PMID: 2536451Jan 1, 1989Paper

Endotoxin-induced reduction of beta-adrenergic binding sites on splenic lymphocytes in vivo and in vitro: its modulation by anterior hypothalamic lesions

Life Sciences
A J Van OosterhoutF P Nijkamp

Abstract

Bacterial endotoxin induced a 38% decrease in the number of beta-adrenergic binding sites (Bmax) on splenic lymphocytes, four days after intraperitoneal administration to guinea pigs. No change in the affinity (Kd) for [125-I]-cyanopindolol ([125-I]-CYP) binding was observed. Incubation of guinea pig splenocytes in vitro with different concentrations of bacterial endotoxin for 24 hours resulted in an increased incorporation of [3H]-thymidine, a parameter for lymphocyte activation. Activation of splenic lymphocytes with the optimal endotoxin concentration of 100 micrograms/ml for 24 hours induced a 27% decrease in the Bmax whereas the Kd for [125-I]-CYP binding was not changed. Based on these findings, we speculate that activation of lymphocytes with endotoxin in vitro and in vivo is associated with a reduction in the number of beta-adrenergic binding sites on these cells. Anterior hypothalamic (AHA) lesions protected against the endotoxin-induced reduction in the number of beta-adrenergic binding sites on lymphocytes. The protective effect of these lesions could not be related to alterations in the plasma levels of cortisol, triiodothyronine (T3), thyroxine (T4), adrenaline and noradrenaline or to splenic noradrenaline content....Continue Reading

References

Apr 30, 1976·Brain Research·J Van der GugtenD H Versteeg
Jan 1, 1987·Annals of the New York Academy of Sciences·H V PeekeV I Reus
Jan 1, 1988·Trends in Pharmacological Sciences·C C MalbonD C Watkins
Feb 1, 1983·The Journal of Endocrinology·M ManinP Delost

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Jan 1, 1990·Life Sciences·A J Van Oosterhout, F P Nijkamp

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