943 resultados para adrenergic receptors


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1. This work investigated the effects of androgens on the norepinephrine sensitivity of vasa deferentia from rats submitted to acute or repeated stress, as well as the participation of alpha(1)-adrenoceptors in the response of intact and bisected vasa deferentia from adult normal rats submitted to acute or repeated stress.2. The acute stress produced subsensitivity to norepinephrine only in intact vasa deferentia from adult normal rats, which was prevented by lack of androgens, suggesting that the sensitivity may be dependent on the physiological level of androgen,3. No change was observed in intact vas deferens sensitivity to norepinephrine in repeated stress, suggesting the occurrence of adaptation to elevated norepinephrine levels or a mild decrease in androgen levers or both.4. The changes in sensitivity observed in acute and repeated stress may also be due to alterations in alpha(1)-adrenergic receptors that are located in the prostatic portion of the vas deferens. (C) 1998 Elsevier B.V.

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In this study we investigated: (a) the effects of intracerebroventricular (i.c.v.) injections of moxonidine (an alpha(2)-adrenergic and imidazoline receptor agonist) on the ingestion of water and NaCl induced by 24 h of water deprivation; (b) the effects of i.c.v. injection of moxonidine on central angiotensin II (ANG II)- and carbachol-induced water intake; (c) the effects of the pre-treatment with i.c.v, idazoxan (an alpha(2)-adrenergic and imidazoline receptor antagonist) and RX 821002 (a selective alpha(2)-adrenergic antagonist) on the antidipsogenic action of central moxonidine. Male Holtzman rats had stainless steel cannulas implanted in the lateral cerebral ventricle. Intracerebroventricular injection of moxonidine (5 and 20 nmol/1 mu l) reduced the ingestion of 1.5% NaCl solution (4.1 +/- 1.1 and 2.9 +/- 2.5 ml/2 h, respectively vs. control = 7.4 +/- 2.1 ml/2 h) and water intake (2.0 +/- 0.6 and 0.3 +/- 0.2 ml/h, respectively vs. control = 13.0 +/- 1.4 ml/h) induced by water deprivation, Intracerebroventricular moxonidine (5 nmol/1 mu l) also reduced i.c.v. ANG Ii-induced water intake (2.8 +/- 0.9 vs. control = 7.9 +/- 1.7 ml/1 h) and i.c.v. moxonidine (10 and 20 nmol/1 mu l) reduced i.c.v. carbachol-induced water intake (4.3 +/- 1.7 and 2.1 +/- 0.9, respectively vs. control = 9.2 +/- 1.0 ml/1 h). The pre-treatment with i.c.v. idazoxan (40 to 320 nmol/1 mu l) abolished the inhibitory effect of i.c.v, moxonidine on carbachol-induced water intake. Intracerebroventricular idazoxan (320 nmol/1 mu l) partially reduced the inhibitory effect of moxonidine on water deprivation-induced water intake and produced only a tendency to reduce the antidipsogenic effect of moxonidine on ANG Ii-induced water intake. RX 821002 (80 and 160 nmol/1 mu l) completely abolished the antidipsogenic action of moxonidine on ANG Ii-induced water intake. The results show that central injections c: moxonidine strongly inhibit water and NaCl ingestion. They also suggest the involvement of central alpha(2)-adrenergic receptors in the antidipsogenic action of moxonidine. (C) 1999 Elsevier B.V.

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1. Tityustoxin (TsTx), a toxic fraction of Tityus serrulatus venom, was studied on the isolated guinea-pig vas deferens. It increased significantly the maximal response of the preparation to both norepinephrine and acetylcholine and decreased the effective median dose of norepinephrine. 2. The effect of TsTx on norepinephrine median dose was unchanged when atropinized or pharmacologically 'denervated' preparations were used but was abolished when both procedures were associated. 3. Atropinization of pharmacologically denervated muscles almost never modify the TsTx-induced increase in the maximal response to norepinephrine. 4. On denervated or phentolamine-treated muscles TsTx-induced increase in the maximal response to acetylcholine was abolished. 5. It was concluded that toxin predominantly induces adrenergic postsynaptic supersensitivity. 6. Of minor significance, it also induces presynaptic cholinergic and adrenergic supersensitivity. 7. Comparison of these results with those of crude venom indicates that TsTx effects may result from the sum of the effects of subcomponents not demonstrated by the chemical procedures here utilized.

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The development of the febrile response to E. coli lipopolysaccharide (1.5 μg/kg, i.v.) in thyroid-deficient rabbits has been studied. Twenty-eight New Zealand White rabbits weighing 2.1-2.3 kg were used. Hypothyroidism was induced by treatment with propylthiouracil (100 or 200 mg/kg body wt./15 days). Thyroid-deficient animals showed a reduction in the febrile response to lipopolysaccharide, but the effect was significantly different (p<0.01) from the control only for rabbits treated with 200 mg/kg of propylthiouracil. Propranolol (2 mg/kg, i.p.) given 30 min before lipopolysaccharide also reduced (p<0.01) the fever response in control rabbits. The results of this experiment are consistent with the hypothesis that the reduction in the febrile response of thyroid-deficient rabbits is due to the reduced number of β-adrenergic receptors, or to a change in the availability of neurotransmitter in thermogenically active tissues, such as brown fat.

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The effects of androgenic deprivation induced by castration on the norepinephrine contractile response of vas deferens from rats, which have been submitted to acute swimming-stress were determined. Acute swimming-stress led to subsensitivity to norepinephrine in vas deferens excised from intact rats. Similarly, castration also induced subsensitivity to norepinephrine, but no further subsensitivity occurred in organs from castrated rats submitted to acute stress. The results indicate a different response to norepinephrine in terms of relative responsiveness ratio, when vas deferens was excised from castrated rats or castrated rats submitted to acute stress. It is suggested that androgenic steroids modulate the recovery of homeostasis in rat vas deferens during acute stress, and that this effect may involve mechanisms that affect both the sensitivity of adrenergic receptors and the system of neuronal uptake of catecholamines.

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Amitraz, an acaricide used to control ectoparasites in animals has a complex pharmacological activity, including α2-adrenergic agonist action. The purpose of this research was to investigate the possible antinociceptive and/or sedative effect of amitraz in horses. The sedative effect of the intravenous (i.v.) injection of dimethylformamide (DMF, 5 mL, control) or amitraz (0.05, 0.10, 0.15 mg/kg), was investigated on the head ptosis test. The participation of α2-adrenergic receptors in the sedative effect provoked by amitraz was studied by dosing yohimbine (0.12 mg/kg, i.v.). To measure the antinociception, xylazine hydrochloride (1 mg/kg, i.v., positive control) and the same doses of amitraz and DMF were used. A focused radiant light/heat directed onto the fetlock and withers of a horse were used as a noxious stimulus to measure the hoof withdrawal reflex latency (HWRL) and the skin twitch reflex latency (STRL). The three doses of amitraz used (0.05, 0.10 and 0.15 mg/kg) provoked a dose-dependent relaxation of the cervical muscles. The experiments with amitraz and xylazine on the HWRL showed that after i.v. administration of all doses of amitraz there was a significant increase of HWRL up to 150 min after the injections. Additionally, there was a significant difference between control (DMF) and positive control (xylazine) values up to 30 min after drug injection. On the other hand, the experiments on the STRL show that after administration of amitraz at the dose of 0.15 mg/kg, a significant increase in STRL was observed when compared with the control group. This effect lasted up to 120 min after injection. However, no significant antinociceptive effect was observed with the 0.05 and 0.10 mg/kg doses of amitraz or at the 1.0 mg/kg dose of xylazine.

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α2-Adrenoceptor activation with moxonidine (α2-adrenergic/imidazoline receptor agonist) into the lateral parabrachial nucleus (LPBN) enhances angiotensin II/hypovolaemia-induced sodium intake and drives cell dehydrated rats to ingest hypertonic sodium solution besides water. Angiotensin II and osmotic signals are suggested to stimulate meal-induced water intake. Therefore, in the present study we investigated the effects of bilateral injections of moxonidine into the LPBN on food deprivation-induced food intake and on meal-associated water and 0.3 M NaCl intake. Male Holtzman rats with cannulas implanted bilaterally into the LPBN were submitted to 14 or 24 h of food deprivation with water and 0.3 M NaCl available (n = 6-14). Bilateral injections of moxonidine (0.5 nmol/0.2 μl) into the LPBN increased meal-associated 0.3 M NaCl intake (11.4 ± 3.0 ml/120 min versus vehicle: 2.2 ± 0.9 ml/120 min), without changing food intake (11.1 ± 1.2 g/120 min versus vehicle: 11.2 ± 0.9 g/120 min) or water intake (10.2 ± 1.5 ml/120 min versus vehicle: 10.4 ± 1.2 ml/120 min) by 24 h food deprived rats. When no food was available during the test, moxonidine (0.5 nmol) into the LPBN of 24 h food-deprived rats produced no change in 0.3 M NaCl intake (1.0 ± 0.6 ml/120 min versus vehicle: 1.8 ± 1.1 ml/120 min), nor in water intake (0.2 ± 0.1 ml/120 min versus vehicle: 0.6 ± 0.3 ml/120 min). The results suggest that signals generated during a meal, like dehydration, for example, not hunger, induce hypertonic NaCl intake when moxonidine is acting in the LPBN. Thus, activation of LPBN inhibitory mechanisms seems necessary to restrain sodium intake during a meal. © 2007 Elsevier B.V. All rights reserved.

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The goal of the present study was to determine if nitric oxide (NO) acting on the brain of bullfrog (Lithobates catesbeianus) is involved in arterial pressure and heart rate (HR) control by influencing sympathetic activity. We investigated the effect of intracerebroventricular injections of l-NMMA (a nonselective NO synthase inhibitor) on mean arterial blood pressure (MAP), HR and cutaneous vascular conductance (CVC) of pelvic skin after intravenous injection of α or β adrenergic blockers, prazosin or sotalol, respectively. Arterial pressure was directly measured by a telemetry sensor inserted in the aortic arch of animals. l-NMMA increased MAP, but did not change HR. This hypertensive response was inhibited by the pre-treatment with prazosin, but accentuated by sotalol. The effect of l-NMMA on MAP was also inhibited by i.v. injections of the ganglionic blocker, hexamethonium. Thus, NO acting on the brain of bullfrog seems to present a hypotensive effect influencing the sympathetic activity dependent on α and β adrenergic receptors in the periphery. © 2013 Elsevier Inc.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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Pós-graduação em Odontologia - FOA

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)