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Made available in DSpace on 2019-09-12T16:26:07Z (GMT). No. of bitstreams: 0 Previous issue date: 2006 As several structures of the central nervous system are involved in the control of hydromineral and cardiovascular balance we investigated whether the natriorhexigenic and pressor response induced by the injection of ANG II into the 3rd V could be mediated by vasopressinergic and nitrergic system. Male Holtzman rats weighing 200-250 g with cannulae implanted into the 3rd V were used. The drugs were injected in 0.5 μL over 30-60 sec. Controls were injected with a similar volume of 0.15 M NaCl. ANGII increased the water intake vs control. AVPA injected into 3rd V prior to ANGII decreased the dipsogenic effect of ANGII. L-arginine also decreased the water intake induced by ANGII. AVPA plus L-arginine inhibit the water intake induced by ANGII. 7NIT injected prior to ANGII potentiated the dipsogenic effect of ANGII. Pre-treatment with ANGII increased the sodium ingestion vs control. AVPA decreased the ANGII effect in sodium intake. L-arginine also decreased the natriorhexigenic effect of ANGII. The combination of L-arginine and AVPA inhibit the sodium intake induced by ANGII. 7NIT injected prior to ANGII potentiated the sodium intake induced by ANGII. ANGII induced an increase in Mean Arterial Pressure (MAP) vs control. AVPA and L-arginine induced a decreased in the pressor effect of ANGII. The combination of L-arginine and AVPA inhibit the pressor effect of ANGII. 7NIT injected prior to ANGII into 3rd V potentiated the pressor effect of ANGII. These data suggest that arginine vasopressin V1 receptors and Nitric Oxide (NO) within the circumventricular structures may be involved in sodium intake and pressor response induced by the activation of ANGII receptors within the circumventricular neurons. These studies revealed the involvement of sodium appetite by utilizing the angiotensinergic, vasopressinergic and nitrergic system in the central regulation of blood pressure. © 2006 Asian Network for Scientific Information. Saad, W.A., Department of Exacts and Naturals Sciences, Uiara, Araraquara São Paulo, Brazil, Institute of Bioscience, UNITAU, Taubaté, SP, Brazil, Department of Physiology and Pathology, School of Dentistry, UNESP, 1680 Humaitá Street, Araraquara, SP 14801-903, Brazil, Department of Surgery, School of Medicine, University of São Paulo, São Paulo, Brazil Guarda, I.F.M.S., Public Medical Hospital, São Paulo, Brazil Camargo, L.A.D.A., Department of Physiology and Pathology, School of Dentistry, UNESP, 1680 Humaitá Street, Araraquara, SP 14801-903, Brazil Guarda, R.S., Department of Exacts and Naturals Sciences, Uiara, Araraquara São Paulo, Brazil Saad, W.A., Department of Exacts and Naturals Sciences, Uiara, Araraquara São Paulo, Brazil, Institute of Bioscience, UNITAU, Taubaté, SP, Brazil, Department of Physiology and Pathology, School of Dentistry, UNESP, 1680 Humaitá Street, Araraquara, SP 14801-903, Brazil, Department of Surgery, School of Medicine, University of São Paulo, São Paulo, Brazil Santos, T.A.F.B.D., Institute of Bioscience, UNITAU, Taubaté, SP, Brazil

We investigated the effects of losartan, an AT1-receptor blocker, and ramipril, a converting enzyme inhibitor, on the pressor response induced by angiotensin II (ANG II) and carbachol (a cholinergic receptor agonist). Male Holtzman rats (250-300 g) with a stainless steel cannula implanted into the lateral ventricle (LV) were used. The injection of losartan (50 nmol/1 µl) into the LV blocked the pressor response induced by ANG II (12 ng/1 µl) and carbachol (2 nmol/1 µl). After injection of ANG II and carbachol into the LV, mean arterial pressure (MAP) increased to 31 ± 1 and 28 ± 2 mmHg, respectively. Previous injection of losartan abolished the increase in MAP induced by ANG II and carbachol into the LV (2 ± 1 and 5 ± 2 mmHg, respectively). The injection of ramipril (12 ng/1 µl) prior to carbachol blocked the pressor effect of carbachol to 7 ± 3 mmHg. These results suggest an interaction between central cholinergic pathways and the angiotensinergic system in the regulation of arterial blood pressure