Decreased endothelial nitric oxide, systemic oxidative stress, and increased sympathetic modulation contribute to hypertension in obese rats (2014)
- Authors:
- USP affiliated authors: GRANDO, MARCELLA DARUGE - FCFRP ; BENDHACK, LUSIANE MARIA - FCFRP
- Unidade: FCFRP
- DOI: 10.1152/ajpheart.00520.2013
- Subjects: ÓXIDO NÍTRICO; ENDOTÉLIO; GLUTAMATOS
- Language: Inglês
- Imprenta:
- Source:
- Título: American Journal of Physiology Heart and Circulatory Physiology
- ISSN: 0363-6135
- Volume/Número/Paginação/Ano: v. 306, n. 10, p. H1472-H1480, 2014
- Este periódico é de acesso aberto
- Este artigo NÃO é de acesso aberto
-
ABNT
CUNHA, Natalia Veronez da et al. Decreased endothelial nitric oxide, systemic oxidative stress, and increased sympathetic modulation contribute to hypertension in obese rats. American Journal of Physiology Heart and Circulatory Physiology, v. 306, n. 10, p. H1472-H1480, 2014Tradução . . Disponível em: https://doi.org/10.1152/ajpheart.00520.2013. Acesso em: 16 fev. 2026. -
APA
Cunha, N. V. da, Pinge-Filho, P., Panis, C., Silva, B. R., Pernomian, L., Grando, M. D., et al. (2014). Decreased endothelial nitric oxide, systemic oxidative stress, and increased sympathetic modulation contribute to hypertension in obese rats. American Journal of Physiology Heart and Circulatory Physiology, 306( 10), H1472-H1480. doi:10.1152/ajpheart.00520.2013 -
NLM
Cunha NV da, Pinge-Filho P, Panis C, Silva BR, Pernomian L, Grando MD, Cecchini R, Bendhack LM, Martins-Pinge MC. Decreased endothelial nitric oxide, systemic oxidative stress, and increased sympathetic modulation contribute to hypertension in obese rats [Internet]. American Journal of Physiology Heart and Circulatory Physiology. 2014 ; 306( 10): H1472-H1480.[citado 2026 fev. 16 ] Available from: https://doi.org/10.1152/ajpheart.00520.2013 -
Vancouver
Cunha NV da, Pinge-Filho P, Panis C, Silva BR, Pernomian L, Grando MD, Cecchini R, Bendhack LM, Martins-Pinge MC. Decreased endothelial nitric oxide, systemic oxidative stress, and increased sympathetic modulation contribute to hypertension in obese rats [Internet]. American Journal of Physiology Heart and Circulatory Physiology. 2014 ; 306( 10): H1472-H1480.[citado 2026 fev. 16 ] Available from: https://doi.org/10.1152/ajpheart.00520.2013 - Endothelial cyclooxygenase differently modulates the contractile response to phenylephrine but not to thromboxane analog in aorta from normotensive and hypertensive rats
- Phenylephrine activates eNOS Ser1177 phosphorylation and nitric oxide signaling in renal hypertensive rat aorta
- Increased resting tension abolishes the endothelial anti-contractile effect induced by phenylephrine in renal hypertensive (2K-1C) rat aorta
- Hydrogen peroxide modulates the contractile response induced by phenylephrine in renal hypertensive rat aorta
- Inibição da NO-sintase normaliza a resposta contrátil estimulada com fenilefrina em aorta de ratos hipertensos renais 2R-1C
- Vascular activation of K+ channels and Na+-K+ ATPase activity of estrogen-deficient female rats
- Hidrogen peroxide decreases the contractile response induced by phenylephrine in renal hypertensive rat aorta
- Augmented nitric oxide production and up-regulation of endothelial nitric oxide synthase during cecal ligation and perforation
- Contractile response induced by phenylephrine in modulated by eNOS phosphorylation and by hydrogen peroxide production in renal hypertensive rat aorta
- Hydrogen peroxide activates the endothelial enzymes no-synthase (eNOS) and cyclooxigenase (COX) in renal hypertensive rat aorta
Informações sobre o DOI: 10.1152/ajpheart.00520.2013 (Fonte: oaDOI API)
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