The vasopressor and oxytocic activities of the hypothalamus and neurohypophysis are influenced by inhibited alpha-adrenergic transmission during dehydration and subsequent rehydration in the white rat.

During equilibrated water metabolism a single dose of dihydroergotamine (DHE) increased vasopressin release from the neurohypophysis; it had no effect on oxytocin content in the hypothalamus and neurohypophysis. After two days of dehydration DHE somewhat restrained the decrease of oxytocin in the hypothalamus; the release of vasopressin from the neurohypophysis was then increased. Under severe dehydration, i.e. under conditions of potent osmoreceptor stimulation, DHE influenced the vasopressin content neither in the hypothalamus nor in the neurohypophysis, but in some way it intensified oxytocin depletion in the neurohypophysis. Following two days of rehydration DHE somewhat restrained the renewal of vasopressin in the hypothalamus. No changes of oxytocin in the hypothalamus could be demonstrated at that time; in the neurohypophysis DHE intensified vasopressin repletion, but inhibited oxytocin repletion. Following four and eight days of rehydration DHE had no influence on vasopressin repletion rate in the hypothalamus and neurohypophysis. At that time oxytocin repletion in the neurohypophysis was increased; in the hypothalamus it was not affected by DHE. It is concluded that the response of the hypothalamo-neurohypophyseal system to alpha-adrenergic blockade-as brought about by dihydroergotamine treatment-seems to be dependent on the actual state of water metabolism. Impulses from the osmoreceptors may be therefore of some important in modifying the change in vasopressin and oxytocin release resulting from inhibition of alpha-adrenergic transmission through neural chains including units susceptible to dihydroergotamine.