Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distribution of high affinity histamine H3 receptors in various tissues from guinea pig has been determined using [3H]N alpha-methylhistamine binding. In the course of those studies, it was observed that the pituitary gland contains H3 receptors. Using this radioligand, we have now identified and characterized H3 receptors on' the AtT-20 cell line from a murine anterior pituitary tumor. This line has approximately 5000 high affinity (KD = 0.7 nM) H3 binding sites per cell. Competition binding with standard H1, H2 and H3 agents has confirmed that these sites are, indeed, H3 receptors. The H3 receptor specific agonist, (R)-alpha-methylhistamine increased the release of adrenocorticotropic hormone (ACTH) from AtT-20 cells in a dose- and time-dependent manner, while histamine and the H2 agonist dimaprit were significantly less potent. Furthermore, this response was blocked by thioperamide, an H3 receptor specific antagonist, but not by the H1 and H3 antagonists, chlorpeniramine and cimetidine. These results identify, for the first time, a cell line expressing H3 receptors and indicate that the high affinity histamine H3 receptor regulates ACTH release from that cell.
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PMID:High affinity histamine H3 receptors regulate ACTH release by AtT-20 cells. 131 2

Histamine H3 receptors have been identified in rat and guinea-pig pituitary glands and in the mouse pituitary tumor cell line, AtT-20. Histamine H3 receptor agonists are reported to stimulate adrenocorticotropic hormone (ACTH) release from AtT-20 cells, an effect blocked by histamine H3 but not H1 or H2 receptor antagonists. To determine whether negative feedback regulation of the histamine H3 receptor-mediated effect might occur, we tested the effects of steroid treatment upon binding of the agonist [3H]N alpha-methylhistamine to AtT-20 cell membranes. Consistent with feedback regulation, steroid treatment of the cells reduced [3H]N alpha-methylhistamine binding. The effect was dose-dependent and was greatest for glucocorticoids among the steroids tested. As the duration of steroid treatment increased, the amount of [3H]N alpha-methylhistamine binding decreased, to 15% of control at 36 h. However, the effect was not specific for histamine H3 receptors. Somatostatin inhibits ACTH release from these cells and its binding was similarly reduced by steroid treatment. Because steroids have been reported to modulate levels of guanine nucleotide-binding proteins, the lack of receptor specificity could reflect an indirect effect of steroids upon agonist binding and, in fact, we show that [3H]N alpha-methylhistamine binding to these cells, like somatostatin, is pertussis toxin-sensitive. However, steroid treatment does not alter the apparent levels of pertussis toxin substrate in these cells. Whether steroid treatment affects histamine H3 receptors of these cells directly or through some more subtle effect upon the guanine nucleotide-binding proteins to which they couple, the result is a negative feedback loop that attenuates [3H]N alpha-methylhistamine binding to these cells.
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PMID:Steroid-sensitivity of agonist binding to pituitary cell line histamine H3 receptors. 808 74