Mechanisms of Inactivation of Neurohypophysial Hormone Release

Abstract

The biosynthesis of the neurohypophysial hormones, followed by packaging into granules and transport to neurosecretory swellings and terminals, provides a large pool of stored product from which hormone secreted into the blood is derived. This chapter describes the mechanism of inactivation of hormone release, using both potassium and electrical stimulation in vitro and the stimulus of 2% saline drinking in vivo . It is found that inactivation of release elicited by potassium stimulation is dependent not only on membrane potential but also on calcium entry. Recovery from the potential-dependent component is much faster than from the calcium-dependent one. Calcium-dependent inactivation of hormone release can also be demonstrated with electrical stimulation, which additionally reveals a third component of inactivation dependent on external sodium. Ex vivo experiments, involving incubation of neurohypophyses from animals previously given 2% NaCl rather than drinking water, suggest that similar mechanisms serve to limit hormone release in vivo . The chapter suggests that all the three components of inactivation exert their effects upon membrane calcium permeability and that it is the magnitude of intracellular calcium entry during stimulation, rather than decreased availability of hormone or fatigue of the exocytotic mechanism, which is responsible for inactivation of release.