Involvement of Potassium Channels in Vasorelaxant Effect Induced by<i>Valeriana prionophylla</i>Standl. in Rat Mesenteric Artery

Assaysin vitroandin vivowere performed on extract from roots and leaves from theValeriana prionophyllaStandl. (VPR and VPF, resp.). In phenylephrine (1 μM) precontracted rings, VPR (0.01–300 μg/mL) induced a concentration-dependent relaxation (maximum response (MR) = 75.4 ± 4.0%, EC50= 5.97 (3.8–9.3)μg/mL,n=6]); this effect was significantly modified after removal of the endothelium (EC50= 39.6 (27.2–57.6)μg/mL,P&lt;0.05). However, VPF-induced vasorelaxation was less effective compared to VPR. When rings were preincubated with L-NAME (100 μM) or indomethacin (10 μM), the endothelium-dependent relaxation induced by VPR was significantly attenuated (MR = 20.9 ± 2.3%, 34.2 ± 2.9%, resp.,P&lt;0.001). In rings denuded endothelium, precontracted with KCl (80 mM), or in preparations pretreated with KCl (20 mM) or tetraethylammonium (1 or 3 mM), the vasorelaxant activity of VPR was significantly attenuated (MR = 40.0 ± 8.2,n=5; 50.5 ± 6.0%; 49.3 ± 6.4%; 46.8 ± 6.2%; resp.,P&lt;0.01). In contrast, neither glibenclamide (10 μM), barium chloride (30 μM), nor 4-aminopyridine (1 mM) affected VPR-induced relaxation. Taken together, these results demonstrate that hypotension induced by VPR seems to involve, at least in part, a vascular component. Furthermore, endothelium-independent relaxation induced by VPR involves K+channels activation, most likely due to BKCachannels, in the rat superior mesenteric artery.</jats:p

Influência das conexões cerebelo-hipotalâmicas sobre as funções autonômicas

Artigo não contém resumo

Brain Research

Texto completo: acesso restrito. p.121–132In the present study, we investigated the role of 5-HT3 and 5-HT2C receptors located within the medial amygdala (MeA) in the control of water and salt intake in sodium-depleted rats. Pharmacological activation of 5-HT3 receptors located in the medial amygdala by the selective 5-HT3 receptor agonist m-CPBG significantly reduced salt intake in sodium-depleted rats, an effect that is reverted by pretreatment with the selective 5-HT3 receptor antagonist ondansetron. In addition, the injection of ondansetron alone into the medial amygdala had no effect on salt intake in sodium-depleted and in sodium-repleted rats. Pharmacological stimulation of 5-HT2C receptors located in the medial amygdala by the selective 5-HT2C receptor agonist m-CPP failed to modify salt intake in sodium-depleted rats, whereas the blockade of these receptors by the selective 5-HT2C receptor antagonist SDZ SER 082 significantly reduced salt intake in this same group of animals. These results lead to the conclusion that the pharmacological activation of 5-HT3 receptors located within the MeA inhibits salt intake in sodium-depleted rats and that, in this same brain region, the functional integrity of 5-HT2C receptors is required to achieve the full expression of sodium appetite in sodium-depleted rats

Hypertensive response to stress: The role of histaminergic H1 and H2 receptors in the medial amygdala

AbstractDifferent brain areas seem to be involved in the cardiovascular responses to stress. The medial amygdala (MeA) has been shown to participate in cardiovascular control, and acute stress activates the MeA to a greater extent than any of the other amygdaloid structures. It has been demonstrated that the brain histaminergic system may be involved in behavioral, autonomic and neuroendocrine responses to stressful situations. The aim of the present study was to investigate the role of the histaminergic receptors H1 and H2 in cardiovascular responses to acute restraint stress. Wistar rats (280–320g) received bilateral injections of cimetidine, mepyramine or saline into the MeA and were submitted to 45min of restraint stress. Mepyramine microinjections at doses of 200, 100 and 50nmol promoted a dose-dependent blockade of the hypertensive response induced by the restraint stress. Cimetidine (200 and 100nmol) promoted a partial blockade of the hypertensive response to stress only at the highest dose administered. Neither drugs altered the typical stress-evoked tachycardiac responses. Furthermore, mepyramine and cimetidine were unable to modify the mean arterial pressure or heart rate of freely moving rats under basal conditions (non-stressed rats). The data suggest that in the MeA the histaminergic H1 receptors appear to be more important than H2 receptors in the hypertensive response to stress. Furthermore, there appears to be no histaminergic tonus in the MeA controlling blood pressure during non-stress conditions

Physiology and Behavior

Texto completo: acesso restrito. p. 531–539The aim of the present study was to investigate the effect of third ventricle injections of zinc on salt intake in rats in the three different experimental models where sodium appetite is increased: fluid deprivation, central angiotensinergic stimulation and sodium depletion. Adult Wistar male rats received third ventricle injections of Zn(Ac)2 in three different doses (0.03, 0.3 and 3.0 nmol/rat). Central angiotensinergic stimulation was achieved by third ventricle injections of angiotensin II in the dose of 25 ng/rat 30 min before central zinc administration. As expected, fluid deprivation, central angiotensinergic stimulation and sodium depletion significantly increased sodium appetite. Water intake was also enhanced after fluid deprivation and central angiotensinergic stimulation. After sodium depletion, no increase in water intake was observed. Third ventricle injections of zinc inhibited salt intake in all three experimental models studied. Water intake was also inhibited by central zinc administration after fluid deprivation and central angiotensinergic stimulation. Conversely, third ventricle injections of zinc were unable to modify food intake or body temperature. It is suggested that zinc, acting on central structures related to the control of body fluid homeostasis, inhibits the drive for salt intake that is normally observed during fluid deprivation, central angiotensinergic stimulation and sodium depletion

Physiology and Behavior

Texto completo: acesso restrito. p. 506–514The role of the central opioid system in the control of water and salt intake is complex, with both stimulatory and inhibitory effects having been observed. The aim of the present study was to investigate the participation of the central κ-opioid receptors in the control of salt appetite. Male Wistar rats were submitted to two different experimental protocols: sodium deficit produced by the diuretic, furosemide, and brain angiotensinergic stimulation in rats under normal sodium balance. Lateral ventricle (LV) injections of Nor-binaltorphimine (Nor-BNI) at different doses (5, 10 and 20 nmol) inhibited hypertonic saline solution (1.5%) intake in sodium-depleted rats. The salt appetite induced by an LV injection of angiotensin II (AngII) (10 ng) was also blocked by Nor-BNI injections into the LV, while no significant change was observed in water intake. Furthermore, the decrease in salt intake seems not to have been due to a general inhibition of locomotor activity or to any change in palatability, since central administration of Nor-BNI failed to modify the intake of a 0.1% saccharin solution when the animals were submitted to a “dessert test” or to induce any significant locomotor deficit in the open-field test. Also the central administration of Nor-BNI was unable to modify blood pressure in sodium-depleted animals. The present results suggest that activation of endogenous κ-opioid receptors modulates salt appetite induced by sodium depletion and by central angiotensinergic stimulation in rats

Brain Research

Trabalho completo: acesso restrito, p.64–72n the present study we investigated the role of central 5-HT2C receptors in the control of blood pressure and heart rate in non-stressed and stressed, adult, male, Wistar rats. Third ventricle injections of the 5-HT2C agonist mCPP elicited a significant increase in blood pressure in non-stressed animals. The initial period of this hypertensive response (10–30 min after mCPP administration) was accompanied by baroreflex-mediated bradycardia, while after this period the coexistence of hypertension and tachycardia was observed. These cardiovascular effects promoted by the central administration of mCPP were blocked by pretreatment with the 5-HT2C antagonist, SDZ SER 082. The administration of SDZ SER 082 alone induced no significant changes in blood pressure or heart rate. The pharmacological stimulation of central 5-HT2C receptors by mCPP did not change the hypertensive or tachycardic responses induced by restraint stress. Conversely, the blockade of central 5-HT2C receptors by SDZ SER 082 blunted stress-induced hypertension without modifying stress-induced tachycardia. It is concluded that the activation of central 5-HT2C receptors induces hypertension in non-stressed rats and that the normal function of these receptors is essential for the rise in blood pressure that occurs in the course of restraint stress

Neuropeptides

p. 219–227The aim of the present work was to investigate the role of brain l, j and d opioid receptors in the central serotonergic mechanisms regulating blood pressure in rats. The data obtained show that: (1) pharmacological activation of central 5-HT3 receptors yields a significant decrease in blood pressure; (2) the blockade of those receptors by a selective antagonist induces an acute hypertensive response; (3) the pharmacological blockade of central opioid receptors by three different opioid antagonists exhibiting variable degrees of selectivity to l, j and d opioid receptors always suppressed the hypotensive response induced by central 5-HT3 receptor stimulation; (4) the blockade of opioid receptors by the same opioid antagonists that impaired the hypotensive effect of central 5-HT3 receptor stimulation failed to modify blood pressure in animals not submitted to pharmacological manipulations of central 5-HT3 receptor function. It is shown that a 5-HT3 receptor-dependent mechanism seems to be part of the brain serotonergic system that contributes to cardiovascular regulation since the hypertensive response observed after ondansetron administration indicates that central 5-HT3 receptors exert a tonic inhibitory drive on blood pressure. Furthermore, the data obtained here clearly indicate that the hypotensive response observed after pharmacological stimulation of central 5-HT3 receptors depends on the functional integrity of brain l, j and d opioid receptors, suggesting that a functional interaction between serotonergic and opiatergic pathways in the brain is part of the complex, multifactorial system that regulates blood pressure in the central nervous system