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Artigo de periodico
Mitochondrial aldehyde dehydrogenase prevents ROS-induced vascular contraction in angiotensin-II hypertensive mice (2011)
Choi, Hyehun; Passaglia, Rita de Cassia Aleixo Tostes; Webb, R. Clinton
Source: Journal of the American Society of Hypertension. Unidade: FMRP
Subjects: HIPERTENSÃO, ALDEÍDOS
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
ABNT
CHOI, Hyehun e PASSAGLIA, Rita de Cassia Aleixo Tostes e WEBB, R. Clinton. Mitochondrial aldehyde dehydrogenase prevents ROS-induced vascular contraction in angiotensin-II hypertensive mice. Journal of the American Society of Hypertension, v. 5, n. 3, p. 154-160, 2011Tradução . . Disponível em: https://doi.org/10.1016/j.jash.2011.02.005. Acesso em: 13 nov. 2024.
APA
Choi, H., Passaglia, R. de C. A. T., & Webb, R. C. (2011). Mitochondrial aldehyde dehydrogenase prevents ROS-induced vascular contraction in angiotensin-II hypertensive mice. Journal of the American Society of Hypertension, 5( 3), 154-160. doi:10.1016/j.jash.2011.02.005
NLM
Choi H, Passaglia R de CAT, Webb RC. Mitochondrial aldehyde dehydrogenase prevents ROS-induced vascular contraction in angiotensin-II hypertensive mice [Internet]. Journal of the American Society of Hypertension. 2011 ; 5( 3): 154-160.[citado 2024 nov. 13 ] Available from: https://doi.org/10.1016/j.jash.2011.02.005
Vancouver
Choi H, Passaglia R de CAT, Webb RC. Mitochondrial aldehyde dehydrogenase prevents ROS-induced vascular contraction in angiotensin-II hypertensive mice [Internet]. Journal of the American Society of Hypertension. 2011 ; 5( 3): 154-160.[citado 2024 nov. 13 ] Available from: https://doi.org/10.1016/j.jash.2011.02.005
Artigo de periodico
S-nitrosylation inhibits protein kinase C-mediated contraction in mouse aorta (2011)
Choi, Hyehun; Passaglia, Rita de Cassia Aleixo Tostes; Webb, R. Clinton
Source: Journal of Cardiovascular Pharmacology. Unidade: FMRP
Subjects: SISTEMA CARDIOVASCULAR, PROTEÍNAS QUINASES
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
ABNT
CHOI, Hyehun e PASSAGLIA, Rita de Cassia Aleixo Tostes e WEBB, R. Clinton. S-nitrosylation inhibits protein kinase C-mediated contraction in mouse aorta. Journal of Cardiovascular Pharmacology, v. 57, n. 1, p. 65-71, 2011Tradução . . Acesso em: 13 nov. 2024.
APA
Choi, H., Passaglia, R. de C. A. T., & Webb, R. C. (2011). S-nitrosylation inhibits protein kinase C-mediated contraction in mouse aorta. Journal of Cardiovascular Pharmacology, 57( 1), 65-71.
NLM
Choi H, Passaglia R de CAT, Webb RC. S-nitrosylation inhibits protein kinase C-mediated contraction in mouse aorta. Journal of Cardiovascular Pharmacology. 2011 ; 57( 1): 65-71.[citado 2024 nov. 13 ]
Vancouver
Choi H, Passaglia R de CAT, Webb RC. S-nitrosylation inhibits protein kinase C-mediated contraction in mouse aorta. Journal of Cardiovascular Pharmacology. 2011 ; 57( 1): 65-71.[citado 2024 nov. 13 ]
Artigo de periodico
O-GlcNAcylation: a novel pathway contributing to the effects of endothelin in the vasculature (2011)
Lima, Victor Vitorino; Giachini, Fernanda Regina; Hardy, David M.; Webb, Robert Clinton; Passaglia, Rita de Cassia Aleixo Tostes
Source: American Journal of Physiology: Regulatory, Integrative and Comparative Physiology. Unidade: FMRP
Subjects: SISTEMA CARDIOVASCULAR, ENDOTELINAS
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
ABNT
LIMA, Victor Vitorino et al. O-GlcNAcylation: a novel pathway contributing to the effects of endothelin in the vasculature. American Journal of Physiology: Regulatory, Integrative and Comparative Physiology, v. 300, n. 2, p. R236-R250, 2011Tradução . . Disponível em: https://doi.org/10.1152/ajpregu.00230.2010. Acesso em: 13 nov. 2024.
APA
Lima, V. V., Giachini, F. R., Hardy, D. M., Webb, R. C., & Passaglia, R. de C. A. T. (2011). O-GlcNAcylation: a novel pathway contributing to the effects of endothelin in the vasculature. American Journal of Physiology: Regulatory, Integrative and Comparative Physiology, 300( 2), R236-R250. doi:10.1152/ajpregu.00230.2010
NLM
Lima VV, Giachini FR, Hardy DM, Webb RC, Passaglia R de CAT. O-GlcNAcylation: a novel pathway contributing to the effects of endothelin in the vasculature [Internet]. American Journal of Physiology: Regulatory, Integrative and Comparative Physiology. 2011 ; 300( 2): R236-R250.[citado 2024 nov. 13 ] Available from: https://doi.org/10.1152/ajpregu.00230.2010
Vancouver
Lima VV, Giachini FR, Hardy DM, Webb RC, Passaglia R de CAT. O-GlcNAcylation: a novel pathway contributing to the effects of endothelin in the vasculature [Internet]. American Journal of Physiology: Regulatory, Integrative and Comparative Physiology. 2011 ; 300( 2): R236-R250.[citado 2024 nov. 13 ] Available from: https://doi.org/10.1152/ajpregu.00230.2010
Artigo de periodico
Dysregulation of renal transient receptor potential melastatin 6/7 but not paracellin-1 in aldosterone-induced hypertension and kidney damage in a model of hereditary hypomagnesemia (2011)
Yogi, Álvaro; Callera, Gláucia Elena; O'Connor, Sarah E.; He, Ying; Corrêa, José W.; Passaglia, Rita de Cassia Aleixo Tostes; Mazur, Andrzej; Touyz, Rhian M.
Source: Journal of Hypertension. Unidade: FMRP
Subjects: RIM (DANOS), MAGNÉSIO, FÁRMACOS, INFLAMAÇÃO, PRESSÃO SANGUÍNEA
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
ABNT
YOGI, Álvaro et al. Dysregulation of renal transient receptor potential melastatin 6/7 but not paracellin-1 in aldosterone-induced hypertension and kidney damage in a model of hereditary hypomagnesemia. Journal of Hypertension, v. 29, n. 7, p. 1400-1410, 2011Tradução . . Disponível em: https://doi.org/10.1097/hjh.0b013e32834786d6. Acesso em: 13 nov. 2024.
APA
Yogi, Á., Callera, G. E., O'Connor, S. E., He, Y., Corrêa, J. W., Passaglia, R. de C. A. T., et al. (2011). Dysregulation of renal transient receptor potential melastatin 6/7 but not paracellin-1 in aldosterone-induced hypertension and kidney damage in a model of hereditary hypomagnesemia. Journal of Hypertension, 29( 7), 1400-1410. doi:10.1097/hjh.0b013e32834786d6
NLM
Yogi Á, Callera GE, O'Connor SE, He Y, Corrêa JW, Passaglia R de CAT, Mazur A, Touyz RM. Dysregulation of renal transient receptor potential melastatin 6/7 but not paracellin-1 in aldosterone-induced hypertension and kidney damage in a model of hereditary hypomagnesemia [Internet]. Journal of Hypertension. 2011 ; 29( 7): 1400-1410.[citado 2024 nov. 13 ] Available from: https://doi.org/10.1097/hjh.0b013e32834786d6
Vancouver
Yogi Á, Callera GE, O'Connor SE, He Y, Corrêa JW, Passaglia R de CAT, Mazur A, Touyz RM. Dysregulation of renal transient receptor potential melastatin 6/7 but not paracellin-1 in aldosterone-induced hypertension and kidney damage in a model of hereditary hypomagnesemia [Internet]. Journal of Hypertension. 2011 ; 29( 7): 1400-1410.[citado 2024 nov. 13 ] Available from: https://doi.org/10.1097/hjh.0b013e32834786d6
Artigo de periodico
Transient receptor potential melastatin 7 (TRPM7) cation channels, magnesium and the vascular system in hypertension (2011)
Yogi, Álvaro; Callera, Gláucia Elena; Antunes, Tayze T.; Passaglia, Rita de Cassia Aleixo Tostes; Touyz, Rhian M.
Source: Circulation Journal. Unidade: FMRP
Subjects: SISTEMA CARDIOVASCULAR, HIPERTENSÃO, MAGNÉSIO
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
ABNT
YOGI, Álvaro et al. Transient receptor potential melastatin 7 (TRPM7) cation channels, magnesium and the vascular system in hypertension. Circulation Journal, v. 75, n. 2, p. 237-245, 2011Tradução . . Acesso em: 13 nov. 2024.
APA
Yogi, Á., Callera, G. E., Antunes, T. T., Passaglia, R. de C. A. T., & Touyz, R. M. (2011). Transient receptor potential melastatin 7 (TRPM7) cation channels, magnesium and the vascular system in hypertension. Circulation Journal, 75( 2), 237-245.
NLM
Yogi Á, Callera GE, Antunes TT, Passaglia R de CAT, Touyz RM. Transient receptor potential melastatin 7 (TRPM7) cation channels, magnesium and the vascular system in hypertension. Circulation Journal. 2011 ; 75( 2): 237-245.[citado 2024 nov. 13 ]
Vancouver
Yogi Á, Callera GE, Antunes TT, Passaglia R de CAT, Touyz RM. Transient receptor potential melastatin 7 (TRPM7) cation channels, magnesium and the vascular system in hypertension. Circulation Journal. 2011 ; 75( 2): 237-245.[citado 2024 nov. 13 ]
Artigo de periodico
Vascular proinflammatory responses by aldosterone are mediated via c-Src trafficking to cholesterol-rich microdomains: role of PDGFR (2011)
Callera, Gláucia Elena; Yogi, Álvaro; Briones, Ana Maria; Montezano, Augusto Cesar Inforzato; He, Ying; Passaglia, Rita de Cassia Aleixo Tostes; Schiffrin, Ernesto L; Touyz, Rhian M.
Source: Cardiovascular Research. Unidade: FMRP
Subjects: ALDOSTERONA, CÉLULAS MUSCULARES
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
ABNT
CALLERA, Gláucia Elena et al. Vascular proinflammatory responses by aldosterone are mediated via c-Src trafficking to cholesterol-rich microdomains: role of PDGFR. Cardiovascular Research, v. 91, n. 4, p. 720-731, 2011Tradução . . Disponível em: https://doi.org/10.1093/cvr/cvr131. Acesso em: 13 nov. 2024.
APA
Callera, G. E., Yogi, Á., Briones, A. M., Montezano, A. C. I., He, Y., Passaglia, R. de C. A. T., et al. (2011). Vascular proinflammatory responses by aldosterone are mediated via c-Src trafficking to cholesterol-rich microdomains: role of PDGFR. Cardiovascular Research, 91( 4), 720-731. doi:10.1093/cvr/cvr131
NLM
Callera GE, Yogi Á, Briones AM, Montezano ACI, He Y, Passaglia R de CAT, Schiffrin EL, Touyz RM. Vascular proinflammatory responses by aldosterone are mediated via c-Src trafficking to cholesterol-rich microdomains: role of PDGFR [Internet]. Cardiovascular Research. 2011 ; 91( 4): 720-731.[citado 2024 nov. 13 ] Available from: https://doi.org/10.1093/cvr/cvr131
Vancouver
Callera GE, Yogi Á, Briones AM, Montezano ACI, He Y, Passaglia R de CAT, Schiffrin EL, Touyz RM. Vascular proinflammatory responses by aldosterone are mediated via c-Src trafficking to cholesterol-rich microdomains: role of PDGFR [Internet]. Cardiovascular Research. 2011 ; 91( 4): 720-731.[citado 2024 nov. 13 ] Available from: https://doi.org/10.1093/cvr/cvr131
Artigo de periodico
Uridine adenosine tetraphosphate-induced contraction is increases in renal but not pulmonary arteries from DOCA-salt hypertensive rats (2011)
Matsumoto, Takayuri; Passaglia, Rita de Cassia Aleixo Tostes; Webb, R. Clinton
Source: American Journal of Physiology: Heart and Circulatory Physiology. Unidade: FMRP
Subjects: HIPERTENSÃO, ENDOTÉLIO, ANTAGONISTAS
A citação é gerada automaticamente e pode não estar totalmente de acordo com as normas
ABNT
MATSUMOTO, Takayuri e PASSAGLIA, Rita de Cassia Aleixo Tostes e WEBB, R. Clinton. Uridine adenosine tetraphosphate-induced contraction is increases in renal but not pulmonary arteries from DOCA-salt hypertensive rats. American Journal of Physiology: Heart and Circulatory Physiology, v. 301, n. 2, p. H409-H417, 2011Tradução . . Disponível em: https://doi.org/10.1152/ajpheart.00084.2011. Acesso em: 13 nov. 2024.
APA
Matsumoto, T., Passaglia, R. de C. A. T., & Webb, R. C. (2011). Uridine adenosine tetraphosphate-induced contraction is increases in renal but not pulmonary arteries from DOCA-salt hypertensive rats. American Journal of Physiology: Heart and Circulatory Physiology, 301( 2), H409-H417. doi:10.1152/ajpheart.00084.2011
NLM
Matsumoto T, Passaglia R de CAT, Webb RC. Uridine adenosine tetraphosphate-induced contraction is increases in renal but not pulmonary arteries from DOCA-salt hypertensive rats [Internet]. American Journal of Physiology: Heart and Circulatory Physiology. 2011 ; 301( 2): H409-H417.[citado 2024 nov. 13 ] Available from: https://doi.org/10.1152/ajpheart.00084.2011
Vancouver
Matsumoto T, Passaglia R de CAT, Webb RC. Uridine adenosine tetraphosphate-induced contraction is increases in renal but not pulmonary arteries from DOCA-salt hypertensive rats [Internet]. American Journal of Physiology: Heart and Circulatory Physiology. 2011 ; 301( 2): H409-H417.[citado 2024 nov. 13 ] Available from: https://doi.org/10.1152/ajpheart.00084.2011

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