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Articles by William Abrao Saad
Total Records ( 6 ) for William Abrao Saad
  Wilson Abrao Saad , Ismael Francisco Motta Siqueira Guarda , Luiz Antonio de Arruda. Camargo , William Abrao Saad , Renata Saad Guarda , Talmir A.F.B. Santos and Sylvio Simoes
  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 AT 2 (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 and a 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.
  Wilson Abrao Saad , Luiz Antonio de Arruda Camargo , Jose Antunes-Rodrigues , William Abrao Saad , Ismael Franscisco Motta Sigueira Guarda and Renata Saad Guarda
  It was speculated whether the influence of lateral pvasopressin (AVP) and angiotensin (ANG II). The present study investigated the effects of central administration of specific AVP and ANG II antagonists (d(CH2)5-Tyr (Me)-AVP (AAVP) and [Adamanteanacetyl1, 0-ET-D-Tyr2, Val4, Aminobutyryl6, Arg8,9]-AVP (ATAVP) antagonists of V1 and V2 receptors of AVP. Also the effects of losartan and CGP42112A (selective ligands of the AT1 and AT2 angiotensin receptors, respectively), was investigated on Na+ uptake and renal fluid and electrolyte excretion. After an acclimatization period of 7 days, the animals were maintained under tribromoethanol (200 mg kg 1 body weight, intraperitoneal) anesthesia and placed in a Kopf stereotaxic instrument. Stainless guide cannula was implanted into the LPO. AAVP and ATAVP injected into the LPO prior to AVP produced a reduction in the sodium intake responses. Both the AT1 and AT2 ligands administered into the LPO elicited a decrease in the sodium intake induced by AVP injected into the LPO, but losartan was more effective than CGP 42112A. AVP injection into LPO increased sodium renal excretion, but this was reduced by prior AAVP administration. The ATAVP produced a decreased in the natriuretic effect of AVP. The losartan injected into LPO previous to AVP decreased the sodium excretion and the CGP 421122A also decreased the natriuretic effect of AVP with a high intensity. The AVP produced an antidiuresis effect that was inhibited by prior administration into LPO of the ATAVP. The AAVP produced no change in the antidiuretic effect of AVP. These results suggest that LPO are implicated in sodium balance that is mediated by V1, V2, AT1 and AT2 receptors.
  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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