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 examine 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 the 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.