論文 - 北村 和雄
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Masuyama H., Tsuruda T., Kato J., Imamura T., Asada Y., Stasch J.P., Kitamura K., Eto T.
Hypertension 48 ( 5 ) 972 - 978 2006年11月
掲載種別：研究論文（学術雑誌） 出版者・発行元：Hypertension
It is unknown whether long-term pharmacological stimulation of soluble guanylate cyclase (sGC), elevating intracellular cGMP levels, has a beneficial effect on hypertension. The purpose of this study is to investigate the effects of BAY41-2272, an orally available sGC stimulator, on cardiovascular remodeling in hypertensive rats. Eight-week-old male Wistar rats with hypertension induced by angiotensin II infused subcutaneously at 250 ng/kg per minute were treated orally with a low ([L] 2 mg/kg per day) or high ([H] 10 mg/kg per day) dose of BAY41-2272 for 14 days. BAY41-2272-H partially suppressed the rise in blood pressure and reduced the heart weight (4.20±0.34 versus 3.68±0.20 mg/g; P<0.01), whereas BAY41-2272-L had no effect. However, both doses decreased the angiotensin II-induced left ventricular accumulation of collagen in the perivascular area (L, -20%, P<0.05; H, -30%, P<0.01) and myocardial interstitium (L, -21%, P<0.05; H, -38%, P<0.01), reducing the number of activated fibroblasts surrounding coronary arteries (L, -74%; H, -79%; P<0.05). BAY41-2272 downregulated the angiotensin II-induced left ventricular gene expression of type 1 collagen (L, -41%, P<0.05; H, -49%, P<0.01) and transforming growth factor-β1 (L, -49%, P<0.05; H, -65%, P<0.01). cGMP levels were elevated by BAY41-2272 not only in the left ventricle, but also in cultured cardiac fibroblasts, resulting in reduced thymidine incorporation into the cells. Thus, stimulation of sGC by BAY41-2272 attenuates fibrosis of the left ventricle in rats with angiotensin II-induced hypertension partly in a pressure-independent manner, suggesting an important role for sGC generating cGMP in inhibiting cardiovascular remodeling. © 2006 American Heart Association, Inc.
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Bone and bone related biochemical examinations. Hormone and hormone related substances. Calcitonin gene-related peptide (CGRP) 査読あり
Kenji Kuwasako 1, Kazuo Kitamura
Clin Calcium 16 ( 6 ) 905 - 912 2006年6月
掲載種別：研究論文（学術雑誌）
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Adrenomedullin in mast cells of abdominal aortic aneurysm 査読あり
Tsuruda T., Kato J., Hatakeyama K., Yamashita A., Nakamura K., Imamura T., Kitamura K., Onitsuka T., Asada Y., Eto T.
Cardiovascular Research 70 ( 1 ) 158 - 164 2006年4月
掲載種別：研究論文（学術雑誌） 出版者・発行元：Cardiovascular Research
Objectives: Produced by vascular walls, adrenomedullin (AM) exerts antifibrotic actions in the process of cardiovascular remodeling. The purpose of this study was to examine the pathophysiological role of AM in the development of human abdominal aortic aneurysm (AAA). Methods and results: Immunohistochemical analyses revealed that vascular smooth muscle cells in the media were positive for AM in the early stage of atherosclerotic aorta. Intense immunoreactivity was observed in mast cells of the outer media and adventitia of AAA, and the number of mast cells was greater (p < 0.01) in AAA than in atherosclerotic aorta without any aneurysmal change. To determine the role of AM in mast cells, we examined cultured human mast cell leukemia line-1 (HMC-1) and fibroblasts isolated from AAA patients. Cultured HMC-1 cells were found to express preproAM gene and release AM peptide into the cultured media. When assessed by collagenase-sensitive [3H]proline incorporation and procollagen type I C-peptide secretion, collagen synthesis in co-culture of HMC-1 and the fibroblasts was reduced by 10- 6 mol/L synthetic AM, while conversely, it increased following blockade of the action of endogenous AM with 10 μg/mL anti-AM monoclonal antibody. Conclusion: The present study suggests an anti-fibrotic role for AM released from mast cells, providing new insight into the biological actions of mast cell-derived AM in the development of AAA. © 2006 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.
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レニン・アンジオテンシン系阻害薬を再考する 査読あり
北村和雄
臨床のあゆみ 69 24 - 25 2006年4月
記述言語：日本語 掲載種別：研究論文（学術雑誌）
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長期のベニジピン療法により降圧を超えた動脈硬化度の改善が得られる 査読あり
北 俊弘、鈴木良彦、江藤胤尚、北村和雄
Arterial Stiffness 10 48 - 49 2006年4月
記述言語：日本語 掲載種別：研究論文（学術雑誌）
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Plasma adrenomedullin level and development of hypertension 査読あり
Kato J, Kitamura K, Eto T
J Hum Hypertens 20 566 - 570 2006年4月
記述言語：英語 掲載種別：研究論文（学術雑誌）
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Increased production of adrenomedullin in glomeruli from anti-glomerular basement membrane (GBM) glomerulonephritis rats treated with methylprednisolone. 査読あり
Iwatsubo S, Fujimoto S, Matsumoto M, Sato Y, Hara S, Kitamura K, Eto T
Nephron Exp Nephrol 104 e41 - e47 2006年4月
記述言語：英語 掲載種別：研究論文（学術雑誌）
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Kuwasako K., Cao Y.N., Chu C.P., Iwatsubo S., Eto T., Kitamura K.
Journal of Biological Chemistry 281 ( 11 ) 7205 - 7213 2006年3月
掲載種別：研究論文（学術雑誌） 出版者・発行元：Journal of Biological Chemistry
Receptor activity-modifying proteins (RAMPs) enable calcitonin receptor-like receptor (CRLR) to function as a calcitonin gene-related peptide receptor (CRLR/RAMP1) or an adrenomedullin (AM) receptor (CRLR/RAMP2 or -3). Here we investigated the functions of the cytoplasmic C-terminal tails (C-tails) of human RAMP1, -2, and -3 (hRAMP1, -2, and -3) by cotransfecting their C-terminal deletion or progressive truncation mutants into HEK293 cells stably expressing hCRLR. Deletion of the C-tail from hRAMP1 had little effect on the surface expression, function, or intracellular trafficking of the mutant heterodimers. By contrast, deletion of the C-tail from hRAMP2 disrupted transport of hCRLR to the cell surface, resulting in significant reductions in 125I-hAM binding and evoked cAMP accumulation. The transfection efficiency for the hRAMP2 mutant was comparable with that for wild-type hRAMP2; moreover, immunocytochemical analysis showed that the mutant hRAMP2 remained within the endoplasmic reticulum. FACS analysis revealed that deleting the C-tail from hRAMP3 markedly enhances AM-evoked internalization of the mutant heterodimers, although there was no change in agonist affinity. Truncating the C-tails by removing the six C-terminal amino acids of hRAMP2 and -3 or exchanging their C-tails with one another had no effect on surface expression, agonist affinity, or internalization of hCRLR, which suggests that the highly conserved Ser-Lys sequence within hRAMP C-tails is involved in cellular trafficking of the two AM receptors. Notably, deleting the respective C-tails from hRAMPs had no effect on lysosomal sorting of hCRLR. Thus, the respective C-tails of hRAMP2 and -3 differentially affect hCRLR surface delivery and internalization. © 2006 by The American Society for Biochemistry and Molecular Biology, Inc.
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テルミサルタンが、あらゆる臓器障害に先行して起こる血管内皮機能障害の指標であるNOを増加させたことは、きわめて意義深い 査読あり
北村和雄
Medical Tribune 2006年2月
記述言語：日本語 掲載種別：研究論文（学術雑誌）
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第14回(最終回) アドレノメデュリン 査読あり
加藤丈司、北村和雄、江藤胤尚
血圧 13 ( 2 ) 225 - 227 2006年
掲載種別：研究論文（学術雑誌）
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PAMP単独過剰発現ラットの開発とPAMPの血管新生作用 査読あり
北村和雄、Yuan-NingCao、江藤胤尚
日本内分泌学会雑誌 82 ( 1 ) 116 - 116 2006年
掲載種別：研究論文（学術雑誌）
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アドレノメデュリン 査読あり
北村和雄
日本臨牀 64 ( 2 ) 217 - 221 2006年
掲載種別：研究論文（学術雑誌）
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降圧因子としてのアドレノメデュリンとPAMP 査読あり
北村和雄
循環制御 27 ( 4 ) 312 - 316 2006年
掲載種別：研究論文（学術雑誌）
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糖尿病患者の心血管発症イベントの抑制を目指して:BNPとCRPのイベント発症予測因子としての有用性 査読あり
鶴田敏博、加藤丈司、隅専浩、三嶋和也、今村卓郎、北村和雄、江藤胤尚
日本内分泌学会雑誌 82 ( 2 ) 506 - 506 2006年
掲載種別：研究論文（学術雑誌）
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閉塞性動脈血栓の形成における5-HT2A受容体の関与‐家兎動脈硬化性血栓モデルでの検討 査読あり
西平賢作、山下篤、田中直子、川本理一朗、今村卓郎、山本隆一、北村和雄、浅田祐士郎
血圧 13 ( 9 ) 951 - 954 2006年
掲載種別：研究論文（学術雑誌）
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Effect of adrenomedullin administration on acetic acid-induced colitis in rats 査読あり
芦塚 伸也,石川 直人,加藤 丈司,山家 純一,稲津 東彦,北村 和雄,江藤 胤尚
Peptides 26 2610 - 2615 2005年12月
記述言語：英語 掲載種別：研究論文（学術雑誌）
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Long-term anti-hypertensive therapy with benidipine improves arterial stiffness over blood pressure lowering 査読あり
北 俊弘,Suzuki Y,江藤 胤尚,北村 和雄
Hypertens Res 28 959 - 964 2005年12月
記述言語：英語 掲載種別：研究論文（学術雑誌）
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Adrenomedullin a protective factor for blood vessels 査読あり
加藤 丈司,鶴田 敏博,北 俊弘,北村 和雄,江藤 胤尚
Arterioscler Thromb Vasc Biol 25 2480 - 2487 2005年12月
記述言語：英語 掲載種別：研究論文（学術雑誌）
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Adrenomedullin release in the rat mesenteric resistance artery 査読あり
Akiyama S,Hobara N,Naruo N,Hashida S,北村 和雄,江藤 胤尚,Kawasaki H
Peptides 26 2222 - 2230 2005年11月
記述言語：英語 掲載種別：研究論文（学術雑誌）
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Cao Y.N., Kuwasako K., Kato J., Nishihira K., Asada Y., Eto T., Kitamura K.
FEBS Letters 579 ( 22 ) 4997 - 5001 2005年9月
記述言語：日本語 掲載種別：研究論文（学術雑誌） 出版者・発行元：FEBS Letters
We developed a transgenic (Tg) rat model that overexpresses human proadrenomedullin N-terminal 20 peptide (PAMP) only and then compared the effects of unilateral nephrectomy followed by a high salt diet for five weeks in Tg and wild-type rats. We found that systolic blood pressure was significantly lower in Tg UNX rats and cardiac hypertrophy and myocardial fibrosis was also attenuated in Tg rats. Evaluation of gene expression showed suppression of cardiac local renin-angiotensin system (RAS) in Tg rat. These results suggest that in addition to reducing blood pressure, PAMP suppresses cardiac hypertrophy through negative regulation of the local cardiac RAS. © 2005 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.