Gender-specific mechanisms in the etiology of the vascular dysfunction of diabetic female rats (2005)
- Authors:
- USP affiliated authors: SCAVONE, CRISTOFORO - ICB ; NIGRO, DOROTHY - ICB ; CARVALHO, MARIA HELENA CATELLI DE - ICB ; PASSAGLIA, RITA DE CASSIA ALEIXO TOSTES - ICB ; BRITTO, LUIZ ROBERTO GIORGETTI DE - ICB ; FORTES, ZULEICA BRUNO - ICB
- Unidade: ICB
- Subjects: FARMACOLOGIA; FISIOLOGIA
- Language: Português
- Abstract: 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 itsexpression. 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
- Imprenta:
- Publisher: Federação de Sociedades de Biologia Experimental
- Publisher place: Águas de Lindóia, São Paulo
- Date published: 2005
- Source:
- Título: Resumos
- Conference titles: Reunião Anual da Federação de Sociedades de Biologia Experimental, FeSBE
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ABNT
AKAMINE, Eliana Hiromi et al. Gender-specific mechanisms in the etiology of the vascular dysfunction of diabetic female rats. 2005, Anais.. Águas de Lindóia, São Paulo: Federação de Sociedades de Biologia Experimental, 2005. . Acesso em: 02 out. 2024. -
APA
Akamine, E. H., Kawamoto, E. M., Scavone, C., Nigro, D., Carvalho, M. H. C. de, Passaglia, R. de C. A. T., et al. (2005). Gender-specific mechanisms in the etiology of the vascular dysfunction of diabetic female rats. In Resumos. Águas de Lindóia, São Paulo: Federação de Sociedades de Biologia Experimental. -
NLM
Akamine EH, Kawamoto EM, Scavone C, Nigro D, Carvalho MHC de, Passaglia R de CAT, Britto LRG de, Fortes ZB. Gender-specific mechanisms in the etiology of the vascular dysfunction of diabetic female rats. Resumos. 2005 ;[citado 2024 out. 02 ] -
Vancouver
Akamine EH, Kawamoto EM, Scavone C, Nigro D, Carvalho MHC de, Passaglia R de CAT, Britto LRG de, Fortes ZB. Gender-specific mechanisms in the etiology of the vascular dysfunction of diabetic female rats. Resumos. 2005 ;[citado 2024 out. 02 ] - Correction of endothelial dysfunction in diabetic female rats by tetrahydrobiopterin and chronic insulin
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- Enhanced oxidative stress as a potential mechanism underlying the programming of hypertension in utero
- Metformin treatment restores the altered microvascular reactivity in neonatal streptozotocin-induced diabetic rats increasing NOS activity, but not NOS expression
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