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J W Guzek

Publications and source records attributed to J W Guzek.

82 records · Page 5Linked to original sources
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Monoaminergic influences on the incorporation of 35S in the hypothalamic and neurohypophysial proteins following intracerebroventricular injection of 35S-cysteine in dehydrated rats.

In the rats dehydrated for 48 h the mean specific activity of hypothalamic and neurohypophysial TCA-precipitable proteins following intracerebroventricular injection of L-cysteine-35S-hydrochloride was significantly higher than that found in the dehydrated and reserpinized. Under influence of amphetamine sulfate however, no change of 35S-uptake by TCA-precipitable hypothalamic and neurohypophysial proteins could be detected in rats similarly dehydrated.

Amphetamine↗
PubMedDate not supplied

The release of neurohypophysial hormones as influenced by stimulation of alpha-adrenergic transmission in long-term dehydrated male white rats. Information 1: hypothalamic and neurohypophysial vasopressor activity.

Rats dehydrated up to 12 days were given intraperitoneally methoxamine hydrochloride in a daily dose of 1.0 mg/100 g of the initial body weight. The single dose of methoxamine administered to normally hydrated animals was followed by a significant increase of the vasopressin content of the neurohypophysis and hypothalamus (both in NSO and NPV regions). Under conditions of severe dehydration a more marked depletion of hypothalamic and neurohypophysial vasopressin stores was noted in methoxamine-treated animals.

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The release of neurohypophysial hormones as influenced by stimulation of alpha-adrenergic transmission in long-term dehydrated male white rats. Information 2: hypothalamic and neurohypophysial oxytocic activity.

Rats dehydrated up to 12 days were given intraperitoneally methoxamine hydrochloride in a daily dose of 1.0 mg/100 g of initial body weight. The only dose of methoxamine injected into normally hydrated animals did not influence significantly the oxytocic activity neither in the hypothalamus nor in the neural lobe. Following four days of dehydration a distinctly more marked depletion of the hypothalamic (both in the NSO and NPV region) and neurohypophysial oxytocin content was found in animals treated with methoxamine. For the neurohypophysis, a similar effect has been noted under severe dehydration (8th and 12th day) as well.

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

Under conditions of equilibrated water metabolism a single dose of methoxamine increased the content of vasopressin in the hypothalamus as well as that of oxytocin both in the hypothalamus and neurohypophysis. During dehydration the depletion of hypothalamic and neurohypophysial vasopressin was more marked in methoxamine-treated animals; this effect, however, was absent in the neurohypophysis on the 2nd day and in the hypothalamus on the 8th day of water deprivation. After two days of dehydration methoxamine inhibited the decrease of oxytocin content in the hypothalamus; simultaneously (2nd and 4th day of dehydration) it intensified this process in the neurohypophysis. During rehydration methoxamine impaired the renewal of vasopressin both in the hypothalamus and neurohypophysis; this effect was most marked on the 8th day of rehydration. On the contrary, it favoured somewhat the renewal of hypothalamic oxytocin in rehydrated rats (such an event was not found on the 8th day of rehydration). Moreover, methoxamine restrained initially (on the 2nd and 4th day of rehydration) the restoration of neurohypophysial oxytocin stores; following eight days of rehydration an opposite effect was here found. It is concluded that the response of the vasopressinergic and oxytocinergic neurons to alpha-adrenergic stimulation, brought about by using methoxamine as pharmacological tool, seems to be depended on the actual state of water metabolism. Impulses from the osmoreceptors may be therefore of some importance in modifying the change in vasopressin and oxytocin synthesis, transport and release resulting from stimulation of alpha-adrenergic transmission through neural chains including units susceptible to methoxamine.

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The effects of stress on the hypothalamic and neurohypophysial vasopressin content and plasma renin activity in rats.

Rats were stressed by immobilization of exposure to cold. The hypothalamic vasopressor activity increased in immobilized animals and did not change in cold-exposed ones. The neurohypophysial vasopressor potency increased in cold-exposed animals and decreased following immobilization. The plasma renin activity in immobilized animals was significantly lower when compared with the respective controls. It seems, therefore, that different kinds of stress (cold exposure and immobilization) may cause different responses of the hypothalamo-neurohypophysial system.

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The content of vasopressin and oxytocin in the hypothalamus and neurohypophysis of pinealectomized male rats.

The content of vasopressin in the neurohypophysis as well as the content of oxytocin in both hypothalamus and neurohypophysis were found to decrease considerably 8 weeks following pinealectomy in male rats. It may be, therefore, concluded that the pineal body is in some way involved in the regulatory mechanisms for vasopressinergic and oxytocinergic neurons.

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The adrenergic influences on the hypothalamic and neurohypophysial oxytocic activity in long-term dehydrated male white rats.

Rats dehydrated up to 12 days were given intraperitoneally phenoxybenzamine hydrochloride or amphetamine sulfate in daily doses of 0.2 mg/100 g or 0.5 mg/100 g, respectively. In not dehydrated animals, both drugs decreased significantly the hypothalamic and neurohypophysial oxytocin content. In dehydrated rats the oxytocin activity in the hypothalamo-neurohypophysial system diminished progressively; under such conditions, inhibition of alpha-adrenergic receptors (brought about by using phenoxybenzamine as pharmacological tool) as well as the stimulation of the alpha- and beta-adrenergic receptors (caused by amphetamine administration) potentiated the effects of osmoreceptor stimulation.

Amphetamine↗
PubMedDate not supplied

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.

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