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  1. AU="Maria Helena C. Carvalho"
  2. AU="Huang, Jiaying"
  3. AU="Kasis, Ata George"
  4. AU="Beuzekom, M.van"
  5. AU="Saecker, Ruth"
  6. AU="Philbert, Sasha A"
  7. AU=Ruan Jue
  8. AU=Koo J Y M AU=Koo J Y M
  9. AU="Ouni, Ala"
  10. AU="Tseng, Li-Wen" AU="Tseng, Li-Wen"
  11. AU="Riemenschneider, G." AU="Riemenschneider, G."
  12. AU="Wessel, Connor"
  13. AU=Chu Xiaogang
  14. AU="Moulding, David J"
  15. AU=Ogawa Makio
  16. AU="Heisel, Curtis J"
  17. AU="Zakharchenko, Artem"
  18. AU="C.K.Cheong, "
  19. AU="Pierfrancesco Franco"
  20. AU="Barutcu, Sezgin"
  21. AU="Saha, Titas"
  22. AU="Lipina, Tatiana V"
  23. AU="Herman, Mariana"
  24. AU="Sicard, Delphine"
  25. AU="Guglielmi, Adele"
  26. AU="Hammond, Ester"
  27. AU="Li, Lanhui"
  28. AU="Hassett, Michael J"
  29. AU="Kyle K. Biggar"
  30. AU="Al-Garawi, Amal"
  31. AU="Freeman, Willard M"
  32. AU="Lussier, A M"
  33. AU="J.Castaneda, "
  34. AU="Izquierdo, Ledys"
  35. AU="Werner, F"
  36. AU="Boddington, Marie E"
  37. AU="N Siddaiah"

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  1. Artikel ; Online: Influence of aerobic training on the reduced vasoconstriction to angiotensin II in rats exposed to intrauterine growth restriction

    Vanessa Oliveira / Eliana Hiromi Akamine / Maria Helena C Carvalho / Lisete Compagno Michelini / Zuleica Bruno Fortes / Tatiana Sousa Cunha / Maria do Carmo Franco

    PLoS ONE, Vol 9, Iss 11, p e

    possible role of oxidative stress and AT2 receptor of angiotensin II.

    2014  Band 113035

    Abstract: Intrauterine growth restriction (IUGR) is associated with impaired vascular function, which contributes to the increased incidence of chronic disease. The aim of this study was to investigate whether aerobic training improves AngII-induced ... ...

    Abstract Intrauterine growth restriction (IUGR) is associated with impaired vascular function, which contributes to the increased incidence of chronic disease. The aim of this study was to investigate whether aerobic training improves AngII-induced vasoconstriction in IUGR rats. Moreover, we assess the role of superoxide dismutase (SOD) isoforms and NADPH oxidase-derived superoxide anions in this improvement. Female Wistar rats were randomly divided into two groups on day 1 of pregnancy. A control group was fed standard chow ad libitum, and a restricted group was fed 50% of the ad libitum intake throughout gestation. At 8 weeks of age, male offspring from both groups were randomly assigned to 4 experimental groups: sedentary control (SC), trained control (TC), sedentary restricted (SRT), and trained restricted (TRT). The training protocol was performed on a treadmill and consisted of a continuous 60-min session 5 days/week for 10 weeks. Following aerobic training, concentration-response curves to AngII were obtained in endothelium-intact aortic rings. Protein expression of SOD isoforms, AngII receptors and the NADPH oxidase component p47phox was assessed by Western blot analysis. The dihydroethidium was used to evaluate the in situ superoxide levels under basal conditions or in the presence of apocynin, losartan or PD 123,319. Our results indicate that aerobic training can prevent IUGR-associated increases in AngII-dependent vasoconstriction and can restore basal superoxide levels in the aortic rings of TRT rats. Moreover, we observed that aerobic training normalized the increased p47phox protein expression and increased MnSOD and AT2 receptor protein expression in thoracic aortas of SRT rats. In summary, aerobic training can result in an upregulation of antioxidant defense by improved of MnSOD expression and attenuation of NADPH oxidase component p47phox. These effects are accompanied by increased expression of AT2 receptor, which provide positive effects against Ang II-induced superoxide generation, resulting in attenuation of AngII-induced vasoconstriction.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 796 ; 571
    Sprache Englisch
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: Upregulation of ERK1/2-eNOS via AT2 receptors decreases the contractile response to angiotensin II in resistance mesenteric arteries from obese rats.

    Graziela N Hagihara / Nubia S Lobato / Fernando P Filgueira / Eliana H Akamine / Danielle S Aragão / Dulce E Casarini / Maria Helena C Carvalho / Zuleica B Fortes

    PLoS ONE, Vol 9, Iss 8, p e

    2014  Band 106029

    Abstract: It has been clearly established that mitogen-activated protein kinases (MAPKS) are important mediators of angiotensin II (Ang II) signaling via AT1 receptors in the vasculature. However, evidence for a role of these kinases in changes of Ang II-induced ... ...

    Abstract It has been clearly established that mitogen-activated protein kinases (MAPKS) are important mediators of angiotensin II (Ang II) signaling via AT1 receptors in the vasculature. However, evidence for a role of these kinases in changes of Ang II-induced vasoconstriction in obesity is still lacking. Here we sought to determine whether vascular MAPKs are differentially activated by Ang II in obese animals. The role of AT2 receptors was also evaluated. Male monosodium glutamate-induced obese (obese) and non-obese Wistar rats (control) were used. The circulating concentrations of Ang I and Ang II, determined by HPLC, were increased in obese rats. Ang II-induced isometric contraction was decreased in endothelium-intact resistance mesenteric arteries from obese compared with control rats and exhibited a retarded AT1 receptor antagonist response. Blocking of AT2 receptors and inhibition of either endothelial nitric oxide synthase (eNOS) or extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) restored Ang II-induced contraction in obese rats. Western blot analysis revealed increased protein expression of AT2 receptors in arteries from obese rats. Basal and Ang II-induced ERK1/2 phosphorylation was also increased in obese rats. Blockade of either AT1 or AT2 receptors corrected the increased ERK1/2 phosphorylation in arteries from obese rats to levels observed in control preparations. Phosphorylation of eNOS was increased in obese rats. Incubation with the ERK1/2 inhibitor before Ang II stimulation did not affect eNOS phosphorylation in control rats; however, it corrected the increased phosphorylation of eNOS in obese rats. These results clearly demonstrate that enhanced AT2 receptor and ERK1/2-induced, NO-mediated vasodilation reduces Ang II-induced contraction in an endothelium-dependent manner in obese rats.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 571
    Sprache Englisch
    Erscheinungsdatum 2014-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: Reduced endothelium-dependent relaxation to anandamide in mesenteric arteries from young obese Zucker rats.

    Nubia S Lobato / Fernando P Filgueira / Roshini Prakash / Fernanda R Giachini / Adviye Ergul / Maria Helena C Carvalho / R Clinton Webb / Rita C Tostes / Zuleica B Fortes

    PLoS ONE, Vol 8, Iss 5, p e

    2013  Band 63449

    Abstract: Impaired vascular function, manifested by an altered ability of the endothelium to release endothelium-derived relaxing factors and endothelium-derived contracting factors, is consistently reported in obesity. Considering that the endothelium plays a ... ...

    Abstract Impaired vascular function, manifested by an altered ability of the endothelium to release endothelium-derived relaxing factors and endothelium-derived contracting factors, is consistently reported in obesity. Considering that the endothelium plays a major role in the relaxant response to the cannabinoid agonist anandamide, the present study tested the hypothesis that vascular relaxation to anandamide is decreased in obese rats. Mechanisms contributing to decreased anandamide-induced vasodilation were determined. Resistance mesenteric arteries from young obese Zucker rats (OZRs) and their lean counterparts (LZRs) were used. Vascular reactivity was evaluated in a myograph for isometric tension recording. Protein expression and localization were analyzed by Western blotting and immunofluorescence, respectively. Vasorelaxation to anandamide, acetylcholine, and sodium nitroprusside, as well as to CB1, CB2, and TRPV1 agonists was decreased in endothelium-intact mesenteric arteries from OZRs. Incubation with an AMP-dependent protein kinase (AMPK) activator or a fatty acid amide hydrolase inhibitor restored anandamide-induced vascular relaxation in OZRs. CB1 and CB2 receptors protein expression was decreased in arteries from OZRs. Incubation of mesenteric arteries with anandamide evoked endothelial nitric oxide synthase (eNOS), AMPK and acetyl CoA carboxylase phosphorylation in LZRs, whereas it decreased phosphorylation of these proteins in OZRs. In conclusion, obesity decreases anandamide-induced relaxation in resistance arteries. Decreased cannabinoid receptors expression, increased anandamide degradation, decreased AMPK/eNOS activity as well as impairment of the response mediated by TRPV1 activation seem to contribute to reduce responses to cannabinoid agonists in obesity.
    Schlagwörter Medicine ; R ; Science ; Q
    Sprache Englisch
    Erscheinungsdatum 2013-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  4. Artikel ; Online: An interaction of renin-angiotensin and kallikrein-kinin systems contributes to vascular hypertrophy in angiotensin II-induced hypertension

    Graziela S Ceravolo / Augusto C Montezano / Maria T Jordão / Eliana H Akamine / Tiago J Costa / Ana P Takano / Denise C Fernandes / Maria L Barreto-Chaves / Francisco R Laurindo / Rita C Tostes / Zuleica B Fortes / Renato P Chopard / Rhian M Touyz / Maria Helena C Carvalho

    PLoS ONE, Vol 9, Iss 11, p e

    in vivo and in vitro studies.

    2014  Band 111117

    Abstract: The kallikrein-kinin and renin-angiotensin systems interact at multiple levels. In the present study, we tested the hypothesis that the B1 kinin receptor (B1R) contributes to vascular hypertrophy in angiotensin II (ANG II)-induced hypertension, through a ...

    Abstract The kallikrein-kinin and renin-angiotensin systems interact at multiple levels. In the present study, we tested the hypothesis that the B1 kinin receptor (B1R) contributes to vascular hypertrophy in angiotensin II (ANG II)-induced hypertension, through a mechanism involving reactive oxygen species (ROS) generation and extracellular signal-regulated kinase (ERK1/2) activation. Male Wistar rats were infused with vehicle (control rats), 400 ng/Kg/min ANG II (ANG II rats) or 400 ng/Kg/min ANG II plus B1 receptor antagonist, 350 ng/Kg/min des-Arg(9)-Leu(8)-bradykinin (ANGII+DAL rats), via osmotic mini-pumps (14 days) or received ANG II plus losartan (10 mg/Kg, 14 days, gavage - ANG II+LOS rats). After 14 days, ANG II rats exhibited increased systolic arterial pressure [(mmHg) 184 ± 5.9 vs 115 ± 2.3], aortic hypertrophy; increased ROS generation [2-hydroxyethidium/dihydroethidium (EOH/DHE): 21.8 ± 2.7 vs 6.0 ± 1.8] and ERK1/2 phosphorylation (% of control: 218.3 ± 29.4 vs 100 ± 0.25]. B1R expression was increased in aortas from ANG II and ANG II+DAL rats than in aortas from the ANG II+LOS and control groups. B1R antagonism reduced aorta hypertrophy, prevented ROS generation (EOH/DHE: 9.17 ± 3.1) and ERK1/2 phosphorylation (137 ± 20.7%) in ANG II rats. Cultured aortic vascular smooth muscle cells (VSMC) stimulated with low concentrations (0.1 nM) of ANG II plus B1R agonist exhibited increased ROS generation, ERK1/2 phosphorylation, proliferating-cell nuclear antigen expression and [H3]leucine incorporation. At this concentration, neither ANG II nor the B1R agonist produced any effects when tested individually. The ANG II/B1R agonist synergism was inhibited by losartan (AT1 blocker, 10 µM), B1R antagonist (10 µM) and Tiron (superoxide anion scavenger, 10 mM). These data suggest that B1R activation contributes to ANG II-induced aortic hypertrophy. This is associated with activation of redox-regulated ERK1/2 pathway that controls aortic smooth muscle cells growth. Our findings highlight an important cross-talk between the DABK and ANG II in the vascular system and contribute to a better understanding of the mechanisms involved in vascular remodeling in hypertension.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2014-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  5. Artikel ; Online: III Consenso Brasileiro de Hipertensão Arterial

    Osvaldo Kohlmann Jr. / Armênio Costa Guimarães / Maria Helena C. Carvalho / Hilton de Castro Chaves Jr. / Carlos Alberto Machado / José Nery Praxedes / José Luiz Santello

    Arquivos brasileiros de Endocrinologia e Metabologia, Vol 43, Iss 4, Pp 247-

    1999  Band 249

    Schlagwörter Diseases of the endocrine glands. Clinical endocrinology ; RC648-665 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Internal medicine ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
    Sprache Portugiesisch
    Erscheinungsdatum 1999-08-01T00:00:00Z
    Verlag Sociedade Brasileira de Endocrinologia e Metabologia
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  6. Artikel ; Online: III Consenso Brasileiro de Hipertensão Arterial

    Osvaldo Kohlmann Jr. / Armênio Costa Guimarães / Maria Helena C. Carvalho / Hilton de Castro Chaves Jr. / Carlos Alberto Machado / José Nery Praxedes / José Luiz Santello / Fernando Nobre / Décio Mion Jr.

    Arquivos brasileiros de Endocrinologia e Metabologia, Vol 43, Iss 4, Pp 257-

    1999  Band 286

    Schlagwörter Diseases of the endocrine glands. Clinical endocrinology ; RC648-665 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Internal medicine ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
    Sprache Portugiesisch
    Erscheinungsdatum 1999-08-01T00:00:00Z
    Verlag Sociedade Brasileira de Endocrinologia e Metabologia
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  7. Artikel ; Online: IV Diretrizes Brasileiras de Hipertensão Arterial Grupos de trabalho IV Brazilian Guidelines on Arterial Hypertension Work groups

    Marco Antonio Mota Gomes / Angela Maria Geraldo Pierin / Antonio Silveira Sbissa / Armando da Rocha Nogueira / Ayrton Pires Brandão / Cibeli I. Saad Rodrigues / Edgar Pessoa de Mello / José Xavier de Mello Filho / Luiz Carlos Bodanese / Paulo Toscano / Sebastião Ferreira Filho / Fernando Nobre / Agostinho Tavares / Antonio Carlos Lopes / Jorge Pinto Ribeiro / José Carlos Aydar Ayoub / José Márcio Ribeiro / Luiz Introcaso / Marcelo Corrêa /
    Mario Maranhão / Pedro Jabur / Raimundo Marques Nascimento / Roberto de Sá Cunha / Rogério Andrade Mulinari / Carlos Alberto Machado / Adriana Avila / Clóvis Oliveira Andrade / João Carlos Rocha / Margarida Maria Veríssimo Lopes / Maria Cecília G. Marinho Arruda / Maria Fátima Azevedo / Maria Helena C. Carvalho / Marilda Novaes Lipp / Nárcia Elisa B. Kohlmann / Neide de Jesus / Paulo César da Veiga Jardim / Celso Amodeo / Carlos Eduardo Negrão / Celso Ferreira / Cláudio Pereira da Cunha / Eli Toscano / Eliuden Galvão de Lima / Estelamaris Tronco Monego / Fátima Lúcia Machado Braga / Hilton de Castro Chaves Jr. / Joel Heiman / Tales de Carvalho / Osvaldo Kohlmann Jr. / Alvaro Avezum / Artur Beltrame Ribeiro / Carlos Alberto Gomes / Dante Marcelo Artigas Giorgi / Gilson Feitosa / Harue Ohashi / José Antonio Franchini Ramirez / Marcelo Marcondes Machado / Natalino Salgado Filho / Rafael Leite Luna / Roberto Jorge da Silva Franco / Robson Augusto dos Santos / Wille Oigman / Istênio Fernandes Pascoal / Airton Massaro / Álvaro Nagib Atallah / Andréa Brandão / Elizabete Viana de Freitas / Ivan Cordovil / José Egídio Paulo de Oliveira / José Geraldo L. Ramos / Maria Teresa Zanella / Maurício Wajngarten / Roberto Dischinger Miranda / Soubihe Kahhale / Vera Koch / Décio Mion Jr. / Armênio C. Guimarães / Catia Sueli Palmeira / Claudia Lucia de Moraes Forjaz / Eduardo B. Coelho / Fernando Antonio Almeida / Isabel Cristina Estefano Pellizari / Marcos Ausenka Ribeiro / Michel Batlouni / Paulo Lotufo / Regina Teresa Capelari / Lucélia C. Magalhães / Abrahão Afiune Neto / Abrão Cury / Alci Moreira / Ana Luisa de Souza / Flavio Danni Fuchs / Ines Lessa / Marcus V. Bolívar Malachias / Romero Bezerra / Sandra Fuchs / José Nery Praxedes / Antonio Cambara / Antonio Marmo Lucon / Berenice Mendonça / Flavio Borelli / Helio B. Silva / João Egidio Romão Jr. / José Gastão Rocha Carvalho / José Luiz Santello / Luiz Bortolotto / Luis Celso Matavelli / Maria Eliete Pinheiro / Valéria Guimarães

    Arquivos Brasileiros de Cardiologia, Vol 82, Pp 5-

    2004  Band 5

    Schlagwörter Diseases of the circulatory (Cardiovascular) system ; RC666-701 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Cardiovascular ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
    Sprache Englisch
    Erscheinungsdatum 2004-03-01T00:00:00Z
    Verlag Sociedade Brasileira de Cardiologia - SBC
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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