Ionic dependence of depolarization-mediated adipokinetic hormone release from the locust corpus cardiacum

The locust corpus cardiacum (CC) is a peripheral neurohemal organ in which are clustered a prodigious array of neurosecretory cells (NSCs), nearly all of which synthesize and release adipokinetic hormones (AKHs). We have examined the extracellular requirements for Na+ and Ca2+ in the process of AKH release following NSC depolarization by high extracellular K+ or veratridine. Na+ is not required for release mediated by high external K+ although Ca2+ is. The Ca2+ channel antagonists cobalt and lanthanum prevent release and support the hypothesis that depolarization with K+ leads to Ca2+ channel activation and subsequent AKH release. Tetrodotoxin does not block K+-mediated release suggesting that Na+ channel activation and Na+ influx are not required for K+-mediated release. The alkaloid veratridine leads to cobalt- and tetrodotoxin-sensitive release and this suggests that cell depolarization by Na+ channel activation is nevertheless capable of opening Ca2+ channels and initiating release. Release mediated by high external K+ is reduced by nifedipine but is not significantly reduced by methoxyverapamil, however veratridine-mediated release is slightly reduced by methoxyverapamil. Glandular lobes accumulated greater amounts of 45Ca2+ following high K+-mediated depolarization compared to glands incubated in normal saline and this enhanced accumulation was blocked by the Ca2+ channel antagonist lanthanum. During prolonged exposure to high K+ saline the release of AKHs and the uptake of 45Ca2+ reach a maximum and then gradually decline. The temporal pattern of the reduction in AKH release is similar to that of 45Ca2+ accumulation by the glandular lobe. This reduction in AKH release and 45Ca2+ uptake may result from inactivation of Ca2+ channels associated with the release process. These results indicate that Ca2+ influx into the NSCs by way of voltage-sensitive Ca2+ channels plays a critical role in the process of depolarization-mediated AKH release.