Participation of B-endorphinergic system in the inhibitory effect of clonidine on induced sodium intake

CAEIRO X; VIVAS L.

Mendoza

Congreso; XXVI Reunión Científica Anual Sociedad de Biología de Cuyo; 2008

Sociedad de Biología de Cuyo

Participation of B-endorphinergic system in the inhibitory effect of clonidine on induced sodium intake Caeiro X, Vivas L. INIMEC-CONICET. Córdoba. E-mail: xcaeiro@immf.uncor.edu Considerable evidence has been gathered involving the interaction of alpha2-adrenergic and B-endorphinergic systems in hydrosaline and cardiovascular homeostatic regulation. In order to evaluate if the inhibitory action of clonidine (alfa2-adrenergic agonist) on sodium appetite is mediated by the B-endorphinergic system, B-endorphin knockout (Bend-/-), heterozygous (Bend+/-) and wild-type (Bend+/+) mice were submitted to a combined treatment of furosemide plus a low sodium diet. Twenty hours later, animals were injected with ip clonidine (0.5 mg/kg). Afterwards, mice were tested by allowing them access to a two bottle choice test (water and 2% NaCl). Although no differences were observed on induced water intake of mice with different genotypes, the present results indicate that Bend-/- mice treated with clonidine showed both an earlier recovery from sodium appetite inhibition, and also a larger consumption of saline solution when compared to the consumption response observed in Bend+/+ and Bend+/- mice. In summary, our results indicate that clonidine exerts a minor inhibitory effect on induced sodium appetite in mice lacking B-endorphin, suggesting that the inhibitory action of alpha2-adrenergic system on induced sodium intake may be mediated, at least in part, by the B-endorphinergic system. Supported by ANPCyT and CONICET