mice. This method is based on (i) a simple method for the preparation of histamine-free enzyme solutions and (ii) a simple manual method for the separation of histamine formed in reaction mixtures containing HDC.抄録全体を表示PDF形式でダウンロード (8604K) -
内井 雅子, 高嶋 みゆき, 杉山 朋美, 小坂 信夫1998 年 112 巻 5 号 p. 315-321
発行日: 1998年
公開日: 2007/01/30
ジャーナル フリー閉経後骨粗繧症モデルである卵巣摘除ラットの骨代謝に対するKW-8232の作用を6週間の経口投与で検討した．KW-8232は，卵巣摘除による大腿骨および脛骨の骨密度低下を1mg/kgから有意に抑制した．卵巣摘除によって，骨代謝の高回転型マーカーである血清アルカリホスファターゼおよびオステオカルシン濃度は上昇し，また，骨吸収のマーカーである尿中ヒドロキシプロリン，ピリジノリンおよびデオキシピリジノリン排泄も増加した．KW-8232は，血清アルカリホスファターゼ濃度の上昇を10mg/kg以上で抑制し，血清オステオカルシン濃度の上昇には3mg/kgで有意に抑制した．一方，KW-8232は尿中ヒドロキシプロリン，ピリジノリンおよびデオキシピリジノリン排泄の増加を1mg/kgでも著明に抑制した．KW-8232は血清カルシウム濃度には影響しなかったが，尿中カルシウム排泄に対しては10mg/kg以上で有意に抑制した．以上の結果から，卵巣摘除により骨代謝の高回転が骨量低下の成因の一つであり，KW-8232は骨吸収を強く抑制することによって，骨量低下を抑制することが示唆された．抄録全体を表示PDF形式でダウンロード (7335K) -
加藤 義則, 田中 衛, 川島 英敏1998 年 112 巻 5 号 p. 323-331
発行日: 1998年
公開日: 2007/01/30
ジャーナル フリー急性胃炎のモデルとして，タウロコール酸と塩酸で誘発した急性胃粘膜傷害モデルを用い，テプレノンの急性胃粘膜傷害抑制作用をゲファルネートと比較した．タウロコール酸160mMおよび塩酸250mMの溶液をラットに経口投与することにより，胃粘膜表層における出血および糜爛が起こり，粘膜下織の浮腫および粘膜表層のPAS染色性も低下した．前記の肉眼的所見の変化に対して，テプレノンは50mg/kg以上の用量で，有意な胃底腺部粘膜傷害の改善を示した．一方，ゲファルネートは50mg/kgで抑制傾向を，200mg/kgで有意な抑制を示した．組織形態学的所見における棄燗に対してテプレノン50mg/kgで抑制傾向を，同部位のPAS反応性低下に対して同薬は50および200mg/kgで有意な抑制および抑制傾向を示し，ゲファルネート両群も有意な抑制を示した．しかし，幽門部粘膜のPAS反応性低下に対して，ゲファルネート群では対照群と変わらなかったが，テプレノン群では抑制傾向を示した．抄録全体を表示PDF形式でダウンロード (11660K)
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