This evidence supports the existence of adrenergic andâ-endorphin plays a role in the alpha 2-adrenergic/Ĭlonidinemay be mediated by the â-endorphinergic system. May be independent of â-endorphin modulation during the first stage however, the long-lasting inhibitory effect ofĬlonidinemay be mediated by the â-endorphinergic system. Considering these results and the fact that plasma half-life of clonidine at the doseĪdministered is approximately 3 h, it is possible to speculate that the inhibitory effect of clonidine on sodiumappetite Moreover no differences in dipsogenic response were observedīetween the genotypes. Genotype however, in the final stage of the test, a reversal of the inhibitory response on induced sodium appetiteīecomes evident in the mice lacking â-endorphin. The results indicate that clonidineĪdministration during the first stage of the test exerts an equivalent inhibition on sodium intake regardless of the Later, the animals were subjected to a two-bottle choice test (water/2% NaCl). Treatment of furosemide and lowsodiumdiet and, 20 h later,were administered with clonidine (0.5 mg/kg). Heterozygous (âend+/−) andwild-type (âend+/+)mice were submitted to acute sodiumdepletion by a combined In order to evaluate whether the inhibitory action ofĬlonidine (an á2-adrenergic/imidazoline receptor agonist) on induced sodium intake is mediated by the â-Įndorphinergic system, we used a â-endorphin deficient mouse line. Imidazoline receptor agonist attenuation of salt appetite. In the present study, we investigated the degree to which â-endorphin plays a role in the alpha 2-adrenergic/
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