Effect of Calcium and Other Ions on Vasopressin Release from Rat Neurohypophyses stimulated electrically in vitro

Abstract

THE rat posterior pituitary in vitro secretes vasopressin in response to a rise in extracellular potassium concentration. This effect of excess potassium is inhibited by magnesium and sodium ions and is strongly dependent on calcium. Secretion is abolished by omitting calcium from the incubation medium; it increases with increasing calcium concentration over a wide range, and is accompanied by uptake of calcium-45. From such evidence it has been concluded that calcium entry into the neurosecretory terminals on their depolarization by action potentials is the normal physiological event initiating secretion^1–3. This concept is supported by the demonstration of vasopressin release from rat^3,4 and guinea-pig⁵ neurohypophyses in vitro in response to electrical stimuli and of action potentials recorded from the supra-opticohypophyseal tract⁶. It would clearly strengthen the hypothesis if it were shown that the effects of calcium and other ions on vasopressin release, elicited by electrical stimulation, were similar to their effects on secretion elicited by excess potassium. This communication presents evidence that this is so.