Anterior hypothalamic lesions prevent the endotoxin-induced reduction of beta-adrenoceptor number in guinea pig lung.
Bacterial endotoxin (E. coli O111:B4) induces, 4 days after intraperitoneal injection, a 30% reduction of guinea pig lung beta-adrenoceptor number (Bmax). No change in affinity (Kd) for the receptors occurred. Bilateral electrolytic lesions centered in the anterior hypothalamic nucleus prevent this reduction in Bmax 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.
D000818:Animals; D004082:Dihydroalprenolol / Q000378:metabolism; D004731:Endotoxins / Q000494:pharmacology*; D004926:Escherichia coli; D006168:Guinea Pigs; D007032:Hypothalamus, Anterior / Q000502:physiology*; D007700:Kinetics; D008168:Lung / Q000294:innervation; D008297:Male; D011943:Receptors, Adrenergic, beta / Q000187:drug effects* / Q000378:metabolism
D004731:Endotoxins; D011943:Receptors, Adrenergic, beta; D004082:Dihydroalprenolol