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HOWARD SACHS, EDWIN W. HALLER, Further Studies on the Capacity of the Neurohypophysis To Release Vasopressin, Endocrinology, Volume 83, Issue 2, 1 August 1968, Pages 251–262, https://doi.org/10.1210/endo-83-2-251
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Abstract
The dog neurohypophysis can release only a fraction of the vasopressin (ADH) it contains in response to repeated stimulation in vivo or in vitro. Experiments have been performed to determine whether this limited release might result from the presence of ADH in the medium or from cellular damage due to anoxia or substrate deprivation. Neural lobes from bled dogs took up O2in vitro at almost twice the rate of neural lobes from unbled animals. Excess K+ in the incubation medium enhanced the rate of O2 consumption in both cases. Incubation of posterior pituitaries (from unbled dogs) in media lacking glucose and O2 resulted in an increase in the basal level of ADH secretion, and a marked inhibition in the rate of hormone release in response to 56 HIM K+. The secretory mechanisms did not appear to have suffered permanent damage due to the extensive period of hypoxia and substrate deprivation. One hr after the readmission of glucose and O2 to the medium, such pituitaries released ADH in response to 56 HIM K+ at a rate equal to that of glands maintained on glucose and O2 throughout. The ability of dog neural lobes to release ADH in vitro in the presence of excess K+ was not impaired by prior exposure of the glands to high concentrations of exogenous hormone. ADH, either added to, or accumulated in the incubation media due to secretion, appears to stimulate the further secretion of hormone. It has been possible to label the pool of neurohypophysial ADH with 35S and to induce such glands to secrete radioactive ADH in vitro or in vivo. The specific activity of the hormone secreted in response to excess K+ in vitro, or to bleeding in vivo, was several times greater than that of the hormone remaining in the gland, thus affording direct evidence for the metabolic heterogeneity of the pool of neurohypophysial ADH. Experiments are also reported on the decline in the rate of ADH release from guinea pig posterior pituitaries during prolonged electrical stimulation in vitro. (Endocrinology83: 251, 1968)