In the present study, we investigated the effect of central serotonergic pathway activation achieved through third ventricle injections of quipazine, a serotonergic agonist, on plasma glucose levels of fasted and fed adult Wistar male rats, whose third ventricles were canulated 7 days before the experiments. Central quipazine administration induced a significant increase in plasma glucose levels in fasted animals, but was unable to modify plasma glucose concentrations in fed rats. Pretreatment with alpha-helical CRH, a CRH antagonist, significantly attenuated quipazine-induced hyperglycemia. Pretreatment with two different 5-HT3 receptor antagonists, LY-278,584 and ondansetron, was also able to produce a significant reduction in the hyperglycemic response evoked by central administration of quipazine. None of the antagonists used was capable of modifying plasma glucose concentrations when injected alone into the third ventricle. Quipazine-treated, hyperglycemic animals did not show any increase in plasma insulin levels. We conclude that acute pharmacological serotonergic stimulation by quipazine produces hyperglycemia by mechanisms that require the functional integrity of both CRH and 5-HT3 receptors, and that impairment in insulin secretion and/or activity may explain hyperglycemia induced by third ventricle injections of quipazine.
The aim of the study was to verify the effect of central angiotensin II AT2 receptor blockade in thermoregulatory responses during exercise in rats. Internal (Tb) and skin tail (Ttail) temperatures were measured in Wistar rats while they were running until fatigue (18 m.min‐¹, 5% inclination) after intracerebroventricular injection of 2µL of PD 123319 (PD; AT2 angiotensin II receptor antagonist; 10 µg) or 0.15 M NaCl (SAL) (n=7/each). Total time of exercise until fatigue (TTE) and workload (W) were determined. Rats treated with PD had an increase of 17% and 20% in TTE and W, respectively, in comparison with SAL animals (p<0.05). During exercise, Tb enhanced in both group, however, no difference was seen between treatments. On the other hand, following the first 15 minutes of exercise, Ttail variation was superior in PD rats until fatigue (3.1 ± 1,5 °C Sal vs. 4.9 ± 1,2 °C PD, p<0.05). Moreover, the increased Ttail at fatigue shown by PD‐rats directly correlated with their enhanced TTE (r = 0.82, P < 0.01). The data shows that AT2 receptor blockade improves heat balance during exercise due to better ability to dissipate heat, which contributes to enhanced exercise performance.
Grant Funding Source: FAPEMIG, CNPq and CAPES
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