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TAKANO Hiromichi

    Graduate School of Medical Sciences Department of Cell Physiology　Assistant Professor
Contact： takanohimed.nagoya-cu.ac.jp
Last Updated :2024/04/24

Researcher Information

J-Global ID

Research Interests

  • ショック   平滑筋   内皮細胞   血管   

Research Areas

  • Life sciences / Physiology

Association Memberships

  • Physiological society of Japan   

Published Papers

MISC

Research Grants & Projects

  • 日本学術振興会：科学研究費助成事業
    Date (from‐to) : 2021/04 -2026/03 
    Author : 高野 博充; 服部 友紀
     
    肺スライス標本作成方法を以下のように確立した。麻酔ご脱血したラットを開胸して気管に挿入したカニューレから37度のゼラチン溶液を注入後、20度以下に冷却した。ゼラチン硬化確認後摘出した肺を冷却クレブス液中でスライスして厚さ500μmの標本を作成した。このスライス標本を36℃のクレブス液で灌流することでゼラチンを洗い流した後、血管直径測定システムを用いて、この断面に見える脈管の直径を測定することができるようになった。次に敗血症モデルラットをラット微静脈からグラム陰性菌リポ多糖類（LPS）を5mg/Kg静注することにより作成し、LPS投与前（control）、翌日（DAY1）、三日後（DAY3）および六日後（DAY6）に肺スライス標本を作製して直径300 - 500μmの肺動脈の血管反応を観察した。全群で1μMのαアゴニストphenylephrine（phe）は持続的な収縮を起こしたが、LPS投与群ではこの収縮は有意に減弱していた。phe収縮中、1μMアセチルコリン（ACh）を投与すると弛緩が生じたが、DAY1では減弱していた。これらの弛緩反応は内皮除去すると観察されなくなった。Controlでは10μMのNO合成酵素阻害剤nitro-L arginine（LNA）存在下によりこのACh弛緩は抑制され、一過性弛緩に転じた。DAY3ではこのLNA非感受性弛緩反応は増大し、intermediate conductance Ca2+ activated K+チャネルブロッカーTRAM-34（1 μM）によりほとんど抑制された。以上の結果から、肺動脈の収縮はLPSにより抑制されること、内皮からのNOによる弛緩反応がLPS暴露翌日には抑制されるが以後回復すること、内皮依存性過分極による弛緩反応がLPS暴露後三日後に増強することが分かった。
  • Japan Society for the Promotion of Science：Grants-in-Aid for Scientific Research
    Date (from‐to) : 2013/04 -2016/03 
    Author : Takano Hiromichi
     
    The hepatic vein was isolated from the liver in guinea pig and was measured the vasoconstriction and the intracellular Ca2+ concentration. By the transmural nerve stimulation (TNS) transiently increased the tension of the vein. Phenylephrine increased the tension. These responses were not inhibited by nifedipne. Cyclopiazonic acid (CPA) and Y-27632 inhibited the responses. TNS also elicited a transient increase of the cytosolic Ca2+ concentrationx The response was inhibited in presence of tetrodotoxin or phentolamin. Phenylephrine also increased the cytosolic Ca2+. These cytosolic Ca2+ responses were inhibited in presence of CPA. These results suggest that, in the guinea pig hepatic vein, adrenergic nerves stimulate α receptor, which induce the increase of the cytosolic Ca2+ mainly through the intracellular Ca2+ stores or ROK signal, and evoked vasoconstriction to increase the vascular resistance.
  • Japan Society for the Promotion of Science：Grants-in-Aid for Scientific Research
    Date (from‐to) : 2011 -2012 
    Author : TAKANO Hiromichi
     
    The hepatic vein in guinea-pig was isolated from the liver to measure the vasoconstriction and membrane potential responses. Transmural nerve stimulation (TNS) evoked a significantly transient increase of the tension of the vessel. Phentolamine inhibited the vasoconstriction. Atropione decreased the duration of the vasoconstriction. In presence of both of atropine and guanethidine, the TNS evoked vasoconstriction was abolished. Phenylephrine (Phe) evoked the vasoconstriction dose-dependent manner. Noradrenaline (NA 1 - 3 μM) also evoked the vasoconstriction, but 10 μM NA inhibited the vasoconstriction. Acetylcholine (ACh)evoked the vasoconstriction. During Phe-evoked vasoconstriction, ACh increased the tension more. The resting membrane potential of the vessel was -45 ±5 mV. Both ACh and Phe depolarized the membrane (3 mV). These results suggests that the guinea-pig hepatic vein innervated by both adrenergic and cholinergic nerves. The vasoconstriction is evoked through α receptors and muscarinic receptors. The vasodilatation is induced by βreceptors.
  • Japan Society for the Promotion of Science：Grants-in-Aid for Scientific Research
    Date (from‐to) : 2011 -2012 
    Author : HASHITANI HIKARU; TAKANO Hiromichi; MITSUI Retsu
     
    Mural cells in bladder suburothelial venules exhibit spontaneous Ca2+ transients arising from IP3-mediated Ca2+ release from sarcoendoplasmic reticulum. Electrical coupling depending on the regenerative nature of L-type Ca2+ channels play a critical role in maintaining intercellular synchrony amongst mural cells. Spontaneous venular constrictions contribute to active drainage of tissue metabolites, and appear to be regulated by sympathetic innervations as well as bioactive substances released from urothelium and detrusor smooth muscle. Mural cells in suburothelial microvasculature consist of NG2(-)/alphaSMA(+) venular mural cells, NG2(+)/alphaSMA(-) capillary pericytes and NG2(+)/alphaSMA(+) arteriolar smooth muscle cells, suggesting that the origin or process of differentiation of venular mural cells may be distinct from that of mural cells in capillary or arteriole.
  • 日本学術振興会：科学研究費助成事業
    Date (from‐to) : 2009 -2010 
    Author : 橋谷 光; 高野 博充
     
    膀胱壁伸展時の粘膜下微小循環の維持に関与していると考えられる粘膜下細静脈の自動性発生の細胞内機構について検討した。 細胞内電位と細静脈径変化の同時記録では、自発活動電位が自動収縮に先行して起こり、いずれの現象もカルシウム(Ca^<2+>)活性化塩素イオンチャネルおよび電位依存性Ca^<2+>チャネル阻害剤により抑制された。細胞内Ca^<2+>イメージングにより輪走・縦走平滑筋細胞において同期した自発Ca^<2+>濃度上昇が認められた。電位依存性Ca^<2+>チャネル阻害剤存在下においても個々の平滑筋細胞においてCa^<2+>Ca^<2+>濃度上昇が認められたが、細胞間の同期性が失われた。平滑筋とは異なる形態を有し、ネットワークを形成する細胞(血管周囲間質細胞)においても同期した自発細胞内Ca^<2+>濃度上昇が発生し、電位依存性Ca^<2+>チャネル阻害剤により同期性は失われたが個々の間質細胞における自発Ca^<2+>濃度上昇は抑制されなかった。以上の結果からは、平滑筋細胞と間質細胞のいずれが自動運動のペースメーカー細胞としての役割を果たしているかは特定できなかったが、小胞体からのCa^<2+>遊離が起点となり、電位依存性Ca^<2+>チャネルによる電気的細胞間連携により自動運動に不可欠な細胞間同期性がもたらされると考えられた。 細静脈の自発収縮は経壁電気刺激により頻度が増加し、その作用はα受容体阻害薬により抑制された。α受容体阻害下では神経刺激により自発収縮の頻度の低下および血管径の拡張を認める場合があり、抑制作用はプβ受容体阻害により拮抗された。外因性アセチルコリンは濃度依存性に自発収縮の頻度を増加させ血管径を減少させた。排尿筋層のみを除去した尿路上皮を含む標本でも自発収縮を認めたが、神経刺激により持続的な収縮が起こり、またカプサイシン投与により自発収縮の抑制が認められた。以上より細静脈の自発収縮は神経および尿路上皮から放出される生理活性物質により制御されることが示唆された。
  • Japan Society for the Promotion of Science：Grants-in-Aid for Scientific Research
    Date (from‐to) : 2008 -2009 
    Author : TAKANO Hiromichi
     
    The effects of endotoxemia on the diameter change and the membrane potential of submucosal arteriole in guinea pig small intestine were simultaneously measured. The endotoxemia did not significantly change the membrane potential. Acetylcholine (Ach) repolarized and relaxed the vessel in presence of BaCl. Endotoximia inhibited these effects of ACh. The repolarization and vasorelaxation were due to the activation of the two types of the calcium dependent potassium channels. No difference on the role of these channels was observed between the control and the endotiximia model.
  • Japan Society for the Promotion of Science：Grants-in-Aid for Scientific Research
    Date (from‐to) : 2006 -2007 
    Author : SHIBAMOTO Toshishige; KURATA Yasutaka; TAKANO Hiromichi
     
    The main purpose of this study is to measure the hepatic microvascular pressure during circulatory shock in anesthetized rats. The transmural pressure (Pμhv) of the hepatic venule (the diameter 30-50μm) at the liver surface was measured, using a servonull micropipette pressure-measuring system. At first, we compared Pphv with the hepatic occlusion pressures determined with the hepatic vascular occlusion methods developed by the authors (Am. J. Physiol. 286:H121-H130, 2004) in isolated perfused rat livers during the basal states and hepatic venoconstriction induced by norepinephrine, increased blood flow and hepatic anaphylaxis. We found that Pphv is close to the double ooclusion pressure rather than the hepatic venous occlusion pressure. The second, we measured Pphv during anaphylactic hypotension in anesthetized rats. Anaphylactic hypotension was induced by an intravenous injection of 0.6 mg ovalbumin. When the antigen was injected, the systemic arterial pressure decreased profoundly to approximately 45 mmHg, which was accompanied by an increase in Ppv and Pphv: Pphv only transiently increased by 5.7 cmH_2O at lmin and then rapidly returned to the baseline within 2 min, when Ppv continued to increase and reached the peak of 36 cm H_2O at 3.5 min. This indicated that the constriction of the portal veins and the sinusoids much predominate over that of the hepatic veins. Along with this hepatic pre and sinusoidal constriction, the liver lobe thickness significantly decreased by 4% after antigen. Presinusoidal constriction during anaphylactic shock in anesthetized rats increased the portal venous pressure while the hepatic venular pressure only increased slightly and transiently. This predominant presinusoidal constriction is accompanied by a passive decrease in liver volume. Finally, we measured Pphv during endotoxin shock in anesthetized rats. Similar to anaphylactic hypotension, only transient and small increase in Pμhv was observed in response to an intravenous injection of E. coli endotoxin (10〜30mg/kg), indicating that the presinusoidal constriction was predominant during endotoxin shock in anesthetized rats.

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