The binding of glucocorticoids to a crude fraction of rat pituitary plasma membranes and to solubilized membrane proteins was measured. The binding characteristics were similar to those exhibited by transcortin: radioactive corticosterone was bound to a greater extent than radioactive dexamethasone and labelled corticosterone, but not labelled dexamethasone, was displaced by unlabelled corticosterone, deoxycorticosterone and progesterone. A Scatchard plot of the binding data revealed the presence of a binding material with a dissociation constant of about 3.2 nmol/l, which sedimented at 4S after sucrose density-gradient centrifugation. It was found that the number of binding sites was inversely related to the concentration of corticosterone in the circulation and was increased after long-term adrenalectomy. These data suggest that a material similar to transcortin is complexed to the plasma membrane of rat pituitary cells.

The effect of castration and adrenalectomy was studied on vasoactive intestinal peptide (VIP) concentrations in various brain and peripheral structures of male rats. Castration has no effect on any of the structures studied, whereas 4 weeks adrenalectomy (ADX) decreases VIP concentrations in the hippocampus and increases them in the adenohypophysis, two structures known to contain large amounts of glucocorticoid receptors. Corticosterone administration restores VIP levels to control values only in the dorsal hippocampus. In contrast, dexamethasone counteracts both the decrease and the increase of VIP concentrations obtained after ADX in the hippocampus and in the adenohypophysis respectively. The present results suggest that corticosteroids can be involved in the regulation of VIP actions both in the brain and in the adenohypophysis.

The effect of various neurotransmitters on adrenocorticotropic hormone (ACTH) release from superfused neurointermediate lobes of rat hypophysis (NIL) was investigated. Acetylcholine, serotonin, and histamine were shown to have no significant effect on the spontaneous release of ACTH. In contrast, dopamine (DA) and noradrenaline (NA) stimulated NIL ACTH release in a dose-dependent manner. The stimulating effect of DA was mimicked by apomorphine and inhibited by haloperidol, whereas that of NA was abolished by phentolamine. In a comparative study, none of these neurotransmitters is shown to have any significant stimulating effect on ACTH release from superfused anterior lobes. It is concluded that the ACTH release from NIL might be controlled, at least in part, by catecholaminergic innervation.

The effects of K⁺-enhanced and Ca⁺⁺-free media on α-MSH and adrenocorticotropic hormone (ACTH) release from superfused neurointermediate lobe (NIL) were studied in the same experiments. High K⁺ caused reversible and repeatable inhibition of α-MSH release and stimulation of ACTH release. Removal of Ca⁺⁺ impaired the effect of K⁺, irreversibly for α-MSH and reversibly for ACTH. The existence of both melanotrophic and corticotrophic cells within the intermediate lobe (IL) of rat hypophysis could account for the different effects of ionic modifications on in vitro α-MSH and ACTH release.