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Articles by Talmir Augusto Faria Brizola dos Santos
Total Records ( 4 ) for Talmir Augusto Faria Brizola dos Santos
  Wilson Abrao Saad , Ismael Francisco Motta Siqueira Guarda , Luiz Antonio de Arruda Camargo , Talmir Augusto Faria Brizola dos Santos , Sylvio Simoes and William Abrao Saad
  The 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.
  Wilson Abrao Saad , Ismael Francisco Motta Sigueira Guarda , Luis Antonio de Arruda Camargo , Talmir Augusto Faria Brizola dos Santos and William Abrao Saad
  We 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.
  Wilson Abrao Saad , Ismael Francisco Motta Siqueira Guarda , Luiz Antonio de Arruda , Camargo , Talmir Augusto Faria Brizola dos Santos , Sylvio Simoes and William Abrao Saad
  The 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.
  Wilson Abrao Saad , Ismael Francisco Motta Sigueira Guarda , Luis Antonio de Arruda Camargo , Talmir Augusto Faria Brizola dos Santos and William Abrao Saad
  We 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.
 
 
 
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