Endothelial and neuronal nitric oxide synthase inhibitors influences angiotensin II pressor effect in central nervous system

Made available in DSpace on 2019-09-12T16:26:07Z (GMT). No. of bitstreams: 0 Previous issue date: 2006The 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, BrazilGuarda, I.F.M.S., Department of Anesthesiology, Clinical Hospital São Paulo, São Paulo, BrazilCamargo, 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, BrazilSaad, 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, BrazilGuarda, R.S., Department of Anesthesiology, Clinical Hospital São Paulo, São Paulo, BrazilSantos, A.F.B.T., Basic Institute of Biosciences, UNITAU, Taubaté, SP, BrazilSimões, S., Basic Institute of Biosciences, UNITAU, Taubaté, SP, Brazi

Effects of nitric oxide and arginine vasopressin on sodium intake induced by central angiotensin II. Part 2

Made available in DSpace on 2019-09-12T16:26:07Z (GMT). No. of bitstreams: 0 Previous issue date: 2007We study the effects of angiotensin receptors antagonists, arginine vasopressin receptor antagonist, L-arginine and L-NAME, injected into supraoptic nucleus of the hypothalamus (SON) on sodium intake induced by the injection of angiotensin II (ANGII). Holtzman rats weighing 200-250 g with canulae implanted into the SON were used. The drugs were injected in 0.5 μL over 30-60 sec. Sodium intake after injection of saline SAL+SAL 0.15 M NaCl was 0.10±00.1 mL 2 h-1; SAL+ANGII injected into SON increased sodium intake. Losartan injected prior to ANGII into SON decreased sodium intake induced by ANGII. PD123319 injected prior to ANGII produced no changes in sodium intake induced by ANGII. AVPA receptor V1 antagonist injected prior to ANGII reduced sodium intake with a less intensity than losartan. L-arginine injected prior to ANGII decreases sodium intake at a same intensity than losartan. L-NAME injected prior to ANGII potentiated sodium intake induced by ANGII. Losartan injected simultaneously with L-arginine prior to ANGII blocked the natriorexigenic effect of ANGII. These results confirm the importance of SON in the control of sodium intake. Also suggest that both AT1 and arginine vasopressin V1 receptors interact with nitrergic pathways within the SON influencing the sodium metabolism by changing sodium appetite induced by ANGII. © 2007 Asian Network for Scientific Information.Saad, W.A., Basic Institute of Bioscience, University of Taubaté, Taubaté, SP, Brazil, Centro Universitário de Araraquarsa, Araraquara, SP Uniara, Brazil, Department of Physiology and Pathology, School of Dentistry, Paulista State University, Araraquara, SP, Brazil, Department of Gatroenterology, School of Medicine, University of São Paulo, São Paulo, Brazil, Rua Humaitá 1680, 14801-903 Araraquara, SP, BrazilGuarda, I.F.M.S., Department of Anesthesiology, Clinic Hospital State of São Paulo, São Paulo, BrazilCarmago, L.A. de A., Department of Physiology and Pathology, School of Dentistry, Paulista State University, Araraquara, SP, Brazildos Santos, T.A.F.B., Basic Institute of Bioscience, University of Taubaté, Taubaté, SP, BrazilSaad, W.A., Basic Institute of Bioscience, University of Taubaté, Taubaté, SP, Brazil, Centro Universitário de Araraquarsa, Araraquara, SP Uniara, Brazil, Department of Physiology and Pathology, School of Dentistry, Paulista State University, Araraquara, SP, Brazil, Department of Gatroenterology, School of Medicine, University of São Paulo, São Paulo, Brazil, Rua Humaitá 1680, 14801-903 Araraquara, SP, Brazi

Effects of nitric oxide and arginine vasopressin on water intake induced by central angiotensin II. Part 1

Made available in DSpace on 2019-09-12T16:26:07Z (GMT). No. of bitstreams: 0 Previous issue date: 2007We determined the effects of AT1 and AT2 (selective no peptides antagonists angiotensin receptors), arginine vasopressin V1 receptor antagonist as well as L-arginine, a nitric oxide donor and NW-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor, injected into supraoptic nucleus (SON) on water and sodium intake induced by the injection of angiotensin II (ANGII). Male Holtzman rats weighing 200-250 g with canulae implanted into the SON were used. The drugs were injected in 0.5 μL over 30-60 sec. The water intake after injection of saline SAL+SAL 0.15 M NaCl was 0.40±0.1 mL 2 h-1; SAL+ANGII increase water intake. Losartan decreased the water intake induced by ANGII. PD123319 injected prior to produce no change in water intake induced by ANGII. AVPA prior to ANGII reduced the water intake with a less intensity than losartan. L-arginine prior to ANGII decreases the water intake at a same intensity than losartan. L-NAME prior to ANGII potentiated the dipsogenic effect of ANGII. Losartan injected simultaneously with L-arginine prior to ANGII blocked the dipsogenic effect of ANGII. These results confirm the importance of SON in the control of water intake and strongly suggest that AT1, V1 receptors interact with nitrergic pathways within the SON influencing the dipsogenic effect of ANGII.Saad, W.A., Basic Institute of Bioscience, University of Taubaté, Taubaté, SP, Brazil, Centro Universitário de Araraquarsa, Araraquara, SP, Brazil, Department of Physiology and Pathology, School of Dentistry, Paulista State University, Araraquara, SP, Brazil, Department of Gastroenterology, School of Medicine, University of São Paulo, São Paulo, Brazil, Rua Humaitá 1680, 14801-903-Araraquara, SP, BrazilGuarda, I.F.M.S., Department of Anesthesiology, Clinic Hospital State of São Paulo, São Paulo, BrazilDe Arruga Camargo, L.A., Department of Physiology and Pathology, School of Dentistry, Paulista State University, Araraquara, SP, BrazilBrizola dos Santos, T.A.F., Basic Institute of Bioscience, University of Taubaté, Taubaté, SP, BrazilSaad, W.A., Basic Institute of Bioscience, University of Taubaté, Taubaté, SP, Brazil, Centro Universitário de Araraquarsa, Araraquara, SP, Brazil, Department of Physiology and Pathology, School of Dentistry, Paulista State University, Araraquara, SP, Brazil, Department of Gastroenterology, School of Medicine, University of São Paulo, São Paulo, Brazil, Rua Humaitá 1680, 14801-903-Araraquara, SP, Brazi

Nitrergic pathways and L-type calcium channel of MnPO influencing cardiovascular homeostasis

Made available in DSpace on 2019-09-12T16:26:07Z (GMT). No. of bitstreams: 0 Previous issue date: 2006The median preoptic nucleus (MnPO) is one of most important site of the lamina terminalis implicated in the regulation of hydro electrolytic and cardiovascular balance. The purpose of this study was to determine the effect of L-Type calcium channel antagonist, nifedipine, on the increase of median arterial blood pressure (MAP) induce by angiotensin II (ANG II) injected into the MnPO. The influence of nitric oxide (NO) on nifedipine antipressor action has also been studied by utilizing NW-nitro-L-arginine methyl ester (L-NAME) (40 μg 0.2 μL-1) a NO synthase inhibitor (NOSI), 7-nitroindazole (7-NIT) (40 μg 0.2 μL-1), a specific neuronal NO synthase inhibitor (nNOSI) and sodium nitroprusside (SNP) (20 μg 0.2 μL-1) a NO donor agent. We have also investigated the central role of losartan and PD123349 (20 nmol 0.2 μL-1), AT1 and AT2, respectively (selective non peptide ANG II receptor antagonists), in the pressor effect of ANG II (25 pmol 0.2 μL-1) injected into the MnPO. Male Wistar rats weighting 200-250 g, with cannulae implanted into the MnPO were utilized. Losartan injected into the MnPO, prior to ANG II, blocked the pressor effect of ANGII. PD 123319 only decreased the pressor effect of ANG II. Rats pre-treated with either 50 μg 0.2 μL-1 or 100 μg 0.2 μL-1 of nifedipine, followed by 25 pmol 0.2 μL-1 of ANG II, decreased ANG II-pressor effect. L-NAME potentiated the pressor effect of ANG II. 7-NIT injected prior to ANG II into the MnPO also potentiated the pressor effect of ANGII but with less intensity than that of L-NAME. SNP injected prior to ANG II blocked the pressor effect of ANG II. The potentiation action of L-NAME and 7-NIT on ANG II-pressor effect was blocked by prior injection of nifedipine. The results described in this study provide evidence that calcium channels play important roles in central ANG II-induced pressor effect. The structures containing NO in the brain, such as MnPO, include both endothelial and neuronal cells, which might be responsible for the influence of nifedipine on the pressor effect of ANG II. These data have shown the functional relationship between L-Type calcium channel and a free radical gas NO in the MnPO, on the control of ANG II-induced pressor effect acting in AT1 and AT2 receptors.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, Rua Humaitá 1680, 14801-903-Araraquara, SP, Brazil, Department of Anesthesiology Clinic Hospital State of Sao Paulo, Sao Paulo, Brazil, Department of Physiology, Federal University of São Carlos, São Carlos, SP, Brazil, Department of Gastroenterology, Clinic Hospital of University of São Paulo, São Paulo, BrazilGuarda, I.F.M.S., Department of Anesthesiology Clinic Hospital State of Sao Paulo, Sao Paulo, BrazilCamargo, L.A. de A., Department of Physiology and Pathology, School of Dentistry, Paulista State University, Rua Humaitá 1680, 14801-903-Araraquara, SP, Brazildos Santos, T.A.F.B., Basic Institute of Biosciences, UNITAU, Taubaté, SP, BrazilSimões, S., Basic Institute of Biosciences, UNITAU, Taubaté, SP, BrazilSaad, 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, Rua Humaitá 1680, 14801-903-Araraquara, SP, Brazil, Department of Anesthesiology Clinic Hospital State of Sao Paulo, Sao Paulo, Brazil, Department of Physiology, Federal University of São Carlos, São Carlos, SP, Brazil, Department of Gastroenterology, Clinic Hospital of University of São Paulo, São Paulo, Brazi

Central nifedipine-induced alterations in salivary flow and compounds: Role of nitric oxide

Made available in DSpace on 2019-09-12T16:26:07Z (GMT). No. of bitstreams: 0 Previous issue date: 2006The aim of this study was to examine the role of nifedipine and Nitric Oxide (NO) on salivary flow and compounds (salivary amylase, saliva total proteins, saliva calcium, sodium and potassium). Male Holtzman rats weighting 200-250 g were anesthetized with zoletil 50 mg kg-1 (tiletamine chloridrate 125.0 mg and zolazepan chloridrate 125.0 mg) into quadriceps muscle and stainless steel cannulas were implanted into their lateral ventricle of the brain (LV). Animals in divided group were injected with nifedipine (50 μg μL-1) alone and in combination with 7-nitroindazol (7-NIT) (40 μg μL-1), neuronal NO Sinthase Inhibitor (nNOSI) and Sodium Nitroprussate (SNP) (30 μg μL-1) NO donor agent. As a secretory stimuli, pilocarpine dissolved in isotonic was administered intraperitoneally (ip) at a dosage of 10 mg kg-1 body weight. Saliva was collected for 7 min with four cotton balls weighing approximately 20 mg each, two of which were placed on either side of the oral cavity, with the other two placed under the tongue. Nifedipine treatment induced a reduction in saliva secretion rate and concentration of amylase, total protein and calcium without changes in sodium and potassium concentration in comparison with controls. Co-treatment of animals with nifedipine and SNP retained flow rate and concentration of amylase, total protein and calcium in normal levels. Co-treatment of animals with nifedipine and 7-NIT potentiated the effect of nifedipine on the reduction of saliva secretion and concentrations of amylase, total protein and calcium. Nifedipine (dihydroperidine) calcium-channel blocker widely in use is associated with salivary dysfunction acting in the central nervous system structures. NO might be the mechanism for protective effect against the nifedipine-induce salivary dysfunction, acting in the CNS. © 2006 Asian Network for Scientific Information.Saad, W.A., Basic Institute of Biosciences, UNITAU, Taubaté, SP, Brazil, Department of Biological and Health Science, UNIARA, Araraquara, SP, Brazil, Department of Physiology and Pathology, School of Dentistry, Paulista State University, 1680 Humaitá Street, Araraquara, SP 14801-903, Brazil, Department of Physiology, Federal University of São Carlos SP, São Paulo, Brazil, Department of Gastroenterology, Clinic Hospital State of São Paulo, São Paulo, BrazilSiqueira Guarda, I.F.M., Department of Anesthesiology, Clinic Hospital State of São Paulo, São Paulo, BrazilCamargo, L.A. de A., Department of Physiology and Pathology, School of Dentistry, Paulista State University, 1680 Humaitá Street, Araraquara, SP 14801-903, Brazil, Department of Physiology, Federal University of São Carlos SP, São Paulo, BrazilBrizola dos Santos, T.A.F., Basic Institute of Biosciences, UNITAU, Taubaté, SP, BrazilSimões, S., Basic Institute of Biosciences, UNITAU, Taubaté, SP, BrazilSaad, W.A., Basic Institute of Biosciences, UNITAU, Taubaté, SP, Brazil, Department of Biological and Health Science, UNIARA, Araraquara, SP, Brazil, Department of Physiology and Pathology, School of Dentistry, Paulista State University, 1680 Humaitá Street, Araraquara, SP 14801-903, Brazil, Department of Physiology, Federal University of São Carlos SP, São Paulo, Brazil, Department of Gastroenterology, Clinic Hospital State of São Paulo, São Paulo, Brazi