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Experiments were performed on male albino rats in urethane anaesthesia. The pituitary gland was exposed, the pituitary stalk was cut and the whole gland was removed. Isotonic sodium chloride solution used for washing the cut pituitary stalk was collected and its antidiuretic activity assayed. Antidiuretic substance was liberated from the infundibular axons into the washing fluid during continuous intravenous infusion of a hypotonic saline. The antidiuretic activity of the washing fluid was assayed in ethanol-anaesthetized rats. A 5 % sodium chloride solution, infused intravenously to the limit of 1 % of the body weight, caused a significant release of antidiuretic substance from the cut infundibular axons. A similar effect was observed after the i.v. infusion of 1 ml. of a solution containing 0\m=.\06 mM-CaCl2. The i.v. infusion of 0\m=.\02 mM-MgCl2 decreased the amount of antidiuretic substance liberated from the pituitary stalk significantly.

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The posterior pituitary lobe of male rats under urethane anaesthesia was incubated in situ. The pituitary gland was exposed by thr transpharyngeal apprach. The posterior lobe remained in neural and partial vascular connexion with the hypothalamus, whereas the anterior lobe was entirely remobed. Incubation fluid was collected and its melanophore-stimulating activity was assayed in hypophysectomized frogs. No effect was observed after the i.v. injection of 1 ml 120 muM-NaC1 with 60 muM-CaC12 or isotonic NcC1 solution. Hypertonic solutions of 5% NaC1 and 25% glucose injected intravenously to the limit of 0-5% of the body weight, transiently enhanced the release of MSH from the posterior pituitary lobe by 66% (significant) and 15% (not significant) respectively. Intracarotid injection of 0-3 ml 5% NaC1 solution resulted in the highest increase (95%) of MSH release.