Caracterização da ação modulatória de citocinas inflamatórias pelo óleo de Melaleuca alternifolia e seus componentes (terpinen-4ol e alfa-terpineol) em macrófagos humanos ativados lipopolissacarídeos de Porphyromonas gingivalis e Escherichia coli

Pós-graduação em Odontologia - FOAR

Ractopamina em dietas para fêmeas suínas

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Ocorrência da agitação no despertar em crianças anestesiadas com isoflurano ou sevoflurano: influência do tratamento com a dexmedetomidina

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Efeitos das catecolaminas sobre a reposição volêmica com solução fisiológica. Repercussão sobre a variabilidade da frequência cardíaca de coelhos submetidos à hemorragia: estudo por análise espectral

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Sevoflurano e dexmedetomidina em isquemia e reperfusão renais no rato

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

Role of α2-adrenoceptors in the lateral parabrachial nucleus in the control of body fluid homeostasis

Central α2-adrenoceptors and the pontine lateral parabrachial nucleus (LPBN) are involved in the control of sodium and water intake. Bilateral injections of moxonidine (α2-adrenergic/imidazoline receptor agonist) or noradrenaline into the LPBN strongly increases 0.3 M NaCl intake induced by a combined treatment of furosemide plus captopril. Injection of moxonidine into the LPBN also increases hypertonic NaCl and water intake and reduces oxytocin secretion, urinary sodium, and water excreted by cell-dehydrated rats, causing a positive sodium and water balance, which suggests that moxonidine injected into the LPBN deactivates mechanisms that restrain body fluid volume expansion. Pretreatment with specific α2-adrenoceptor antagonists injected into the LPBN abolishes the behavioral and renal effects of moxonidine or noradrenaline injected into the same area, suggesting that these effects depend on activation of LPBN α2-adrenoceptors. In fluid-depleted rats, the palatability of sodium is reduced by ingestion of hypertonic NaCl, limiting intake. However, in rats treated with moxonidine injected into the LPBN, the NaCl palatability remains high, even after ingestion of significant amounts of 0.3 M NaCl. The changes in behavioral and renal responses produced by activation of α2-adrenoceptors in the LPBN are probably a consequence of reduction of oxytocin secretion and blockade of inhibitory signals that affect sodium palatability. In this review, a model is proposed to show how activation of α2-adrenoceptors in the LPBN may affect palatability and, consequently, ingestion of sodium as well as renal sodium excretion.

Citral: A monoterpene with prophylactic and therapeutic anti-nociceptive effects in experimental models of acute and chronic pain

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Doramectin reduces sexual behavior and penile erection in male rats

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

ANGIOTENSINERGIC AND CHOLINERGIC RECEPTORS OF THE SUBFORNICAL ORGAN MEDIATE SODIUM INTAKE INDUCED BY GABAergic ACTIVATION OF THE LATERAL PARABRACHIAL NUCLEUS

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Cardiovascular responses to injections of angiotensin II or carbachol into the rostral ventrolateral medulla in rats with AV3V lesions

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

ATP in the locus coeruleus as a modulator of cardiorespiratory control in unanaesthetized male rats

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

Effects of catecholamines on volemic replacement with saline solution and the impact on heart rate variability in rabbits subjected to hemorrhage. A study by spectral analysis

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

Exercise reduces angiotensin II responses in rat femoral veins

The control of blood flow during exercise involves different mechanisms, one of which is the activation of the renin-angiotensin system, which contributes to exercise-induced blood flow redistribution. Moreover, although angiotensin II (Ang II) is considered a potent venoconstrictor agonist, little is known about its effects on the venous bed during exercise. Therefore, the present study aimed to assess the Ang II responses in thefemoral vein taken from sedentary and trained rats at rest or subjected to a single bout of exercise immediately before organ bath experiments. Isolated preparations of femoral veins taken from resting-sedentary, exercised-sedentary, resting-trained and exercised-trained animals were studied in an organ bath. In parallel, the mRNA expression of prepro-endothelin-1 (ppET-1), as well as the ETA and ETB receptors, was quantified by real-time PCR in this tissue. The results show that, in the presence of L-NAME, Ang II responses in resting-sedentary animals were higher compared to the other groups. However, this difference disappeared after co-treatment with indomethacin, BQ-123 or BQ-788. Moreover, exercise reduced ppET-1 mRNA expression. These reductions in mRNA expression were more evident in resting-trained animals. In conclusion, either acute or repeated exercise adapts the rat femoral veins, thereby reducing the Ang II responses. This adaptation is masked by the action of locally produced nitric oxide and involves, at least partially, the ETB- mediated release of vasodilator prostanoids. Reductions in endothelin-1 production may also be involved in these exercise-induced modifications of Ang II responses in the femoral vein.

Exercise increases the angiotensin II effects in isolated portal vein of trained rats

Training in rats adapts the portal vein to respond vigorously to sympathetic stimuli even when the animal is re-exposed to exercise. Moreover, changes in the exercise-induced effects of angiotensin II, a potent venoconstrictor agonist, in venous beds remain to be investigated. Therefore, the present study aimed to assess the effects of angiotensin II in the portal vein and vena cava from sedentary and trained rats at rest or submitted to an exercise session immediately before organ bath experiments. We found that training or exposure of sedentary animals to a single bout of running exercise does not significantly change the responses of the rat portal vein to angiotensin II. However, the exposure of trained animals to a single bout of running exercise enhanced the response of the rat portal vein to angiotensin II. This enhancement appeared to be territory-specific because it was not observed in the vena cava. Moreover, it was not observed inendothelium-disrupted preparations and in preparations treated with Nω-nitro-l-arginine methyl esterhydrochloride, indomethacin, BQ-123 or BQ-788. These data indicate that training causes adaptations in the rat portal vein that respond vigorously to angiotensin II even upon re-exposure to exercise. This increased response to angiotensin II requires an enhancement of the vasocontractile influence of endothelin beyond the influence of nitric oxide and vasodilator prostanoids.

Angiotensin II AT(1) receptor mutants expressed in CHO cells caused morphological change and inhibition of cell growth

To assess the importance of the leucine residues in positions 262 and 265 of the angiotensin AT, receptor for signaling pathways and receptor expression and regulation, we compared the properties of CHO cells transfected with the wild type or the L262D or L265D receptor point mutants. It was found that the two mutants significantly increased the basal intracellular cyclic AMP (cAMP) formation in an agonist-independent mode. The morphology transformation of CHO cells was correlated with the increased cAMP formation, since forskolin, a direct activator of adenylate cyclase mimicked this effect on WT-expressing CHO cells. DNA synthesis was found to be inhibited in these cell lines, indicating that cAMP may also have determined the inhibitory effect on cell growth, in addition to the cell transformation from a tumorigenic to a non-tumorigenic phenotype. However a role for an increased Ca2(+) influx induced by the mutants in non-stimulated cells cannot be ruled out since this ion also was shown to cause transformed cells to regain the morphology and growth regulation. (c) 2005 Elsevier B.V. All rights reserved.