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Year 2010 - Volume 30, Number 7
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Lesão vascular mediada pelo receptor AT1 em miocárdio, rins e fígado de ratos, 30(7):605-611
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ABSTRACT.- Vailati M.C.F., Rocha N.S., Matsubara L.S., Padovani C.R., Schwartz D.S. & Matsubara B.B. 2010. AT1-receptor mediated vascular damage in myocardium, kidneys and liver in rats. Pesquisa Veterinária Brasileira 30(7):605-611. Departamento de Clínica Veterinária, Faculdade de Medicina Veterinária e Zootecnia, Universidade Estadual Paulista, Distrito de Rubião Júnior s/n, Botucatu, SP 18618-000, Brazil. E-mail: mfvailati@yahoo.com.br
The systemic aspect of vascular damage induced by angiotensin II (ANG II) has been poorly explored in the literature. Considering the presence of ANG II and its specific receptor AT1, in several organs, all tissues might be potentially affected by its effects. The aims of this study were: To evaluate the early histological changes in the heart, liver and kidneys, produced by ANG II infusion, to evaluate the protective effect of losartan. Wistar rats were distributed into three groups: control (no treatment), treated with ANG II, and treated with ANG II + losartan. ANG II was continuously infused over 72 hours by subcutaneous osmotic pumps. Histological sections of the myocardium, kidneys and liver were stained and observed for the presence of necrosis. There were ANG II-induced perivascular inflammation and necrosis of the arteriolar wall in the myocardium, kidney, and liver by, which were partially prevented by losartan. There was no significant correlation between heart and kidney damage. Tissue lesion severity was lower than that of vascular lesions, without statistical difference between groups. ANG II causes vascular injury in the heart, kidneys and liver, indicating a systemic vasculotoxic effect; the mechanisms of damage/protection vary depending on the target organ; perivascular lesions may occur even when anti-hypertensive doses of losartan are used. |
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