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Gender-specific mechanisms in the etiology of the vascular dysfunction of diabetic female rats

Eliana Hiromi Akamine E. M Kawamoto; Cristoforo Scavone; Dorothy Nigro; Maria Helena Catelli de Carvalho; Rita de Cássia Aleixo Tostes Passaglia; Luiz Roberto Giorgetti de Britto; Zuleica Bruno Fortes; Reunião Anual da Federação de Sociedades de Biologia Experimental, FeSBE (20. 2005 Águas de Lindóia, SP)

Resumos Águas de Lindóia, São Paulo: Federação de Sociedades de Biologia Experimental, 2005

Águas de Lindóia, São Paulo Federação de Sociedades de Biologia Experimental 2005

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  • Título:
    Gender-specific mechanisms in the etiology of the vascular dysfunction of diabetic female rats
  • Autor: Eliana Hiromi Akamine
  • E. M Kawamoto; Cristoforo Scavone; Dorothy Nigro; Maria Helena Catelli de Carvalho; Rita de Cássia Aleixo Tostes Passaglia; Luiz Roberto Giorgetti de Britto; Zuleica Bruno Fortes; Reunião Anual da Federação de Sociedades de Biologia Experimental, FeSBE (20. 2005 Águas de Lindóia, SP)
  • Assuntos: FARMACOLOGIA; FISIOLOGIA
  • É parte de: Resumos Águas de Lindóia, São Paulo: Federação de Sociedades de Biologia Experimental, 2005
  • Notas Locais: Disponível somente em CD-ROM
  • Descrição: Objetivo: Insulin and tetrahydrobiopterin (BH4) deficiency may be involved with the endothelial dysfunction in male diabetic rats.Yet this dysfunction exhibits some differential aspects in females. Here we analyzed the effects of BH4 and chronic insulin upon several aspects of the physiology of mesenteric arterioles of alloxan-diabetic female rats. Métodos e Resultados: The parameters studied were the mesenteric arteriolar reactivity (intravital microscopy), NO synthase (NOS) activity (conversion of L-arginine to L-citrulline), eNOS gene expression (RT-PCR), NO production (diaminofluorescein histochemistry), ROS generation (intravital fluorescence microscopy), and Cu/Zn superoxide dismutase (SOD) activity (spectrophotometry) and gene expression (RT-PCR). The response of mesenteric arterioles to acetylcholine, reduced by 39.7% in female diabetic rats, was corrected by both BH4 and insulin. NOS activity was reduced by diabetes (38.2%), and insulin did not correct it. NOS expression was not, however, modified by either diabetes or insulin. The lower NO production (55.1% of control) in female diabetic arterioles was fully corrected by BH4 and only partially corrected by insulin (74.5% of control). ROS generation, increased in diabetic female arterioles (140% above the control), was normalized by both BH4 and insulin. Diabetes did not change SOD activity and gene expression. However, insulin increased SOD activity (169.7% above the control), but not its
    expression. Conclusões: Our data suggest that, similarly to males, the endothelial dysfunction of female diabetic rats involves an altered ROS/NO imbalance, which is possibly caused by a deficiency of BH4 and only partially by a deficiency of insulin. Differently from males, however, insulin does not regulate NOS in the microcirculation of diabetic females
  • Editor: Águas de Lindóia, São Paulo Federação de Sociedades de Biologia Experimental
  • Data de criação/publicação: 2005
  • Formato: res. 17.050.
  • Idioma: Português
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  • Realização: ABCD-USP USP   Logos de Redes Sociais: Freepik

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