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Artigo de periodico
High-fat diet increases O-GlcNAc levels in cerebral arteries: a link to vascular dysfunction associated with hyperlipidaemia/obesity ? (2016)
Lima, Victor L.; Giachini, Fernanda R.; Matsumoto, Takayuki; Li, Weiguo; Bressan, Alecsander F. M.; Chawla, Dhruv; Webb, R. Clinton; Ergul, Adviye; Tostes, Rita de Cássia Aleixo
Fonte: Clinical Science. Unidade: FMRP
Assuntos: ARTÉRIAS CEREBRAIS, HIPERLIPIDEMIA, PROTEÍNAS QUINASES, OBESIDADE
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ABNT
LIMA, Victor L. et al. High-fat diet increases O-GlcNAc levels in cerebral arteries: a link to vascular dysfunction associated with hyperlipidaemia/obesity ?. Clinical Science, v. 130, n. 11, p. 871-881, 2016Tradução . . Disponível em: https://doi.org/10.1042/CS20150777. Acesso em: 13 set. 2024.
APA
Lima, V. L., Giachini, F. R., Matsumoto, T., Li, W., Bressan, A. F. M., Chawla, D., et al. (2016). High-fat diet increases O-GlcNAc levels in cerebral arteries: a link to vascular dysfunction associated with hyperlipidaemia/obesity ? Clinical Science, 130( 11), 871-881. doi:10.1042/CS20150777
NLM
Lima VL, Giachini FR, Matsumoto T, Li W, Bressan AFM, Chawla D, Webb RC, Ergul A, Tostes R de CA. High-fat diet increases O-GlcNAc levels in cerebral arteries: a link to vascular dysfunction associated with hyperlipidaemia/obesity ? [Internet]. Clinical Science. 2016 ; 130( 11): 871-881.[citado 2024 set. 13 ] Available from: https://doi.org/10.1042/CS20150777
Vancouver
Lima VL, Giachini FR, Matsumoto T, Li W, Bressan AFM, Chawla D, Webb RC, Ergul A, Tostes R de CA. High-fat diet increases O-GlcNAc levels in cerebral arteries: a link to vascular dysfunction associated with hyperlipidaemia/obesity ? [Internet]. Clinical Science. 2016 ; 130( 11): 871-881.[citado 2024 set. 13 ] Available from: https://doi.org/10.1042/CS20150777
Artigo de periodico
Constrictor prostanoids and uridine adenosine tetraphosphate: vascular mediators and therapeutic targets in hypertension and diabetes (2015)
Matsumoto, Takayuki; Goulopoulou, Styliani; Taguchi, Kumiko; Tostes, Rita de Cássia Aleixo; Kobayashi, Tsuneo
Fonte: British Journal of Pharmacology. Unidade: FMRP
Assuntos: ENDOTÉLIO VASCULAR, ADENOSINA, HIPERTENSÃO, DIABETES MELLITUS
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ABNT
MATSUMOTO, Takayuki et al. Constrictor prostanoids and uridine adenosine tetraphosphate: vascular mediators and therapeutic targets in hypertension and diabetes. British Journal of Pharmacology, v. 172, n. 16, p. 3980-4001, 2015Tradução . . Disponível em: https://doi.org/10.1111/bph.13205. Acesso em: 13 set. 2024.
APA
Matsumoto, T., Goulopoulou, S., Taguchi, K., Tostes, R. de C. A., & Kobayashi, T. (2015). Constrictor prostanoids and uridine adenosine tetraphosphate: vascular mediators and therapeutic targets in hypertension and diabetes. British Journal of Pharmacology, 172( 16), 3980-4001. doi:10.1111/bph.13205
NLM
Matsumoto T, Goulopoulou S, Taguchi K, Tostes R de CA, Kobayashi T. Constrictor prostanoids and uridine adenosine tetraphosphate: vascular mediators and therapeutic targets in hypertension and diabetes [Internet]. British Journal of Pharmacology. 2015 ; 172( 16): 3980-4001.[citado 2024 set. 13 ] Available from: https://doi.org/10.1111/bph.13205
Vancouver
Matsumoto T, Goulopoulou S, Taguchi K, Tostes R de CA, Kobayashi T. Constrictor prostanoids and uridine adenosine tetraphosphate: vascular mediators and therapeutic targets in hypertension and diabetes [Internet]. British Journal of Pharmacology. 2015 ; 172( 16): 3980-4001.[citado 2024 set. 13 ] Available from: https://doi.org/10.1111/bph.13205
Artigo de periodico
Diabetes impairs the vascular effects of aldosterone mediated by G protein-coupled estrogen receptor activation (2015)
Ferreira, Nathanne S.; Cau, Stefany B. A; Silva, Marcondes A. B.; Manzato, Carla Pavan; Mestriner, Fabiola Leslie Antunes Cardoso; Matsumoto, Takayuki; Carneiro, Fernando Silva; Passaglia, Rita de Cassia Aleixo Tostes
Fonte: Frontiers in Pharmacology. Unidade: FMRP
Assuntos: ALDOSTERONA, CÉLULAS ENDOTELIAIS, DIABETES MELLITUS, RECEPTORES HORMONAIS, MODELOS ANIMAIS
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ABNT
FERREIRA, Nathanne S. et al. Diabetes impairs the vascular effects of aldosterone mediated by G protein-coupled estrogen receptor activation. Frontiers in Pharmacology, v. 6, 2015Tradução . . Disponível em: https://doi.org/10.3389/fphar.2015.00034. Acesso em: 13 set. 2024.
APA
Ferreira, N. S., Cau, S. B. A., Silva, M. A. B., Manzato, C. P., Mestriner, F. L. A. C., Matsumoto, T., et al. (2015). Diabetes impairs the vascular effects of aldosterone mediated by G protein-coupled estrogen receptor activation. Frontiers in Pharmacology, 6. doi:10.3389/fphar.2015.00034
NLM
Ferreira NS, Cau SBA, Silva MAB, Manzato CP, Mestriner FLAC, Matsumoto T, Carneiro FS, Passaglia R de CAT. Diabetes impairs the vascular effects of aldosterone mediated by G protein-coupled estrogen receptor activation [Internet]. Frontiers in Pharmacology. 2015 ; 6[citado 2024 set. 13 ] Available from: https://doi.org/10.3389/fphar.2015.00034
Vancouver
Ferreira NS, Cau SBA, Silva MAB, Manzato CP, Mestriner FLAC, Matsumoto T, Carneiro FS, Passaglia R de CAT. Diabetes impairs the vascular effects of aldosterone mediated by G protein-coupled estrogen receptor activation [Internet]. Frontiers in Pharmacology. 2015 ; 6[citado 2024 set. 13 ] Available from: https://doi.org/10.3389/fphar.2015.00034
Artigo de periodico
Linking the beneficial effects of current therapeutic approaches in diabetes to the vascular endothelin system (2014)
Matsumoto, Takayuki; Lopes, Rheure A. M.; Taguchi, Kumiko; Kobayashi, Tsuneo; Tostes, Rita de Cassia Aleixo
Fonte: Life Science. Unidade: FMRP
Assuntos: DIABETES MELLITUS, ENDOTÉLIO VASCULAR, MÚSCULO LISO VASCULAR, ENDOTELINAS
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ABNT
MATSUMOTO, Takayuki et al. Linking the beneficial effects of current therapeutic approaches in diabetes to the vascular endothelin system. Life Science, v. 118, n. 2, p. 129-135, 2014Tradução . . Disponível em: https://doi.org/10.1016/j.lfs.2013.12.216. Acesso em: 13 set. 2024.
APA
Matsumoto, T., Lopes, R. A. M., Taguchi, K., Kobayashi, T., & Tostes, R. de C. A. (2014). Linking the beneficial effects of current therapeutic approaches in diabetes to the vascular endothelin system. Life Science, 118( 2), 129-135. doi:10.1016/j.lfs.2013.12.216
NLM
Matsumoto T, Lopes RAM, Taguchi K, Kobayashi T, Tostes R de CA. Linking the beneficial effects of current therapeutic approaches in diabetes to the vascular endothelin system [Internet]. Life Science. 2014 ; 118( 2): 129-135.[citado 2024 set. 13 ] Available from: https://doi.org/10.1016/j.lfs.2013.12.216
Vancouver
Matsumoto T, Lopes RAM, Taguchi K, Kobayashi T, Tostes R de CA. Linking the beneficial effects of current therapeutic approaches in diabetes to the vascular endothelin system [Internet]. Life Science. 2014 ; 118( 2): 129-135.[citado 2024 set. 13 ] Available from: https://doi.org/10.1016/j.lfs.2013.12.216
Artigo de periodico
Alterations in vaso constrictor responses to the endothelium-derived contracting factor uridine adenosine tetraphosphate are region specific in DOCA-salt hypertensive rats (2012)
Matsumoto, Takayuki; Tostes, Rita de Cassia Aleixo; Webb, R. Clinton
Fonte: Pharmacological Research. Unidade: FMRP
Assuntos: HIPERTENSÃO, NUCLEOTÍDEOS, FÁRMACOS (SISTEMA CARDIOVASCULAR)
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ABNT
MATSUMOTO, Takayuki e TOSTES, Rita de Cassia Aleixo e WEBB, R. Clinton. Alterations in vaso constrictor responses to the endothelium-derived contracting factor uridine adenosine tetraphosphate are region specific in DOCA-salt hypertensive rats. Pharmacological Research, v. 65, n. 1, p. 81-90, 2012Tradução . . Disponível em: https://doi.org/10.1016/j.phrs.2011.09.005. Acesso em: 13 set. 2024.
APA
Matsumoto, T., Tostes, R. de C. A., & Webb, R. C. (2012). Alterations in vaso constrictor responses to the endothelium-derived contracting factor uridine adenosine tetraphosphate are region specific in DOCA-salt hypertensive rats. Pharmacological Research, 65( 1), 81-90. doi:10.1016/j.phrs.2011.09.005
NLM
Matsumoto T, Tostes R de CA, Webb RC. Alterations in vaso constrictor responses to the endothelium-derived contracting factor uridine adenosine tetraphosphate are region specific in DOCA-salt hypertensive rats [Internet]. Pharmacological Research. 2012 ; 65( 1): 81-90.[citado 2024 set. 13 ] Available from: https://doi.org/10.1016/j.phrs.2011.09.005
Vancouver
Matsumoto T, Tostes R de CA, Webb RC. Alterations in vaso constrictor responses to the endothelium-derived contracting factor uridine adenosine tetraphosphate are region specific in DOCA-salt hypertensive rats [Internet]. Pharmacological Research. 2012 ; 65( 1): 81-90.[citado 2024 set. 13 ] Available from: https://doi.org/10.1016/j.phrs.2011.09.005
Artigo de periodico
Impaired β-adrenoceptor-induced relaxation in small mesenteric arteries from DOCA-salt hypertensive rats is due to reduced Kca channel activity (2012)
Matsumoto, Takayuki; Szasz, Theodora; Tostes, Rita de Cassia Aleixo; Webb, R. Clinton
Fonte: Pharmacological Research. Unidade: FMRP
Assuntos: VASODILATAÇÃO, ADRENORECEPTORES, ARTÉRIAS, HIPERTENSÃO
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
ABNT
MATSUMOTO, Takayuki et al. Impaired β-adrenoceptor-induced relaxation in small mesenteric arteries from DOCA-salt hypertensive rats is due to reduced Kca channel activity. Pharmacological Research, v. 65, n. 5, p. 537-545, 2012Tradução . . Disponível em: https://doi.org/10.1016/j.phrs.2012.02.004. Acesso em: 13 set. 2024.
APA
Matsumoto, T., Szasz, T., Tostes, R. de C. A., & Webb, R. C. (2012). Impaired β-adrenoceptor-induced relaxation in small mesenteric arteries from DOCA-salt hypertensive rats is due to reduced Kca channel activity. Pharmacological Research, 65( 5), 537-545. doi:10.1016/j.phrs.2012.02.004
NLM
Matsumoto T, Szasz T, Tostes R de CA, Webb RC. Impaired β-adrenoceptor-induced relaxation in small mesenteric arteries from DOCA-salt hypertensive rats is due to reduced Kca channel activity [Internet]. Pharmacological Research. 2012 ; 65( 5): 537-545.[citado 2024 set. 13 ] Available from: https://doi.org/10.1016/j.phrs.2012.02.004
Vancouver
Matsumoto T, Szasz T, Tostes R de CA, Webb RC. Impaired β-adrenoceptor-induced relaxation in small mesenteric arteries from DOCA-salt hypertensive rats is due to reduced Kca channel activity [Internet]. Pharmacological Research. 2012 ; 65( 5): 537-545.[citado 2024 set. 13 ] Available from: https://doi.org/10.1016/j.phrs.2012.02.004

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