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Articles by R.S. Guarda
Total Records ( 2 ) for R.S. Guarda
  W.A. Saad , I.F.M.S Guarda , L.A.A. Camargo , W.A. Saad and R.S. Guarda
  In this study we focused on the effect of injection of 7-nitroindazol (7NI) a neuronal nitric oxide synthase inhibitor (nNOSI), L-rginine (LA) a nitric oxide donor agent and atropine a muscarinic receptor antagonist, on the salivary secretion, induced by pilocarpine injection into antero ventral third ventricle (AV3V). Rats were anesthetized with 2,2,2-tribromoethanol (200 mg kg-1 b. wt.) and a stainless steel cannula was implanted into their AV3V. The amount of saliva secretion was studied over a ten minute period after injection of pilocarpine into AV3V. Injection of pilocarpine (10, 20, 40, 80, 160 μg/0.5 μL) into AV3V produced a dose-dependent increase in salivary secretion. 7-NI (40 μg/0.5 μL), was injected into AV3V prior to the injection of pilocarpine produced an increase in salivary secretion due to the effect of pilocarpine. LA (30 μg/0.5 μL) was injected into AV3V prior to pilocarpine attenuated the increase in salivary secretion induced by pilocarpine. The injection of atropine (20 μg/0.5 μL) prior to pilocarpine blocked the sialogogue effect of it. All these roles of pilocarpine depend on the release of nitric oxide into the AV3V and circumventricular structures of central nervous system that are implicated in the control of hydroeletrolitic balance of the body. We may also conclude that these structures are involved with the cholinergic excitatory mechanism that induces salivary secretion by implication of muscarinic receptors.
  W.A. Saad , I.F.M.S. Guarda , L.A.D.A. Camargo , R.S. Guarda , W.A. Saad and T.A.F.B.D. Santos
  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.
 
 
 
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