Anterior hypothalamic lesions prevent the endotoxin-induced reduction of beta-adrenoceptor number in guinea pig lung

Abstract

Bacterial endotoxin ( E. coli O 111:B 4) induces, 4 days after intraperitoneal injection, a 30% reduction of guinea pig lung beta-adrenoceptor number (B max). No change in affinity ( K d ) for the receptors occurred. Bilateral electrolytic lesions centered in the anterior hypothalamic nucleus prevent this reduction in B max and even reverse the reduction into a small increase in beta-adrenoceptor number. Since it is known from the literature data that anterior hypothalamic lesions as well as beta-adrenoceptor stimulants have an inhibitory influence on the immune system, the mechanism by which these lesions inhibit the reduction of beta-adrenoceptor sites after bacterial endotoxin and influence immune functions, may be related.