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Biomedical subjects

J W Guzek

Publications and source records attributed to J W Guzek.

At least 55 records · Page 3Linked to original sources

The influence of melatonin on the content of vasopressin and oxytocin in the hypothalamus and neurohypophysis in euhydrated and dehydrated male rats.

Melatonin injected in a single intraperitoneal dose of 100 micrograms/100 g b.w. to euhydrated rats resulted in a decrease of neurohypophysial oxytocin content but the hypothalamic oxytocin storage as well as the hypothalamo-neurohypophysial storage of vasopressin were not changed. Following 8 d of once-daily melatonin treatment the hypothalamic and neurohypophysial oxytocin and vasopressin content was decreased. It might be therefore suggested that melatonin increases the release of neurohypophysial hormones and/or decreases their synthesis. Melatonin did not significantly modify the neurohypophysial vasopressin depletion rate in animals deprived of water up to 8 days. No consistent effects of melatonin on the decrease of hypothalamo-neurohypophysial content of oxytocin were noted under conditions of dehydration and simultaneous administration of melatonin up to 8 d.

Animals↗

The hypothalamic and neurohypophysial oxytocin content as influenced by desmethylimipramine in normal and pinealectomized white male rats.

Pinealectomized, sham-operated and non operated control rats were injected intracerebroventricularly (i.c.v.) with a single dose of desmethylimipramine hydrochloride (DMI; 20 micrograms, dissolved in 10 microliters of normal saline); after 4 hours they were decapitated and the hypothalamic and neurohypophysial oxytocin content was bioassayed using the milk-ejection effect in vitro. DMI decreased oxytocin content of the hypothalamus and neurointermediate lobe in non operated and sham-operated animals. In pinealectomized rats the oxytocin content of the hypothalamus and neurointermediate lobe diminished and could be further reduced by an i.c.v. DMI injection. As shown in animals pretreated with phenoxybenzamine, these events might be only partially related to an increase of alpha-adrenergic transmission.

Adrenergic Fibers↗

The hypothalamic and neurohypophysial oxytocic activities in stressed rats: independence from beta-adrenergic blockade.

A distinct decrease of oxytocin was found in the hypothalamus of immobilized rats but not of those exposed to cold. Similarly, the content of oxytocin was lower in the neurohypophysis of rats immobilized for 24 hr but, on the contrary, increased in animals exposed to cold for 24 hr. Propranolol did not modify the mentioned changes brought about by immobilization or exposure to cold.

Animals↗

The hypothalamic and neurohypophysial vasopressor and oxytocic activities as influenced by beta-adrenergic blockade during long-term dehydration in the white male rat.

Rats dehydrated up to 12 days were given intraperitoneally propranolol hydrochloride in daily dose of 1.0 mg/100 g of initial body weight. In not dehydrated animals the only dose of propranolol increased significantly the vasopressin and oxytocin release from the neurohypophysis. In dehydrated animals propranolol restrained somewhat the decrease of vasopressin in the neurohypophysis, but intensified the vasopressin depletion in the hypothalamus. The oxytocic potency of both the neurohypophysis and hypothalamus decreased progressively in animals deprived of water. Propranolol potentiated this effect of osmoreceptor stimulation.

Animals↗

The neurohypophysial vasopressin content as influenced by modified cholinergic or adrenergic transmission during long-term dehydration in the white rat.

In rats dehydrated up to 12 days the neurohypophysial vasopressin content was determined by Dekański's method. Carbamylcholine inhibited somewhat the vasopressin depletion in the neurohypophysis, but not earlier than under severe dehydration (8th and 12th day). A single dose of atropine given 24 h prior to sacrifice to not dehydrated animals resulted in a diminution of the vasopressin content in the neurohypophysis; in animals dehydrated for four days and parallely atropinized the decrease of the neurohypophyseal vasopressin content was, on the contrary, considerably inhibited. Under severe dehydration, the treatment with atropine did not change the vasopressin stores in the neural lobe. Phenoxybenzamine inhibited the vasopressin depletion in the neural lobe following four days of dehydration. Under severe dehydration, amphetamine potentiated the effect of osmoreceptor stimulation. It is supposed that impulses of osmoreceptor origin are of some importance in determining the vasopressin release following changes of cholinergic or adrenergic transmission.

Amphetamine↗

The vasopressin and oxytocin content in the hypothalamus and neurohypophysis as influenced by reserpine treatment during long-term dehydration in the white rat.

In dehydrated rats both neurohypophysial hormones diminished in hypothalamus as well as in the neurohypophysis. Oxytocin disappearef from the hypothalamus and neurohypophysis at a more rapid rate than vasopressin did. The minimal content of vasopressin and oxytocin in the hypothalamus was observed during 3rd--4th day, but even in extreme dehydration it was found to be relatively high: 65 per cent of vasopressin and 27 per cent of oxytocin as compared with intact animals. At that time the neurohypophysial vasopressin and oxytocin content were almost fully exhausted. In dehydrated and additionally reserpinized animals (10 mg/kg intraperitoneally, then each 48 hr 5 mg/kg of initial body weight) the vasopressin and and oxytocin hypothalamus and neurohypophysis changed in a similar manner. In some experimental groups the decrease of neurohormones in both sites was more marked under reserpine treatment. The drug seems therefore rather to potentiate the effects of physiological stimulation of osmodetectors. So the existence of monoaminergic stimulatory synapses, directly involved in the neural pathway between the osmodetector and the neurosecretory cell, appears to be hardly probable.

Animals↗