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Studies were carried out in the rat to investigate whether glutamic acid is involved in the regulation of vasopressin (VP) release. For this purpose plasma VP levels were measured in rats treated with the glutamate agonist N-methyl-D-aspartate (NMDA). In our experimental conditions NMDA induced dose-related increases in plasma VP levels in normohydrated rats. The effect of NMDA were prevented by 3[(+)-2 carboxy-piperazine-4-yl]propyl-1-phosphonic acid (CPP), a selective and competitive antagonist of NMDA receptors. These data show that glutamate may contribute to the physiological release of VP from the neurohypophysis.

The coexistence of Atrial Natriuretic Factor (ANF) and Angiotensin II (Ang II) receptors in the subfornical organ suggested that ANF may influence the action of Ang II at this level. To test this hypothesis the effect of ANF pre injected into subfornical organ (SFO) on Ang II-induced vasopressin release was investigated in rats. ANF blunted vasopressin release elicited by circulating Ang II. This study indicates SFO as one of the main sites at which ANF-Ang II interactions occur.

The hypothesis that alpha-adrenergic receptor blockade accounts for the ability of ergotamine to stop migraine attacks was tested, in migraine patients, in an experimental migraine model based on nitroderivative- induced attacks. In a preliminary single blind, placebo controlled study, thymoxamine, a prevalently post-synaptic alpha adrenergic receptor antagonist, was able to abort migraine attack in 9 out of 10 patients, as opposed to 2 out of 10 by placebo (p < 0.005 Fisher's exact test). In a subsequent randomized, crossover, placebo controlled double blind study, the ability of a selective alpha-1 adrenergic receptor agonist, methoxamine, to block ergotamine antimigraine effect was studied. In 26 patients migraine was induced in two separate tests and then ergotamine was administered once after methoxamine pretreatment and once after placebo; methoxamine was significantly more effective than placebo in blocking antimigraine effect of ergotamine (p = 0.0055 Fisher's exact test). These results support the hypothesis that ergotamine alpha-1 adrenolytic properties may account for its antimigraine effect suggesting that this action takes place outside the blood-brain barrier, since methoxamine can cross it very poorly. Ergotamine target structure could be the trigeminal innervation of the extracranial and/or dural vessels.

A number of pharmacological evidence supports the view that somatostatin (SS) may be importantly involved in the seizure susceptibility both in humans and in laboratory animals. In a previous report the Authors have provided the finding that a short-term carbamazepine (CBZ) administration is able to reduce SS-CSF-IR in epileptic patients. The present study has been carried out to investigate whether a long-term treatment with CBZ affects in a similar way SS-IR content in CSF from temporal lobe epileptics (CPS). The results confirm and expand previous evidence suggesting that CBZ lowering effect on CSF-SS-IR may be relevant to its anticonvulsivant action.