L A Camargo

Publications (90)154.82 Total impact

• Article: Role of the alpha(1)- and alpha(2)-adrenoceptors of the paraventricular nucleus on the water and salt intake, renal excretion, and arterial pressure induced by angiotensin II injection into the medial septal area.

  L A Camargo, W A Saad
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  ABSTRACT: In this study we investigated the influence of alpha-adrenergic antagonists injections into the paraventricular nucleus (PVN) of the hypothalamus on the thirst and salt appetite, diuresis, natriuresis, and pressor effects of angiotensin II (ANG II) stimulation of medial septal area (MSA). ANG II injection into the MSA induced water and sodium intake, diuresis, natriuresis, and pressor responses. The previous injection of prazosin (an alpha(1)-adrenergic antagonist) into the PVN abolished, whereas previous administration of yohimbine (an alpha(2)-adrenergic antagonist) into the PVN increased the water and sodium intake, urinary, natriuretic, and pressor responses induced by ANG II injected into the MSA. Previous injection of a nonselective alpha-adrenergic antagonist, regitin, into the PVN blocked the urinary excretion, and reduced the water and sodium intake, sodium intake, and pressor responses induced by ANG II injected into the MSA. The present results suggest that alpha-adrenergic pathways involving the PVN are important for the water and sodium excretion, urine and sodium excretion, and pressor responses, induced by angiotensinergic activation of the MSA.
  Brain Research Bulletin 05/2001; 54(6):595-602. · 2.82 Impact Factor
• Article: Effects of subtypes alpha- and beta-adrenoceptors of the lateral hypothalamus on the water and sodium intake induced by angiotensin II injected into the subfornical organ.

  L A Camargo, W A Saad, G P Camargo
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  ABSTRACT: The present experiments were conducted to investigate the role of the alpha(1A)-, alpha(1B), beta(1)- and beta(2)-adrenoceptors of the lateral hypothalamus (LH) on the water and salt intake responses elicited by subfornical organ (SFO) injection of angiotensin II (ANG II) in rats. 5-methylurapidil (an alpha(1A)-adrenergic antagonist), cyclazosin (an alpha(1B)-adrenergic antagonist) and ICI-118,551 (a beta(2)-adrenergic antagonist) injected into the LH produced a dose-dependent reduction, whereas efaroxan (an alpha(2)-antagonist) increased the water intake induced by administration of ANG II into the SFO. These data show that injection of 5-methylurapidil into the LH prior to ANG II into the SFO increased the water and sodium intake induced by the injection of ANG II. The present data also show that atenolol (a beta(1)-adrenergic antagonist), ICI-118,551, cyclazosin, or efaroxan injected into the LH reduced in a dose-dependent manner the water and sodium intake to angiotensinergic activation of SFO. Thus, the alpha(1)- and beta-adrenoceptors of the LH are possibly involved with central mechanisms dependent on ANG II and SFO that control water and sodium intake.
  Brain Research 11/2000; 881(2):176-81. · 2.73 Impact Factor
• Article: Effect of injection of L-NAME on drinking response.

  W A Saad, L A Camargo, R Saad, A F Pereira, S Simões
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  ABSTRACT: The drinking behavior responses to centrally administered N G-nitro-L-arginine methyl ester (L-NAME; 10, 20 or 40 microg/microl), an inhibitor of nitric oxide synthase, were studied in satiated rats, with cannulae stereotaxically implanted into the lateral ventricle (LV) and subfornical organ (SFO). Water intake increased in all animals after angiotensin II (ANG II) injection into the LV, with values of 14.2 +/- 1.4 ml/h. After injection of L-NAME at doses of 10, 20 or 40 microg/microl into the SFO before injection of ANG II (12 ng/microl) into the LV, water intake decreased progressively and reached basal levels after treatment with 0.15 M NaCl and with the highest dose of L-NAME (i.e., 40 microg). The water intake obtained after 40 microg/microl L-NAME was 0.8 +/- 0.01 ml/h. Also, the injection of L-NAME, 10, 20 or 40 microg/microl, into the LV progressively reduced the water intake induced by hypertonic saline, with values of 5.3 +/- 0.8, 3.2 +/- 0.8 and 0.7 +/- 0.01 ml/h, respectively. These results indicate that nitric oxide is involved in the regulation of drinking behavior induced by centrally administered ANG II and cellular dehydration and that the nitric oxide of the SFO plays an important role in this regulation.
  Brazilian Journal of Medical and Biological Research 12/1999; 32(11):1413-6. · 1.13 Impact Factor
• Article: Role of angiotensin II and vasopressin receptors within the supraoptic nucleus in water and sodium intake induced by the injection of angiotensin II into the medial septal area.

  V R Antunes, G M Camargo, R Saad, W A Saad, A C Luiz, L A Camargo
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  ABSTRACT: In this study we investigated the effects of the injection into the supraoptic nucleus (SON) of non-peptide AT1- and AT2-angiotensin II (ANG II) receptor antagonists, DuP753 and PD123319, as well as of the arginine-vasopressin (AVP) receptor antagonist d(CH2)5-Tyr(Me)-AVP, on water and 3% NaCl intake induced by the injection of ANG II into the medial septal area (MSA). The effects on water or 3% NaCl intake were assessed in 30-h water-deprived or in 20-h water-deprived furosemide-treated adult male rats, respectively. The drugs were injected in 0.5 microliter over 30-60 s. Controls were injected with a similar volume of 0.15 M NaCl. Antagonists were injected at doses of 20, 80 and 180 nmol. Water and sodium intake was measured over a 2-h period. Previous administration of the AT1 receptor antagonist DuP753 into the SON decreased water (65%, N = 10, P < 0.01) and sodium intake (81%, N = 8, P < 0.01) induced by the injection of ANG II (10 nmol) into the MSA. Neither of these responses was significantly changed by injection of the AT2-receptor antagonist PD123319 into the SON. On the other hand, while there was a decrease in water intake (45%, N = 9, P < 0.01), ANG II-induced sodium intake was significantly increased (70%, N = 8, P < 0.01) following injection of the V1-type vasopressin antagonist d(CH2)5-Tyr(Me)-AVP into the SON. These results suggest that both AT1 and V1 receptors within the SON may be involved in water and sodium intake induced by the activation of ANG II receptors within the MSA. Furthermore, they do not support the involvement of MSA AT2 receptors in the mediation of these responses.
  Brazilian Journal of Medical and Biological Research 12/1998; 31(12):1597-600. · 1.13 Impact Factor
• Article: Imidazoline receptors of the paraventricular nucleus on the pressor response induced by stimulation of the subfornical organ.

  W A Saad, L A Camargo, J E Silveira, R Saad, G M Camargo
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  ABSTRACT: In the present experiments we investigated a possible involvement of imidazoline receptors of the paraventricular nucleus (PVN) of the hypothalamus on the pressor effects of the angiotensin II (ANG II) injected into the subfornical organ (SFO), in male Holtzman rats (250-300 g) with a cannula implanted into the third ventricle (3rdV), PVN and SFO. At first we tested the participation of alpha 2 and imidazoline agonist and antagonist compounds on the pressor effect of ANG II injected into the 3rdV. Based on the results we may conclude that clonidine associated with rilmenidine was able to block the hypertensive response to ANG II. The ANG II (20 pmol) injected into SFO induced a robust increase in blood pressure (37 +/- 2 mmHg). Isotonic saline (0.15 M) NaCl did not produce any change in blood pressure (5 +/- 2 mmHg). The injection of rilmenidine (30 micrograms/kg/1 microL), an imidazoline agonist agent injected into PVN before ANG II injection into SFO, blocked the pressor effect of ANG II (5 +/- 2 mmHg). Also, the injection of idazoxan (60 micrograms/kg/microL) before rilmenidine blocked the inhibitory effect of rilmenidine on blood pressure (39 +/- 4 mmHg). The injection of clonidine (20 nmol/microL) prior to ANG II into the 3rdV produced a decreased in arterial blood pressure (37 +/- 2 mmHg) to (15 +/- 4 mmHg). The injection of yohimbine (80 nmol/microL) prior to clonidine blocked the effect of clonidine on the effect of ANG II (27 +/- 2 mmHg). The injection of rilmenidine prior to ANG II also induced a decrease in arterial blood pressure (10 +/- 3 mmHg). The injection of idazoxan prior to rilmenidine also blocked the inhibitory effect of rilmenidine (24 +/- 3 mmHg). In summary, the present study demonstrated that rilmenidine decreases the hypertensive effect of ANG II, with more potency than clonidine, even when injected into 3rdV or PVN. This study established that the PVN interacts with SFO by imidazoline receptors in order to control the arterial blood pressure.
  Journal of Physiology-Paris 03/1998; 92(1):25-30. · 1.31 Impact Factor
• Article: Effect of ibotenate lesions of the ventromedial hypothalamus on the water and salt intake induced by activation of the median preoptic nucleus in sodium-depleted rats.

  C F do Vale, G M Camargo, W A Saad, J V Menani, A Renzi, A C Luiz, P S Cerri, L A Camargo
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  ABSTRACT: In this study we investigated the influence of a ventromedial hypothalamus (VMH) lesion with ibotenic acid on water and sodium intake and pressor responses induced by combined treatment of the median preoptic nucleus (MnPO) with angiotensin II (ANG II) and adrenergic agonists (phenylephrine, norepinephrine, isoproterenol and clonidine). Male Holtzman rats with a stainless steel cannula implanted into the MnPO and bilateral sham (vehicle) or VMH lesions with ibotenic acid were used. The ingestion of water and sodium and mean arterial pressure (MAP) were determined in separate groups submitted to sodium depletion with the diuretic furosemide (20 mg/rat). ANG II (10 pmol) injection into the MnPO of sham-lesioned rats induced water and sodium intake and pressor responses. VMH-lesion reduced ANG II-induced water intake and increased saline intake. In sham rats phenylephrine (80 nmol) into MnPO increased, whereas norepinephrine (80 nmol) and clonidine (40 nmol) reduced ANG II-induced water intake while sodium intake was reduced only by clonidine into MnPO. In VMH-lesioned rats, phenylephrine reduced, noradrenaline increased and clonidine produced no effect on ANG II-induced water intake. In lesioned rats ANG II-induced sodium intake was reduced by phenylephrine and noradrenaline, whereas clonidine produced no change. ANG II-induced pressor response was reduced in VMH-lesioned rats, but the pressor response combining ANG II and phenylephrine or noradrenaline in VMH-lesioned rats was bigger than sham rats. These results show that the VMH is important for the changes in water and sodium intake and cardiovascular responses induced by angiotensinergic and adrenergic activation of the MnPO.
  Journal of the Autonomic Nervous System 10/1997; 66(1-2):19-25.
• Article: Ventromedial hypothalamus lesions increase the dipsogenic responses and reduce the pressor responses to median preoptic area activation.

  R Bastos, J V Menani, W A Saad, A Renzi, J E Silveira, L A Camargo
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  ABSTRACT: In this study, we investigated the participation of adrenergic receptors of the median preoptic area (MnPO) and the participation of ventromedial hypothalamus (VMH) in angiotensin II-(ANG II)-induced water intake and pressor responses. Male rats with sham or electrolytic VMH lesions and a stainless steel cannula implanted into the MnPO were used. Noradrenaline, clonidine (an alpha2-adrenergic receptor agonist), or phenylephrine (an alpha1-adrenergic receptor agonist) injected into the MnPO of sham-lesioned rats reduced water ingestion induced by ANG II injected into the same area. In VMH-lesioned rats ANG II-induced water intake increased with a previous injection of noradrenaline, phenylephrine, or isoproterenol. The pressor response induced by ANG II injected into the MnPO was reduced in VMH-lesioned rats, whereas the pressor response induced by clonidine was abolished. Previous treatment with noradrenaline and phenylephrine into the MnPO of sham-lesioned rats produced a pressor response, and a hypotensive response was obtained with the previous administration of noradrenaline, phenylephrine or isoproterenol into the MnPO of VMH-lesioned rats. These results show that VMH is essential for the dipsogenic and pressor responses induced by adrenergic and angiotensinergic activation of the MnPO in rats.
  Physiology & Behavior 09/1997; 62(2):311-6. · 2.87 Impact Factor
• Article: Functional evidence that the central renin-angiotensin system plays a role in the pressor response induced by central injection of carbachol.

  W A Saad, A C Luiz, L A Camargo, J E Silveira, S Fóglia, J V Menani
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  ABSTRACT: 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 microliter) into the LV blocked the pressor response induced by ANG II (12 ng/1 microliter) and carbachol (2 nmol/1 microliter). 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 microliter) 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.
  Brazilian Journal of Medical and Biological Research 05/1997; 30(4):493-6. · 1.13 Impact Factor
• Article: Effect of rilmenidine injection into the paraventricular nucleus of the hypothalamus on the water intake induced by application of angiotensin II to the subfornical organ.

  C A Arrais, W A Saad, L A Camargo, A Renzi, J V Menani, J E Silveira, R Saad
  Journal of Physiology-Paris 05/1997; 91(2):97-8. · 1.31 Impact Factor
• Article: Ibotenate lesion of the medial hypothalamus alters the salt intake and pressor responses to activation of the median preoptic nucleus in rats.

  C F do Vale, G M Camargo, A Renzi, A C Luiz, W A Saad, S Hetem, L A Camargo
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  ABSTRACT: We investigated the influence of ibotenic acid lesions of the medial hypothalamus (MH) on salt appetite and arterial blood pressure responses induced by angiotensinergic and adrenergic stimulation of the median preoptic nucleus (MnPO) of rats. Previous injection of the adrenergic agonists norepinephrine, clonidine, phenylephrine, and isoproterenol into the MnPO of sham MH-lesioned rats caused no change in the sodium intake induced by ANG II. ANG II injected into the MnPO of MH-lesioned rats increased sodium intake compared with sham-lesioned rats. Previous injection of clonidine and isoproterenol increased, whereas phenylephrine abolished the salt intake induced by ANG II into the MnPO of MH-lesioned rats. Previous injection of norepinephrine and clonidine into the MnPO of sham MH-lesioned rats caused no change in the mean arterial pressure (MAP) induced by ANG II. Under the same conditions, previous injection of phenylephrine increased, whereas isoproterenol reversed the increase in MAP induced by angiotensin II (ANG II). ANG II injected into the MnPO of MH-lesioned rats induce a decrease in MAP compared with sham-lesioned rats. Previous injection of phenylephrine or norepinephrine into the MnPO of MH-lesioned rats induced a negative MAP, whereas pretreatment with clonidine or isoproterenol increased the MAP produced by ANG II injected into the MnPO of sham- or MH-lesioned rats. These data show that ibotenic acid lesion of the MH increases the sodium intake and pressor responses induced by the concomitant angiotensinergic, alpha 2 and beta adrenergic activation of the MnPO, whereas alpha 1 activation may have opposite effects. MH involvement in excitatory and inhibitory mechanisms related to sodium intake and MAP control is suggested.
  Journal of Physiology-Paris 03/1997; 91(1):31-7. · 1.31 Impact Factor
• Article: Receptor-mediated effects of clonidine on need-induced 3% NaCl and water intake.

  M M Yada, P M de Paula, J V Menani, A Renzi, L A Camargo, W A Saad, L A De Luca
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  ABSTRACT: Clonidine combined with adrenergic antagonists were injected in the medial septal area in order to characterize the type of receptors involved with its inhibitory effect on 3% NaCl and water intake of sodium-depleted (furosemide + 24 h of removal of ambient sodium) and 30-h water-deprived rats, respectively. The inhibitory effect of clonidine (20 nmol) on need-induced water intake was reduced 50% by an 80-nmol dose of either idazoxan, yohimbine or prazosin. The inhibitory effect of clonidine (30 nmol) on need-induced 3% NaCl intake was completely antagonized by idazoxan (80, 160 nmol), not altered by yohimbine (40-160 nmol), and partially potentiated (40 nmol) or inhibited (160 nmol) by prazosin. Propranolol did not alter the effects of clonidine on either water (80 nmol) or 3% NaCl (40-160 nmol) intake. The results suggest that the inhibitory effects of clonidine on 3% NaCl and water intake are mediated by different types of alpha2-adrenergic receptors.
  Brain Research Bulletin 02/1997; 42(3):205-9. · 2.82 Impact Factor
• Article: Central interaction between atrial natriuretic peptide and angiotensin II in the control of sodium intake and excretion in female rats.

  P R De-Angelis, V R Antunes, G M Camargo, W A Saad, A Renzi, L A Camargo
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  ABSTRACT: We investigated the effects of estrogen on sodium intake and excretion induced by angiotensin II (ANG II), atrial natriuretic peptide (ANP) or ANG II plus ANP injected into the median nucleus (MnPO). Female Holtzman rats weighing 250-300 g were used. Sodium ingestion and excretion 120 min after the injection of 0.5 microliters of 0.15 M NaCl into the MnPO were 0.3 +/- 0.1 ml (N = 12) and 29 +/- 7 microEq in intact rats, 0.5 +/- 0.2 ml (N = 10) and 27 +/- 6 microEq in ovariectomized rats, and 0.2 +/- 0.08 (N = 11) and 36 +/- 8 microEq in estrogen-treated ovariectomized (50 micrograms/day for 21 days) rats, respectively. ANG II (21 microM) injection in intact, ovariectomized, and estrogen-treated ovariectomized rats increased sodium intake (3.8 +/- 0.4, 1.8 +/- 0.3 and 1.2 +/- 0.2 ml/120 min, respectively) (N = 11) and increased sodium excretion (166 +/- 18, 82 +/- 22 and 86 +/- 12 microEq/120 min, respectively) (N = 11). ANP (65 microM) injection in intact (N = 11), ovariectomized (N = 10) and estrogen-treated ovariectomized (N = 10) rats increased sodium intake (1.4 +/- 0.2, 1.8 +/- 0.3, and 1.7 +/- 0.3 ml/120 min, respectively) and sodium excretion (178 +/- 19, 187 +/- 9, and 232 +/- 29 microEq/120 min, respectively). Concomitant injection of ANG II and ANP into the MnPO of intact (N = 12), ovariectomized (N = 10) and estrogen-treated ovariectomized (N = 10) rats caused smaller effects than those produced by each peptide given alone: 1.3 +/- 0.2, 0.9 +/- 0.2 and 0.3 +/- 0.1 ml/120 min for sodium intake, respectively, and 86 +/- 9, 58 +/- 7, and 22 +/- 4 microEq/120 min for sodium excretion, respectively. Taken together, these results demonstrate that there is an antagonistic interaction of ANP and ANG II on sodium intake and excretion, and that reproductive hormones affect this interaction.
  Brazilian Journal of Medical and Biological Research 01/1997; 29(12):1671-4. · 1.13 Impact Factor
• Article: Antagonism of clonidine injected intracerebroventricularly in different models of salt intake.

  M A Sato, M M Yada, A Renzi, L A Camargo, W A Saad, J V Menani, L A De Luca Júnior
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  ABSTRACT: Clonidine, an alpha 2-adrenergic agonist, injected into the brain inhibits salt intake of animals treated by the diuretic model of sodium depletion. In th present study, we address the question of whether central injection of clonidine also inhibits salt intake in animals deprived of water or in the need-free state. Saline or clonidine (30 nmol) was injected into the anterior third ventricle of 24-h sodium-depleted (furosemide + removal of ambient sodium), of 24-h water-deprived and of normovolemic (need-free state) adult male rats. Clonidine injected intracerebroventricularly (i.c.v.) inhibited the 1.5% NaCl intake for 1209 min by 50 to 90% in every model tested. Therefore, different models of salt intake are inhibited by i.c.v. injection of clonidine. Idazoxan, an alpha 2-adrenergic antagonist, injected i.c.v. at a dose of 160 nmol, inhibited the effect of clonidine only in the furosemide + removal of ambient sodium model of salt intake. This indicates that the antagonism of this effect by idazoxan is dependent on the body fluid/sodium status of the animal.
  Brazilian Journal of Medical and Biological Research 01/1997; 29(12):1663-6. · 1.13 Impact Factor
• Article: On a dual role for clonidine stimulation of the ventromedial nucleus of the hypothalamus in sodium and potassium renal excretions of rats.

  W A Saad, G P Camargo, L A Camargo
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  ABSTRACT: The effects of clonidine on sodium and potassium excretions were examined after previous administration of prazosin (an alpha 1-adrenergic receptor antagonist) and yohimbine (an alpha 2-adrenergic receptor antagonist) into the ventromedial nucleus of the hypothalamus of conscious rats. Clonidine injected into the ventromedial nucleus of the hypothalamus induced inhibitory and facilitatory effects on the urinary sodium and potassium excretions. The results suggest that facilitatory effects of clonidine on natriuresis and kaliuresis are mediated through activation of alpha 1-adrenoceptors and that inhibitory effects require alpha 2A-adrenoceptors.
  Pharmacology 12/1996; 53(5):281-8. · 1.79 Impact Factor
• Article: Paraventricular nucleus administration of DuP753 or PD123319 inhibits the effects of angiotensin on water and sodium intake.

  M H do-Prado, G M Camargo, A Renzi, W A Saad, A C Luiz, R C Queiróz, L A Camargo
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  ABSTRACT: We determined the effects of DuP753 and PD123319 (both nonpeptides and selective antagonists of the AT1 and AT2 angiotensin receptors, respectively), and [Sar1, Ala8]ANG II(a non-selective peptide antagonist of angiotensin receptors) on water and 3% NaCl intake induced by administration of angiotensin II (ANG II) into the paraventricular nucleus (PVN) of sodium-depleted Holtzman rats weighing 250-300 g. Twenty hours before the experiments, the rats were depleted of sodium using furosemide (10 ng/rat, sc). The volume of drug solution injected was 0.5 microliters over a period of 10-15 sec. Water and sodium intake were measured at 0.25, 0.5, 1.0 and 2.0 h. Pre-treatment with DuP753 (14 rats) at a dose of 60 ng completely abolished the water intake induced by injection of 12 ng of ANG II (15 rats) (6.4 +/- 0.6 vs 1.4 +/- 0.3 ml/2 h), whereas [Sar1, Ala8] ANG II (12 rats) and PD123319 (10 rats) at the doses of 60 ng partially blocked water intake (6.4 +/- 0.6 vs 2.9 +/- 0.5 and 2.7 +/- 0.2 ml/h, respectively). In the same animals, [Sar1, Ala8]ANG II, DuP753, and PD123319 blocked the sodium intake induced by ANG II (9.2 +/- 1.6 vs 3.3 +/- 0.6, 1.8 +/- 0.3, and 1.4 +/- 0.2 ml/2 h respectively). These results indicate that both DuP753 and PD123329, administered into the PVN, blocked the water and sodium intake induced by administration of ANG II into the same site.
  Brazilian Journal of Medical and Biological Research 12/1996; 29(11):1499-502. · 1.13 Impact Factor
• Article: Effect of intracerebroventricular injection of ramipril on the drinking response caused by injection of noradrenaline into the third ventricle.

  V M Barros, W A Saad, L A Camargo, A Renzi, J V Menani
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  ABSTRACT: We studied the effect of ramipril injected into the third ventricle (3rdV) on the control of water intake induced by injection of noradrenaline into the 3rdV of adult male Holtzman rats (250-300 g) implanted with a chronic stainless steel cannula into the 3rdV. The injection volume was always 1 microliter and was injected over a period of 30-60 sec. Control animals were injected with 0.15 M NaCl. After the injection of isotonic saline (control, 0.15 M NaCl) into the 3rdV, water ingestion was 0.3 +/- 0.1 ml/h. Ramipril (1 mircogram/microliter) injected into the 3rdV prior to isotonic saline produced no changes in water ingestion (0.4 +/- 0.2 ml/h). The injection of noradrenaline (40 nmol/microliter) after isotonic saline induced an increase in water intake (3.0 +/- 1.1 ml/h). The prior injection of ramipril decreased this ingestion to 1.8 +/- 0.3 ml/h. These data show that the inhibition of converting enzyme in the brain reduces the water intake induced by catecholaminergic stimulation. We conclude that the brain is able to transform the prodrug ramipril into the active drug ramiprilat.
  Brazilian Journal of Medical and Biological Research 12/1996; 29(11):1503-5. · 1.13 Impact Factor
• Article: Losartan (DUP-753) blocks the natriuretic, kaliuretic and antidiuretic effect of intracerebroventricular injection of carbachol in water-loaded rats.

  W A Saad, A C Luiz, L A Camargo, A Renzi, J V Menani
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  ABSTRACT: We determined the effect of intracerebroventricular (icv) administration of losartan, an angiotensin II (ANG II) subtype 1 receptor (AT1) antagonist, on icv carbachol-induced natriuresis, kaliuresis and antidiuresis in water-loaded male Holtzman rats (250-300 g) with a cannula implanted into the lateral ventricle (LV). The rats were water loaded with 5% of their body weight by gavage twice, with the second gavage one hour after the first. Carbachol (2 nmol in 1 microliter) was injected icv immediately after the second load. When losartan (DUP-753, 50 nmol in 1 microliter) was administered icv, it was given 3 min before carbachol. Previous icv treatment with losartan significantly reduced the icv carbachol-induced natriuresis (324 +/- 17 microEq/120 min), kaliuresis (103 +/- 15 microEq/120 min) and antidiuresis (13.5 +/- 2.1 ml/120 min) compared to the effects of previous icv injection of saline (Na+ excretion = 498 +/- 22 microEq/120 min; K+ excretion = 167 +/- 20 microEq/120 min; urine volume = 5.2 +/- 1.2 ml/120 min). These results, reported as means +/- SEM for 12 rats in each group, are consistent with the hypothesis that AT1 subtype receptors participate in the regulation of body electrolyte balance.
  Brazilian Journal of Medical and Biological Research 05/1996; 29(4):511-3. · 1.13 Impact Factor
• Article: Inhibitory effect of DUP-753 on the drinking responses of rats to central administration of noradrenaline and angiotensin II and to dehydration.

  L C Reis, W A Saad, L A Camargo, A Renzi, V Menani, J E Silveira
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  ABSTRACT: We investigated the effect of losartan (DUP-753) on the dipsogenic responses produced by intracerebroventricular (icv) injection of noradrenaline (40 nmol/microliters) and angiotensin II (ANG II) (2 ng/microliters) in male Holtzman rats weighing 250-300 g. The effect of DUP-753 was also studied in animals submitted to water deprivation for 30 h. After control injections of isotonic saline (0.15 M NaCl, 1 microliter) into the lateral ventricle (LV) the water intake was 0.2 +/- 0.01 ml/h. DUP-753 (50 nmol/microliters) when injected alone into the LV of satiated animals had no significant effect on drinking (0.4 +/- 0.02 ml/h) (N = 8). DUP-753 (50 nmol/microliters) injected into the LV prior to noradrenaline reduced the water intake from 2.4 +/- 0.8 to 0.8 +/- 0.2 ml/h (N = 8). The water intake induced by injection of ANG II and water deprivation was also reduced from 9.2 +/- 1.4 and 12.7 +/- 1.4 ml/h to 0.8 +/- 0.2 and 1.7 +/- 0.3 ml/h (N = 6 and N = 8), respectively. These data indicate a correlation between noradrenergic pathways and angiotensinergic receptors and lead us to conclude that noradrenaline-induced water intake may be due to the release of ANG II by the brain. The finding that water intake was reduced by DUP-753 in water-deprived animals suggests that dehydration releases ANG II, and that AT1 receptors of the brain play an important role in the regulation of water intake induced by deprivation.
  Brazilian Journal of Medical and Biological Research 05/1996; 29(4):507-10. · 1.13 Impact Factor
• Article: Role of the alpha 1-, and alpha 2- and beta-adrenoceptors of the median preoptic area on the water intake, renal excretion, and arterial pressure induced by ANG II.

  R K da Silva, J V Menani, W A Saad, A Renzi, J E Silveira, A C Luiz, L A Camargo
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  ABSTRACT: The present experiments were conducted to investigate the role of the alpha 1-, alpha 2- and beta-adrenergic receptors of the median preoptic area (MnPO) on the water intake and urinary electrolyte excretion, elicited by central injections of angiotensin II (ANG II). Prazosin (an alpha 1-adrenergic receptor antagonist) and yohimbine (an alpha 2-adrenergic receptor antagonist) antagonized the water ingestion, Na+, K+, and urine excretion induced by ANG II. Administration of propranolol, a beta-adrenergic receptor antagonist increased the Na+, K+, and urine excretion induced by ANG II. Previous treatment with prazosin and yohimbine reduced the pressor responses to ANG II. These results suggest that the adrenergic neurotransmission in the MnPO may actively participate in ANG II-induced dipsogenesis, natriuresis, kaliuresis, diuresis and pressor responses in a process that involves alpha 1-, alpha 2-, and beta-adrenoceptors.
  Brain Research 05/1996; 717(1-2):38-43. · 2.73 Impact Factor
• Article: Effect of a non-peptide angiotensin receptor antagonist on water intake caused by centrally administered carbachol in the rat.

  L C Reis, W A Saad, L A Camargo, A Renzi, J V Menani
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  ABSTRACT: Angiotensin II (ANG II) administered centrally produces drinking by acting on subtype 1 ANG II (AT1) receptors. Carbachol, a cholinergic receptor agonist, also induces drinking behavior by a central action. In the present study we determined whether the response to carbachol also involves AT1 receptors. Male Holtzman rats (250-300 g) with stainless steel cannula implanted into the lateral ventricle (LV) were used. Water intake after injection of 0.15 M NaCl (1.0 microliter) into the LV was 0.2 +/- 0.01 ml/h (N = 8). The AT1 receptor antagonist DUP-753 (50 nmol/microliters) injected into the LV reduced water intake induced by ANG II (10 nmol/microliters) from 9.2 +/- 1.4 to 0.4 +/- 0.1 ml/h (N = 8), and water intake induced by carbachol (2 nmol/microliters) from 9.8 +/- 1.4 ml/h to 3.7 +/- 0.8 ml/h (N = 8). These results suggest that AT1 receptors play a role in the drinking behavior observed after central cholinergic stimulation in rats.
  Brazilian Journal of Medical and Biological Research 03/1996; 29(2):245-7. · 1.13 Impact Factor