Octopamine and cyclic AMP mediate release of adipokinetic hormone I and II from isolated locust neuroendocrine tissue.

Octopamine serves as a neurotransmitter in the glandular lobe of the locust corpus cardiacum where it regulates adipokinetic hormone (AKH) secretion from intrinsic neurosecretory cells. Two AKHs (AKH I and II) from the corpus cardiacum of Locusta have been sequenced and synthesized. We have now demonstrated that octopamine mediates release of both AKH I and II from Locusta corpora cardiaca in vitro. Octopamine, IBMX, and forskolin have previously been shown to elevate levels of cAMP in the glandular lobe. In this paper we demonstrate that IBMX and forskolin mediate secretion of AKH I and AKH II thus mimicking the effects of octopamine in this tissue. The cAMP analogs dibutyryl cAMP and 8-bromo cAMP also elicit release of AKH and a subthreshold concentration of IBMX potentiates the effects of octopamine. These observations demonstrate that cAMP participates in regulating AKH release and support the hypothesis that octopamine mediates hormone release at least in part via changes in intracellular levels of cAMP. The release of AKH I and AKH II is apparently regulated by similar mechanisms. The hyperlipemic activity of AKH II released into the perfusates following stimulation by octopamine and agents which elevate cAMP levels is significantly lower than that of AKH I. This differential response is probably due both to the reduced lipid-mobilizing effect of AKH II relative to AKH I, as well as to the release of greater amounts of AKH I.