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Made available in DSpace on 2019-09-12T16:26:07Z (GMT). No. of bitstreams: 0 Previous issue date: 2006 O presente estudo investigou o papel central da angiotensina II e do óxido nítrico na pressão arterial (PAM) em ratos. Losartan e PD123349 AT1 e AT2 (seletivos sem peptídeos antagonizam os receptores da angiotensina), bem como FK 409 (um doador de óxido nítrico), éster metílico da NW-nitro-L-arginina (L-NAME), um inibidor da óxido nítrico sintetase endotelial (eNOSI ) e 7-nitroindazol (7NI), um inibidor neuronal específico da óxido nítrico sintase (nNOSI) foi usado. A cepa Holtzman (Rattus norvergicus), com peso de 200 a 250 g, foi anestesiada com zoletil 50 mg kg-1 (cloridrato de tiletamina 125 mg e cloridrato de zolazepan 125 mg) no músculo quadríceps e cânula de aço inoxidável foi estereotaxicamente implantada em seu ventrículo lateral (LV). Os controles foram injetados com um volume de 0,5 mL de NaCl 0,15 M. A angiotensina II injetada no VE aumentou a PAM (19 ± 3 vs. controle 3 ± 1 mm Hg), que é potencializado pela injeção prévia de L-NAME no mesmo local 26 ± 2 mm Hg. O 7NI injetado antes do ANG II no VE também potencializou o efeito pressor do ANG II, mas com uma intensidade maior que o L-NAME de 32 ± 3 mm Hg. A FK 409 inibiu o efeito pressor da ANG II (6 ± 1 mm Hg). O losartan injetado no VE antes do ANG II influencia o efeito pressor do ANG II (8 ± 1 mm Hg). O PD 123319 diminuiu os efeitos pressores do ANG II (16 ± 1 mm Hg). Losartan injetado simultaneamente com FK 409 bloqueou o efeito pressor do ANG II (3 ± 1 mm Hg). O L-NAME produziu um aumento no efeito pressor da ANG II, pode ser devido à vasoconstrição local e de uma só vez pela inibição neuronal da NOS, mas o principal efeito é do 7-NIT um inibidor específico da nNOS. Os receptores antagonistas AT1 melhoram a produção e liberação de óxido nítrico (NO). Esses dados sugerem o envolvimento de NOS constitutiva e neuronal no controle da pressão arterial induzida centralmente por ANG II, evoluindo a vasoconstrição mediada pelo receptor AT1 e a vasodilatação mediada pelo receptor AT2. Estes resultados foram confirmados pelo experimento usando FK 409. The present study investigated the central role of angiotensin II and nitric oxide on arterial blood pressure (MAP) in rats. Losartan and PD123349 AT1 and AT2 (selective no peptides antagonists angiotensin receptors), as well as FK 409 (a nitric oxide donor), NW-nitro-L-arginine methyl ester (L-NAME) a constituve nitric oxide synthase inhibitor endothelial (eNOSI) and 7-nitroindazol (7NI) a specific neuronal nitric oxide synthase inhibitor (nNOSI) were used. Holtzman strain, (Rattus norvergicus) weighting 200-250 g were anesthetized with zoletil 50 mg kg-1 (tiletamine chloridrate 125 mg and zolazepan chloridrate 125 mg) into quadriceps muscle anda stainless steel cannula was stereotaxically implanted into their Lateral Ventricle (LV). Controls were injected with a 0.5 μl volume of 0.15 M NaCl. Angiotensin II injected into LV increased MAP (19±3 vs. control 3±1 mm Hg), which is potentiated by prior injection of L-NAME in the same site 26±2 mm Hg. 7NI injected prior to ANG II into LV also potentiated the pressor effect of ANG II but with a higher intensity than L-NAME 32±3 mm Hg. FK 409 inhibited the pressor effect of ANG II (6±1 mm Hg). Losartan injected into LV before ANG II influences the pressor effect of ANG II (8±1 mm Hg). The PD 123319 decreased the pressor effects of ANG II (16±1 mm Hg). Losartan injected simultaneously with FK 409 blocked the pressor effect of ANG II (3±1 mm Hg). L-NAME produced an increase in the pressor effect of ANG II, may be due to local vasoconstriction and all at once by neuronal NOS inhibition but the main effect is of the 7-NIT an specific nNOS inhibitor. The AT1 antagonist receptors improve basal nitric oxide (NO) production and release. These data suggest the involvement of constitutive and neuronal NOS in the control of arterial blood pressure induced by ANG II centrally, evolving AT1 receptor-mediated vasoconstriction and AT2 receptor-mediated vasodilatation. These results were confirmed by the experiment using FK 409. © 2006 Asian Network for Scientific Information. Saad, W.A., Basic Institute of Biosciences, UNITAU, Taubaté, SP, Brazil, Department of Exact and Natural Science, UNIARA, Araraquara, SP, Brazil, Department of Physiology and Pathology School of Dentistry, Paulista State University, UNESP, 1680 Humaitá Street, 14801-903-Araraquara, SP, Brazil, Department of Gastroenterology, Clinic Hospital School of Medicine, University of São Paulo, São Paulo, Brazil, Department of Physiology, Federal University of São Carlos, São Carlos, SP, Brazil Guarda, I.F.M.S., Department of Anesthesiology, Clinical Hospital São Paulo, São Paulo, Brazil Camargo, L.A. de A., Department of Physiology and Pathology School of Dentistry, Paulista State University, UNESP, 1680 Humaitá Street, 14801-903-Araraquara, SP, Brazil, Department of Physiology, Federal University of São Carlos, São Carlos, SP, Brazil Saad, W.A., Basic Institute of Biosciences, UNITAU, Taubaté, SP, Brazil, Department of Exact and Natural Science, UNIARA, Araraquara, SP, Brazil, Department of Physiology and Pathology School of Dentistry, Paulista State University, UNESP, 1680 Humaitá Street, 14801-903-Araraquara, SP, Brazil, Department of Gastroenterology, Clinic Hospital School of Medicine, University of São Paulo, São Paulo, Brazil, Department of Physiology, Federal University of São Carlos, São Carlos, SP, Brazil Guarda, R.S., Department of Anesthesiology, Clinical Hospital São Paulo, São Paulo, Brazil Santos, A.F.B.T., Basic Institute of Biosciences, UNITAU, Taubaté, SP, Brazil Simões, S., Basic Institute of Biosciences, UNITAU, Taubaté, SP, Brazil