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Your search keyword '"Shirahase, Hiroaki"' showing total 162 results
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162 results on '"Shirahase, Hiroaki"'

3. CDK8 maintains stemness and tumorigenicity of glioma stem cells by regulating the c-MYC pathway

Author

Fukasawa, Kazuya, Kadota, Takuya, Horie, Tetsuhiro, Tokumura, Kazuya, Terada, Ryuichi, Kitaguchi, Yuka, Park, Gyujin, Ochiai, Shinsuke, Iwahashi, Sayuki, Okayama, Yasuka, Hiraiwa, Manami, Yamada, Takanori, Iezaki, Takashi, Kaneda, Katsuyuki, Yamamoto, Megumi, Kitao, Tatsuya, Shirahase, Hiroaki, Hazawa, Masaharu, Wong, Richard W., Todo, Tomoki, Hirao, Atsushi, and Hinoi, Eiichi

Published
2021
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18. Endothelium-dependent relaxation followed by contraction mediated by NK1 receptors in precontracted rabbit intrapulmonary arteries

Author

Shirahase, Hiroaki, Kanda, Mamoru, Kurahashi, Kazuyoshi, and Nakamura, Shohei

Subjects
Male, Nitric Oxide Synthase Type III, Muscle Relaxation, In Vitro Techniques, Pulmonary Artery, Receptors, Neurokinin-1, Substance P, NG-Nitroarginine Methyl Ester, Piperidines, Papers, Benzamides, Benzoquinones, Animals, Endothelium, Vascular, Lipoxygenase Inhibitors, Rabbits, Enzyme Inhibitors, Nitric Oxide Synthase, Muscle Contraction
Abstract

In the present study, we examined whether substance P (SP) and SP methyl ester (SPME), a selective NK(1) agonist, cause biphasic responses consisting of endothelium-dependent relaxation (EDR) and contraction (EDC) in precontracted rabbit intrapulmonary arteries. In arteries contracted with PGF(2alpha) (2x10(-6) M), SP as well as SPME caused only EDR at low concentration (10(-9) M) and EDR followed by EDC at higher concentrations, indicating the involvement of NK(1) receptors. The SP (10(-8) M)-induced EDR was abolished in arteries moderately contracted by PGF(2alpha) (5x10(-7) M) and the EDC in arteries maximally contracted by PGF(2alpha) (10(-5) M), indicating that EDR and EDC are inversely dependent on preexisting tone. Indomethacin (10(-8) - 10(-6) M), a cyclo-oxygenase inhibitor, and ozagrel (10(-8) - 10(-6) M), a TXA(2) synthetase inhibitor attenuated the EDC in the SPME (10(-7) M)-induced biphasic response and markedly potentiated the EDR. AA-861 (10(-8) - 10(-6) M), a 5-lipoxygenase inhibitor, did not affect the EDR or EDC. L-N(G)-nitro-arginine methyl ester (10(-5) - 10(-4) M), a nitric oxide synthase inhibitor, attenuated the EDR and slightly potentiated the EDC. CP-99994 (10(-10) - 10(-8) M), an NK(1) antagonist, attenuated the EDC and potentiated the EDR in the SPME (10(-7) M)-induced biphasic response, while the NK(2) antagonist SR-48968 (10(-9) - 10(-7) M) had no effect. CP-99994 attenuated the SPME (10(-7) M)-induced EDC under EDR-blockade to a greater extent than the EDR under EDC-blockade, indicating that CP-99994 enhanced the EDR component by preferential inhibition of the EDC component. In conclusion, NK(1) agonists caused a biphasic endothelium-dependent response (EDR and EDC) in submaximally precontracted intrapulmonary arteries. The EDC and EDR mediated by NK(1) receptors may play physiological and/or pathophysiological roles in modulation of vascular tone.

Published
2000

23. Hypolipidemic and Antioxidant Activity of the Novel Acyl-CoA:Cholesterol Acyltransferase (ACAT) Inhibitor KY-455 in Rabbits and Hamsters.

Author

Nakamura, Shohei, Kamiya, Shoji, Shirahase, Hiroaki, Kanda, Mamoru, Yoshimi, Akihisa, Tarumi, Tadatsugu, and Kurahashi, Kazuyoshi

Subjects
ANTICHOLESTEREMIC agents, ACYLTRANSFERASES, ANTILIPEMIC agents, HYPOLIPEMIA, ANTIOXIDANTS, DRUGS
Abstract

The hypolipidemic and antioxidant effects of N-(4,6-dimethyl-1-pentylindolin7-yl)-2,2-dimethylpropanamide (CAS 178469-71-1, KY-455), a novel acylCoA:cholesterol acyltransferase (ACAT) inhibitor, were examined in hyperlipidemic rabbits and normolipidemic hamsters. KY-455 inhibited rabbit intestinal, hepatic, macrophage and adrenal ACAT with IC50 values of 0.4, 0.9, 2.9 and 4.1 µmol/l, respectively. KY-455 also inhibited rabbit plasma and LDL-peroxidation (IC50: 0.4 and 1.7 µmol/l, respectively). In rabbits fed a high-cholesterol diet, treatment with KY-455 (30 mg/kg/day) for 8 days markedly lowered serum esterified, free, low-density lipoprotein (LDL)-cholesterol, and hepatic esterified cholesterol levels. KY-455 tended to inhibit ex vivo hepatic ACAT activity 5 h after the final administration. KY-455 also inhibited ex vivo peroxidation of plasma lipids 1 and 5 h after the final administration in rabbits. In normolipidemic hamsters fed a regular diet, treatment with KY-455 (30 mg/kg, twice a day) for 4 days significantly reduced serum esterified, free and LDL-cholesterol, and hepatic esterified and free cholesterol levels. A single administration of KY-455 (30 mg/kg) significantly inhibited ex vivo hepatic ACAT activity in hamsters. In conclusion, KY-455 showed in vitro inhibitory effects on LDL-peroxidation and macrophage ACAT activity at similar concentrations, and in vivo hypolipidemic and ex vivo antioxidative effects at the same dose. Long-term administration of KY-455 is expected to prevent the progress of atherosclerosis by lowering plasma lipid levels, inhibiting both LDLoxidation and accumulation of cholesterol in macrophages. [ABSTRACT FROM AUTHOR]

Published
2004

27. Protective Effects of Iganidipine on Morphological and Functional Changes of Arteries in Hypertensive Dahl Rats.

Author

Shirahase, Hiroaki, Uehara, Yoshio, Kanda, Mamoru, Wada, Katsuo, Ichikawa, Atsuko, Kobayashi, Yoshihiko, and Funahashi, Norio

Subjects
CALCIUM antagonists, CARDIOVASCULAR agents, ARTERIAL diseases, LABORATORY rats, PHARMACODYNAMICS
Abstract

The article presents a study to examine the protective effects of iganidipine, a new water-soluble calcium antagonist, on the morphological and functional changes of arteries in Dahl salt-sensitive (Dahl-S) rats. The results show that iganidipine, in Dahl-S rats fed a high-salt diet, completely prevented all the changes at a sustained-hypotensive dose, and prevented the injuries of peripheral mesenteric arteries (PMA).

Published
1998
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