Protein Malnutrition Induces Endothelial Dysfunction in Mesenteric and Pancreatic Resistance Arteries by Different Mechanisms: Protective Role of Taurine

Protein Malnutrition Induces Endothelial Dysfunction in Mesenteric and Pancreatic Resistance Arteries by Different Mechanisms: Protective Role of Taurine

• Autor
• Daniele Mendes Guizoni
• Co-autores
• Israelle Netto Freitas , Jamaira Aparecida Victorio , Everardo Magalhaes Carneiro , Ana Paula Davel
• Resumo

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  Protein malnutrition increases the risk for the development of diabetes and hypertension. The treatment with taurine has been demonstrated to reduce cardiometabolic risk improving islet hormone secretion and reducing blood pressure. Therefore, we hypothesized a beneficial effect of taurine treatment in pancreatic and peripheral vasculature during protein restriction. Since lieno-pancreatic artery (LPA) is important for pancreas blood flow and islet activity, and small mesenteric arteries (SMA) contribute to total peripheral resistance, these arteries were investigated. Post-weaned male C57BL/6Junib mice fed normal (NP, 14%) or low-protein (LP, 6%) diet for 90 days, and a group of LP mice were concomitantly treated with 2.5% taurine in drinking water (CEUA-UNICAMP 4533-1/2017). As results, protein malnutrition reduced the acetylcholine-induced relaxation without changed the relaxation to the nitric oxide (NO)-donor sodium nitroprusside in SMA and LPA. Incubation with L-NAME (300?M) or KCl (20mM) reduced acetylcholine-induced relaxation in both arteries but L-NAME abolished differences between groups only in SMA while KCl did it only in LPA. This result suggests NO as the main factor involved in protein malnutrition-induced SMA dysfunction and endothelium-derived hyperpolarization (EDH) in LPA dysfunction. Those alterations were normalized by taurine. It has been suggested that taurine stimulates H2S synthesis and H2S has EDH activity. Therefore, we investigated H2S production and vasorelaxation to H2S donor NaHS and found both reduced in LPA from LP. Taurine treatment increased H2S production, H2S-synthesizing enzyme CBS expression and vasodilatory response to NaHS in LPA. Such effects were not observed in SMA. Take together our data suggest that protein malnutrition results in SMA and LPA endothelial dysfunction by distinct mechanisms: impaired NO in SMA and reduced CBS-H2S pathway in LPA. Taurine rescued endothelial function in both arteries. Therefore, taurine emerges as a potential therapy for vascular and metabolic dysfunction associated with malnutrition.

• Palavras-chave
• Protein restriction, resistance arteries, endothelial dysfunction.
• Modalidade
• Pôster
• Área Temática
• Disfunção endotelial