Papers - ITOH Hiroshi

メタボリックドミノから考える治療戦略とPPAR-γの役割

Itoh Hiroshi, Theodore W. Kurz

Pharma Medica 25 ( 5 ) 199-203 2007.05

Research paper (scientific journal), Joint Work

メタボリックドミノ

Wakino Shu, Itoh Hiroshi

アンチ・エイジング医学 3 ( 2 ) 40(180)-46(186) 2007.05

Research paper (scientific journal), Single Work

E. Addison病

Yokota Kenichi, Shibata Hirotaka, Itoh Hiroshi

内分泌代謝専門医ガイドブック (株式会社診断と治療社)     177-181 2007.04

Research paper (scientific journal), Joint Work

「循環器病学の論点—controversy in cardiology—」メタボリックは存在するか？

Ura Nobuyuki, Itoh Hiroshi, Sone Hirohito, Shimozawa Tatsuo

Therapeutic Research 28 ( 4 ) 547-556 2007.04

Research paper (scientific journal), Joint Work

偽アルドステロン症の重症副作用への疾患別対応

Shibata Hirotaka, Itoh Hiroshi

日本内科学会雑誌 96 ( 4 ) 805（153）-810（158） 2007.04

Research paper (scientific journal), Joint Work

メタボリックシンドロームと高血圧管理—生活習慣病発症予防の観点から—

Sasamura Hiroyuki, Itoh Hiroshi

動脈硬化予防 6 ( 1 ) 63-71 2007.04

Research paper (scientific journal), Joint Work

RA系阻害による高血圧発症抑制の可能性

Sasamura Hiroyuki, Itoh Hiroshi

血圧 14 ( 4 ) 70（426）-75（431） 2007.04

Research paper (scientific journal), Joint Work

アンジオテンシンとアディポカイン（メタボリックシンドロームを含む）

Wakino Shu, Itoh Hiroshi

血圧 14 ( 4 ) 56(412)-60(416) 2007.04

Research paper (scientific journal), Joint Work

メタボリックシンドロームをめぐって—実地医家としての対処法

Itoh Hiroshi, Funabashi Toru, Tshkamoto Kazuhisa, Kadowaki Takashi

Vita 24 ( 2 ) 39526 2007.04

Research paper (scientific journal), Joint Work

メタボリックドミノの概念と治療

Kawai Toshihide, Itoh Hiroshi

PHYSICIAN'S THERAPY MANUAL 4 ( 2 )  2007.04

Research paper (scientific journal), Single Work,  ISSN  1343-3598

メタボリックシンドロームでなぜ組織レニン−アンジオテンシン系が活性されるのか

Ichihara Atsuhiro, Itoh Hiroshi

医学のあゆみ 220 ( 13 ) 1118-1122 2007.03

Research paper (scientific journal), Joint Work

Novel axonal projection from the caudal end of the ventrolateral medulla to the intermediolateral cell column

Iigaya, K., Kumagai, H., Onimaru, H., Kawai, A., Oshima, N., Onami, T., Takimoto, C., Kamayachi, T., Hayashi, K., Saruta, T. and Itoh, H.

Am J Physiol Regul Integr Comp Physiol 292 ( 2 ) R927 - 36 2007.02

ISSN  0363-6119

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We used an optical imaging technique to investigate whether axons of neurons in the caudal end of the ventrolateral medulla (CeVLM), as well as axons of neurons in the rostral ventrolateral medulla (RVLM), project to neurons in the intermediolateral cell column (IML) of the spinal cord. Brain stem-spinal cord preparations from neonatal normotensive Wistar-Kyoto and spontaneously hypertensive rats were stained with a voltage-sensitive dye, and responses to electrical stimulation of the IML at the Th2 level were detected as changes in fluorescence intensity with an optical imaging apparatus (MiCAM-01). The results were as follows: 1) depolarizing responses to IML stimulation during low-Ca high-Mg superfusion were detected on the ventral surface of the medulla at the level of the CeVLM, as well as at the level of the RVLM, 2) depolarizing responses were also detected on cross sections at the level of the CeVLM, and they had a latency of 24.0 +/- 5.5 (SD) ms, 3) antidromic action potentials in response to IML stimulation were demonstrated in the CeVLM neurons where optical images were detected, and 4) glutamate application to the CeVLM increased the frequency of excitatory postsynaptic potentials (EPSPs) and induced depolarization of the IML neurons. The optical imaging findings suggested a novel axonal and functional projection from neurons in the CeVLM to the IML. The increase in EPSPs of the IML neurons in response to glutamate application suggests that the CeVLM participates in the regulation of sympathetic nerve activity and blood pressure and may correspond to the caudal pressor area.

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Developmental activity of the renin-angiotensin system during the "critical period" modulates later L-NAME-induced hypertension and renal injury

Ishiguro, K., Sasamura, H., Sakamaki, Y., Itoh, H. and Saruta, T.

Hypertens Res 30 ( 1 ) 63 - 75 2007.01

ISSN  0916-9636

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The incidence of hypertension and hypertensive renal disease is increasing worldwide, and new strategies to prevent these diseases need to be investigated. The aims of this study were 1) to examine if transient exposure to an angiotensin receptor blocker (ARB) during an early period in hypertension development confers protection against subsequent worsening of hypertension and renal injury induced by the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME), and 2) conversely, to examine the effects of transient exposure to angiotensin II (Ang II) during the same period. First, spontaneously hypertensive rats (SHR) were treated transiently from age 3 to 10 weeks with an ARB (candesartan cilexetil), a calcium channel antagonist or a vasodilator, then taken off treatment for 2 months. Administration of L-NAME at age 18 weeks caused severe hypertension and renal injury. However, the rats that had been exposed to the ARB not only had a lower blood pressure, but also failed to show signs of renal injury or increase of oxidative stress. Furthermore, the elevation of components of the renin-angiotensin-aldosterone system was also suppressed in these rats. In the second study, Wistar-Kyoto rats (WKY) and SHR were exposed to Ang II from age 4 to 8 weeks. The follow-up showed that the blood pressures in the WKY remained elevated compared to controls, while the SHR had heightened increases in blood pressure, renal renin mRNA, and urinary 8-hyroxydeoxyguanosine after L-NAME administration. Together, these experiments demonstrate that transient treatment of rats during an early phase in the development of hypertension with an ARB suppresses the renin-angiotensin-aldosterone system and confers long-term protection against subsequent L-NAME-induced renal injury and increases in renal oxidative stress. Conversely, developmental exposure to Ang II during this "critical" period had the opposite effect, predisposing rats to higher blood pressure, renal injury, and oxidative stress after L-NAME administration.

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Regression of Nephropathy Developed in Diabetes by (Pro)rennin Receptor Blockade

Hidena Takahashi, Atsuhiro Ichihara, Yuki Kaneshiro, Kenta Inomata, Mariyo Sakoda, Tomoko Takemitsu, Akira Nishiyama, Itoh Hiroshi

J Am Soc Nephrol 18   2054-2061 2007

Research paper (scientific journal), Joint Work

Coactivation of the N-terminal transactivation of mineralocorticoid receptor by Ubc9

K. Yokota, H. Shibata, I. Kurihara, S. Kobayashi, N. Suda, A. Murai-Takeda, I. Saito, H. Kitagawa, S. Kato, T. Saruta, Itoh Hiroshi

J Biol Chem 282   1998-2010 2007

Research paper (scientific journal), Joint Work

Novel axonal projection from the caudal end of the ventrolateral medulla to the intermediolateral cell column

K. Iigaya, H. Kumagai, H. Onimaru, A. Kawai, N. Ohshima, T. Onami, C. Takimoto, T. Kamayachi, K. Hayashi, T. Saruta, Itoh Hiroshi

Am. J. Physiol. Regul Integr Comp Physiol  ( 292 ) 927-936 2007

Research paper (scientific journal), Joint Work

Role of nonproteolytically activated prorenin in pathologic, but not physiologic, retinal neovascularization

S. Satofuka, A. Ichihara, N. Nagai, T. Koto, H. Shinoda, K. Noda, Y. Ozawa, M. Inoue, K. Tsubota, Itoh Hiroshi, Y. Oike, S. Ishida

Investigative Ophthalmology & Visual Science  ( 48 ) 422-429 2007

Research paper (scientific journal), Joint Work

Add-on amlodipine improves arterial function and structure in hypertensive patients treated with an angiotensin receptor blocker

A. Ichihara, Y. Kaneshiro, M. Sakoda, T. Takemitsu, Itoh Hiroshi

J. Cardiovasc. Pharmacol  ( 49 ) 161-166 2007

Research paper (scientific journal), Joint Work

Developmental Activity of the Renin-Angiotensin System during the “Critical Period” Modulates Later L-NAME-Induced Hypertension and Renal Injury

Kimiko Ishiguro, Hiroyuki Sasamura, Yusuke Sakamaki, Itoh Hiroshi, Takao Saruta

Hypertens Res 30 ( 1 ) 63-75 2007

Research paper (scientific journal), Joint Work

Adrenomedullin/cyclic AMP pathway induces Notch activation and differentiation of arterial endothelial cells from vascular progenitors

Yurugi-Kobayashi, T., Itoh, H., Schroeder, T., Nakano, A., Narazaki, G., Kita, F., Yanagi, K., Hiraoka-Kanie, M., Inoue, E., Ara, T., Nagasawa, T., Just, U., Nakao, K., Nishikawa, S. and Yamashita, J. K.

Arterioscler Thromb Vasc Biol 26 ( 9 ) 1977 - 84 2006.09

ISSN  1079-5642

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OBJECTIVE: The acquisition of arterial or venous identity is highlighted in vascular development. Previously, we have reported an embryonic stem (ES) cell differentiation system that exhibits early vascular development using vascular endothelial growth factor (VEGF) receptor-2 (VEGFR2)-positive cells as common vascular progenitors. In this study, we constructively induced differentiation of arterial and venous endothelial cells (ECs) in vitro to elucidate molecular mechanisms of arterial-venous specification. METHODS AND RESULTS: ECs were induced from VEGFR2+ progenitor cells with various conditions. VEGF was essential to induce ECs. Addition of 8bromo-cAMP or adrenomedullin (AM), an endogenous ligand-elevating cAMP, enhanced VEGF-induced EC differentiation. Whereas VEGF alone mainly induced venous ECs, 8bromo-cAMP (or AM) with VEGF supported substantial induction of arterial ECs. Stimulation of cAMP pathway induced Notch signal activation in ECs. The arterializing effect of VEGF and cAMP was abolished in recombination recognition sequence binding protein at the Jkappa site deficient ES cells lacking Notch signal activation or in ES cells treated with gamma-secretase inhibitor. Nevertheless, forced Notch activation by the constitutively active Notch1 alone did not induce arterial ECs. CONCLUSIONS: Adrenomedullin/cAMP is a novel signaling pathway to activate Notch signaling in differentiating ECs. Coordinated signaling of VEGF, Notch, and cAMP is required to induce arterial ECs from vascular progenitors.

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