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Your search keyword '"Nakagawa, Masao"' showing total 20 results
Start Over Author "Nakagawa, Masao" Journal journal of cardiovascular pharmacology
20 results on '"Nakagawa, Masao"'

2. Bradykinin Inhibits Serum-Depletion-Induced Apoptosis of Human Vascular Endothelial Cells by Inducing Nitric Oxide via Calcium Ion Kinetics

Author

Kono, Yoshihito, primary, Sawada, Shohei, additional, Kawahara, Takeshi, additional, Tsuda, Yutaka, additional, Higaki, Tadashi, additional, Yamasaki, Seiki, additional, Imamura, Hitoshi, additional, Tada, Yusuke, additional, Sato, Toshiyuki, additional, Hiranuma, Osamu, additional, Akamatsu, Naoaki, additional, Komatsu, Sumio, additional, Tamagaki, Toshiyuki, additional, Nakagawa, Katsumi, additional, Tsuji, Hajime, additional, and Nakagawa, Masao, additional

Published
2002
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3. Effect of Cicletanine on the Nitric Oxide Pathway in Human Umbilical Vein Endothelial Cells

Author

Akamatsu, Naoaki, primary, Sawada, Shohei, additional, Komatsu, Sumio, additional, Tamagaki, Toshiyuki, additional, Hiranuma, Osamu, additional, Kawahara, Takeshi, additional, Tsuda, Yutaka, additional, Kono, Yoshihito, additional, Higaki, Tadashi, additional, Tada, Yusuke, additional, Yamasaki, Seiki, additional, Imamura, Hitoshi, additional, Sato, Toshiyuki, additional, Tsuji, Hajime, additional, and Nakagawa, Masao, additional

Published
2001
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4. Interleukin-1α Stimulated Prostacyclin Release by Increasing Gene Transcription of Prostaglandin H Synthase and Phospholipase A2 in Human Vascular Endothelial Cells

Author

Toratani, Akihisa, primary, Sawada, Shohei, additional, Kono, Yoshihito, additional, Higaki, Tadashi, additional, Imamura, Hitoshi, additional, Tada, Yusuke, additional, Yamasaki, Seiki, additional, Sato, Toshiyuki, additional, Komatsu, Sumio, additional, Akamatsu, Naoaki, additional, Tamagaki, Toshiyuki, additional, Nakagawa, Katsumi, additional, Tsuji, Hajime, additional, and Nakagawa, Masao, additional

Published
1999
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6. Blockade of Angiotensin II Receptors Inhibits the Increase in Blood Pressure Induced by Insulin

Author

Nakata, Tetsuo, primary, Takeda, Kazuo, additional, Hatta, Tsuguru, additional, Kiyama, Masahiro, additional, Moriguchi, Jiro, additional, Miki, Shigeyuki, additional, Kawa, Tetsuyoshi, additional, Morimoto, Satoshi, additional, Nakamura, Kazue, additional, Uchida, Atsushi, additional, Itoh, Hiroshi, additional, Sasaki, Susumu, additional, and Nakagawa, Masao, additional

Published
1998
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17. Interleukin-1α Stimulated Prostacyclin Release by Increasing Gene Transcription of Prostaglandin H Synthase and Phospholipase A2in Human Vascular Endothelial Cells

Author

Toratani, Akihisa, Sawada, Shohei, Kono, Yoshihito, Higaki, Tadashi, Imamura, Hitoshi, Tada, Yusuke, Yamasaki, Seiki, Sato, Toshiyuki, Komatsu, Sumio, Akamatsu, Naoaki, Tamagaki, Toshiyuki, Nakagawa, Katsumi, Tsuji, Hajime, and Nakagawa, Masao

Abstract

This study was conducted to evaluate the effects of interleukin-1α (IL-1α) on prostacyclin (PGI2) production in cultured human vascular endothelial cells in association with intracellular Ca2+, inositol 1,4,5-trisphosphate (IP3), and with prostaglandin H synthase (PGHS) and phospholipase A2(PLA2) gene expression by using the competitive polymerase chain reaction (PCR) method. IL-1α did not increase PGI2production for 15 min, but induced an increase of about three-fold relative to that in controls at 60 and 180 min. IL-1α had no effect on intracellular Ca2+levels throughout the experimental period. In this study, consistent with previous reports, PGHS-1 messenger RNA (mRNA) was constitutively expressed, whereas PLA2mRNA was not. After stimulation with IL-1α, PLA2mRNA level showed an eightfold increase within 15 min, and PGHS-2 mRNA level increased by 76-fold within 180 min. PGHS-1 mRNA level was increased 1.6-fold at 180 min. These results suggest the existence of regulatory mechanisms of IL-1α-induced PGI2production, which involve PGHS and PLA2gene transcription.

Published
1999

19. Kinetics of FrequencyDependent Conduction Delay by Class I Antiarrhythmic Drugs in Human Atrium

Author

Sakai, Ryuta, Inoue, Daisuke, Ishibashi, Kazuya, Inoue, Miho, Shirayama, Takeshi, Yamahara, Yasuhiro, Asayama, Jun, and Nakagawa, Masao

Abstract

We investigated use-dependent prolongation of interatrial conduction time (IACT) by class I antiar-rhythmic drugs in 16 patients. Changes in IACT at the initiation of atrial pacing were used to evaluate the onset kinetics. We examined recovery kinetics by giving a single extra stimulus with a varying coupling interval after discontinuing train stimulation. Time constants of the onset kinetics were 1.52 ± 0.15/n(fast) and 0.087 ± 0.031/ n(slow) for mexiletine, 0.075 ± 0.015/n for aprindine, 0.078 ± 0.019/n for disopyramide, and 0.050 ± 0.006/n for pilsicainide. The recovery time constants were 203 ± 66 ms for mexiletine, 1,021 ± 162 ms for aprindine, 993 ± 101 ms for disopyramide, and 2,930 ± 569 ms for pilsicainide. Class I antiarrhythmic drugs produced use-dependent IACT prolongation in humans, with characteristic kinetics for each agent similar to that of depression of the maximum upstroke velocity of cardiac action potential (Vmax) reported in in vitro studies.

Published
1995

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