962 resultados para area of the circle


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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Cholinergic activation of the medial septal area (MSA) with carbachol produces thirst, natriuresis, antidiuresis and pressor response. In the brain, hydrogen peroxide (H2O2) modulates autonomic and behavioral responses. In the present study, we investigated the effects of the combination of carbachol and H2O2 injected into the MSA on water intake, renal excretion, cardiovascular responses and the activity of vasopressinergic and oxytocinergic neurons in the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei. Furthermore, the possible modulation of carbachol responses by H2O2 acting through K+ATP channels was also investigated. Male Holtzman rats (280–320 g) with stainless steel cannulas implanted in the MSA were used. The pre-treatment with H2O2 in the MSA reduced carbachol-induced thirst (7.9 ± 1.0, vs. carbachol: 13.2 ± 2.0 ml/60 min), antidiuresis (9.6 ± 0.5, vs. carbachol: 7.0 ± 0.8 ml/120 min,), natriuresis (385 ± 36, vs. carbachol: 528 ± 46 μEq/120 min) and pressor response (33 ± 5, vs. carbachol: 47 ± 3 mmHg). Combining H2O2 and carbachol into the MSA also reduced the number of vasopressinergic neurons expressing c-Fos in the PVN (46.4 ± 11.2, vs. carbachol: 98.5 ± 5.9 c-Fos/AVP cells) and oxytocinergic neurons expressing c-Fos in the PVN (38.5 ± 16.1, vs. carbachol: 75.1 ± 8.5 c-Fos/OT cells) and in the SON (57.8 ± 10.2, vs. carbachol: 102.7 ± 7.4 c-Fos/OT cells). Glibenclamide (K+ATP channel blocker) into the MSA partially reversed H2O2 inhibitory responses. These results suggest that H2O2 acting through K+ATP channels in the MSA attenuates responses induced by cholinergic activation in the same area.

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Background: The aim of this study was to determine the perception of smile esthetics among orthodontists and laypeople with respect to the presence of diastemas in the upper lateral incisor in the mesial, distal, and both surfaces using an oblique smile analysis. Methods: Two standardized oblique photos of pleasant smiles from two white women were selected. Images were digitally altered to create diastemas in the lateral incisor, in 0.5-mm increments, in the mesial, distal, or both surfaces. Final images were randomly assembled in a photo album, which was given to 120 judgesd60 orthodontists and 60 laypersons. Each rater was asked to evaluate the attractiveness of the images on a visual analog scale. The data collected were submitted to statistical analysis by the means of one-way ANOVA with the Tukey post hoc test and the unpaired Student’s t test. Results: The most attractive smile was the one without spacing, and the presence of diastemas was considered unattractive by both groups of raters, following a pattern: the greater and the more mesially located, the more unattractive was the smile. Conclusions: The results of this study suggest that diastemas in the upper lateral incisor area were considered unattractive, following a pattern: the greater and the more mesially located, the more unattractive was the smile.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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To determine whether central α1 and α2-adrenergic mechanisms are involved in urinary sodium and potassium excretion and urine volume induced by angiotensin II (ANGII), these renal parameters were measured in volume-expanded Holtzman rats with cannulas implanted into lateral ventricle (LV) and lateral hypothalamus (LH). The injection of ANGII into LV in rats with volume expansion reduced the sodium, potassium and urine excretion in comparison to the control injections of isotonic saline, whereas prazosin (α1 antagonist) potentiated these effects. Clonidine (α2 agonist) and yohimbine (α2 antagonist) injected into LH previous to injection of ANGII into LV also abolished the inhibitory effect of ANGII. These results suggest that the discharge of central alpha-adrenergic receptors has dual inhibitory and excitatory effect on antinatriuretic, antikaliuretic and antidiuretic effect induced by central ANGII in volume-expanded rats. © 1995.

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In this study, we investigated an interaction between noradrenergic and cholinergic pathways of the medial septal area (MSA) on the control of water intake and urinary electrolyte excretion by means of injection of their respective agonists. Noradrenaline (a nonspecific α-adrenergic agonist) and clonidine (an α2-adrenergic agonist), but not phenylephrine (an α1-adrenergic agonist), induced natriuresis and kaliuresis. α-Adrenergic activation had no effect on the natriuresis and kaliuresis induced by carbachol (a cholinergic agonist) and it inhibited the antinatriuresis and antikaliuresis induced by isoproterenol (a ß-adrenergic agonist). Interactions related to volume excretion are complex. α-Adrenergic activation induced a mild diuresis and inhibited the antidiuresis induced by isoproterenol, but phenylephrine combined with carbachol induced antidiuresis. The water intake induced by carbachol was inhibited by clonidine and noradrenaline, but not phenylephrine. These results show an asymmetry in the interaction between α-adrenergic and cholinergic receptors concerning water intake and electrolyte excretion. © 1992.

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In the present experiments, we investigated a possible involvement of noradrenergic receptors of the lateral hypothalamus (LH) in the water intake and pressor response induced by cholinergic stimulation of the medial septal area (MSA) in rats. The cholinergic agonist carbachol (2 nmol) injected into the MSA induced water intake and pressor response. The injection of an α2-adrenergic agonist, clonidine (20 and 40 nmol), but not of an α1-adrenergic agonist, phenylephrine (80 and 160 nmol), into the LH inhibits the water intake induced by carbachol injected into the MSA. The injection of clonidine or phenylephrine into the LH produced no change in the MAP increase induced by carbachol injected into the MSA. The present results suggest that adrenergic pathways involving the LH are important for the water intake, but not for the pressor response, induced by cholinergic activation of the MSA. © 1994.

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Rats bearing lesions in the septal area followed by lesions in the subfornical organ were submitted to various thirst-eliciting procedures. The rats with hyperdipsia induced by lesions of the septal area drank more water than either during the control period or after lesion of the subfornical organ under the same thirst-eliciting or angiotensin-liberating stimuli (polyethyleneglycol, isoproterenol, water deprivation and ligation of the inferior vena cava). The overdrinking elicited by lesions in the septal area was blocked after lesion of the subfornical organ. Neither hypovolemia, nor hypotension or water deprivation could elicit increased water intake in animals whose subfornical organ had been destroyed. Animals with lesions in the subfornical organ showed decreased water intake after cellular dehydration. The results obtained suggest that the subfornical organ acts as a more important structure than the septal area in the regulation of water intake elicited by angiotensin, with two opposite effects: a direct one facilitating water intake, and an indirect one inhibiting the septal area. The septal area has an inhibitory effect on the subfornical organ and on water intake. © 1980.

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In the present study we investigated the effect of electrolytic lesion of the medial septal area (MSA) on the pressor and dipsogenic response to cholinergic activation and angiotensin II (ANGII) injection into the subfornical organ (SFO) in rats. In addition the effect of MSA lesion on the natriuresis, kaliuresis and diuresis after cholinergic activation of the SFO was also investigated. Sham- and MSA-lesioned rats with a stainless steel cannula implanted into the SFO was used. The injection of ANGII (12 ng) into the SFO in sham rats produced pressor (24 ± 2 mmHg) and dipsogenic (9.6 ± 1.1 ml/h) responses. MSA lesion, both acute (2-6 days) and chronic (15-19 days), reduced the pressor (14 ± 2 mmHg) and dipsogenic (2.7 ± 1 ml/h) responses to ANGII into SFO. The injection of the cholinergic agonist carbachol (2 nmol) into the SFO in sham rats produced pressor (48 ± 4 mmHg), dipsogenic (10 ± 1.2 ml/h), natriuretic (457 ± 58 μEq/2 h) and kaliuretic (249 ± 16 μEq/2 h) responses. Acute, but not chronic MSA lesion reduced the pressor (27 ± 3 mmHg), natriuretic (198 ± 55 μEq/2 h) and kaliuretic (128 ± 16 μEq/2 h) responses to carbachol into SFO. No change in the dipsogenic response to carbachol into the SFO was observed in MSA-lesioned rats. Antidiuresis after carbachol was observed only in MSA-lesioned rats. The present results show that the MSA plays a role on the pressor, natriuretic and kaliuretic responses to cholinergic activation of the SFO in rats and on the pressor and dipsogenic responses to ANGII into the same area. In addition, they provide circumstancial evidence for separate circuits subserving the dipsogenic response to central cholinergic and angiotensinergic activation. A facilited diuresis after MSA lesion is also suggested.

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The present experiments were conducted to investigate the role of the α1-, α2- and β-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 α1-adrenergic receptor antagonist) and yohimbine (an α2-adrenergic receptor antagonist) antagonized the water ingestion, Na +, K +, and urine excretion induced by ANG II. Administration of propranolol, a β-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 α1-, α2-, and β-adrenoceptors.