Adrenocorticotropic hormone stimulation of lacrimal peroxidase secretion.
The effect of adrenocorticotropic hormone (ACTH) on secretion of lacrimal gland peroxidase was studied using an in vitro perifusion technique. The peptide stimulated a dose-dependent (1 nM to 100 nM) release of peroxidase, with the maximum level of secretion induced by 20 nM ACTH. Secretion in the presence of submaximal ACTH was potentiated with either 100 microM iso-butylmethylxanthine or 0.3 microM carbachol. In contrast, the combination of ACTH and phenylephrine was additive. Time-dependence studies demonstrated that the stimulation of peroxidase release by ACTH, as with other cyclic adenosine monophosphate mediated secretagogues, showed a latency in reaching the maximum rate which was not evident with either cholinergic or alpha-adrenergic stimulation. Furthermore, where potentiation of the response to ACTH occurred, the time course was distinctly altered from that obtained with either ACTH or the potentiating agonist alone. The data suggest that lacrimal gland function is regulated by a multiple system of neurotransmitters and (or) neuromodulators that involves the activation of peptidergic as well as cholinergic and alpha-adrenergic receptors.
D015056:1-Methyl-3-isobutylxanthine / Q000494:pharmacology; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology*; D000818:Animals; D002217:Carbachol / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004357:Drug Synergism; D066298:In Vitro Techniques; D007765:Lacrimal Apparatus / Q000187:drug effects / Q000201:enzymology*; D008297:Male; D010544:Peroxidases / Q000378:metabolism*; D010656:Phenylephrine / Q000494:pharmacology; D051381:Rats; D011916:Rats, Inbred F344; D012636:Secretory Rate / Q000187:drug effects; D013997:Time Factors
D010656:Phenylephrine; D002217:Carbachol; D000324:Adrenocorticotropic Hormone; D010544:Peroxidases; D015056:1-Methyl-3-isobutylxanthine