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J W Guzek

Publications and source records attributed to J W Guzek.

At least 37 records · Page 2Linked to original sources
PubMed1992

The vasopressin and oxytocin neurohypophysial content as influenced by bleeding or dehydration: effect of cholecystokinin octapeptide.

The effect of CCK-8 (50 ng, i.c.v.) on the neurohypophysial vasopressin and oxytocin storage was estimated in haemorrhaged (1 ml per 100 g b.w.) male Wistar rats. In another experimental series rats dehydrated for three days were given CCK-8 in a daily i.c.v. dose of 50 ng. The neurohypophysial vasopressin and oxytocin content was bioassayed by pressor effect following Dekański or milk-ejection activity in vitro following van Dongen and Hays, respectively. The decrease of neurohypophysial vasopressin and oxytocin content, brought about by dehydration, was significantly less marked in animals treated with CCK-8. The depletion of neurohypophysial vasopressin and oxytocin content in haemorrhaged animals could be completely inhibited by earlier i.c.v. administration of CCK-8. It is suggested that hypothalamic cholecystokinin may serve as a modulator of neurohypophysial function.

Animals↗
PubMed1992

Atrial natriuretic peptide inhibits neurohypophysial hormones' release in the rat (in vitro and in vivo studies).

Intracerebroventricular hANP (50 nmol) inhibits release of vasopressin and oxytocin following dehydration as well as after haemorrhage. 10 nmol/L hANP markedly inhibits vasopressin and oxytocin release in vitro from the neurointermediate lobes both under basal condition as well as during stimulation with excess (56 mM) potassium. It is suggested that ANP may serve as a modulator of vasopressin and oxytocin release. The respective processes are localized, at least in part, at the neurohypophysial level.

Animals↗
PubMed1991

Inhibition of prostaglandin synthesis and the release of vasopressin and oxytocin from the rat neurohypophysis: in vitro studies.

The basal and K(+)-evoked release of vasopressin (VP) and oxytocin (OT) from the neurointermediate lobes in vitro was determined under conditions of indomethacin-induced inhibition of prostaglandin (PG) synthesis. The in vivo treatment with indomethacin (IM), administered to donor animals, did not modify the release of VP during resting conditions as well as during the potassium stimulation; on the contrary, both base-line and K(+)-evoked release of OT was significantly inhibited under such conditions. Incubation of neurointermediate lobes in a solution containing indomethacin resulted in an inhibition of VP and OT release both during resting conditions and during depolarization due to excess potassium.

Animals↗
PubMed1990

(6R)-5,6,7,8-tetrahydro-alpha-biopterin affects vasopressin and oxytocin release from rat neurointermediate lobe in vitro.

Incubation of neurointermediate lobes in Locke's solution containing 0.13 mumol.l-1 (6R)-5,6,7,8-tetrahydro-alpha-biopterin dihydrochloride (THB4) resulted in an inhibition of bioassayed vasopressin secretion and in an increase of that of oxytocin both under resting conditions as well as during depolarization due to excess potassium. It is suggested that some events related to THB4 and localized in the neural lobe are involved in the mechanism of vasopressin and oxytocin release.

Animals↗
PubMed1990

The vasopressin and oxytocin content in the neurohypophysis under conditions of increased beta-adrenergic transmission in euhydrated and dehydrated rats.

In rats euhydrated or dehydrated for two or four days the neurohypophysial vasopressin and oxytocin content was estimated. Rats were given intracerebroventricularly (i.c.v.) isoprenaline in a daily dose of 10 micrograms dissolved in 10 microliters of 0.9% sodium chloride. The neurohypophysial vasopressor and oxytocic activity diminished progressively during deprivation of water. A single dose of isoprenaline diminished the neurohypophysial content of vasopressin in euhydrated rats. In animals dehydrated for two or four days the depletion of neurohypophysial vasopressin storage (as brought about by osmoreceptor stimulation) was distinctly less marked under treatment with isoprenaline. The neurohypophysial oxytocin storage was diminished by a single dose of isoprenaline; on the contrary, during dehydration isoprenaline distinctly intensified the oxytocin depletion in the neurohypophysis.

Adrenergic Fibers↗
PubMed1990

The effect of intracerebroventricular insulin on the hypothalamic and neurohypophysial oxytocin activity in euhydrated or dehydrated rats.

Rats dehydrated up to four days were given intracerebroventricularly insulin in a daily dose of 100 ng. Insulin decreased significantly the hypothalamic and neurohypophysial oxytocin content in euhydrated rats. In dehydrated animals the oxytocin activity in the hypothalamo-neurohypophysial system, markedly depleted after deprivation of water, could be further reduced by intracerebroventricular treatment with insulin. These results seem to suggest a possible regulatory role of brain insulin in the mechanisms of oxytocin release.

Animals↗
PubMed1988

Vasopressin and oxytocin neurohypophysial content under conditions of beta-adrenergic blockade in euhydrated and dehydrated rats: further studies.

Rats euhydrated and dehydrated for two days were given intracerebroventricularly (i.c.v.) propranolol hydrochloride in a daily dose of 10 micrograms. In euhydrated rats the single dose of propranolol diminished significantly the vasopressin and oxytocin content in the neurohypophysis. On the contrary, in animals dehydrated for two days the depletion of the vasopressin and oxytocin neurohypophysial storage was distinctly less marked during i.c.v. treatment with propranolol.

Animals↗
PubMed1988

Insulin and release of neurohypophysial hormones: in vivo and in vitro studies.

No significant effect of intracerebroventricular administration of insulin on the bioassayed neurohypophysial storage of vasopressin and oxytocin could be found. This finding, however, only indirectly reflects possible changes of vasopressin and oxytocin release. Incubation of neurointermediate lobes in Locke's solution containing 3.3 mumol/l insulin resulted in an inhibition of oxytocin release under resting conditions as well as in a decrease of both vasopressin and oxytocin release during depolarization due to excess potassium. These results seem to suggest a possible regulatory role of brain insulin in the mechanisms of release of neurohypophysial hormones.

Animals↗
PubMed1988

Hypothalamic and neurohypophysial vasopressin and oxytocin in melatonin-treated pinealectomized male rats.

The effect of melatonin on hypothalamic and neurohypophysial vasopressin and oxytocin was investigated in normal and pinealectomized rats. Pinealectomy was followed by a decrease of both vasopressin and oxytocin content in the hypothalamus and neurohypophysis. In unpinealectomized rats, melatonin decreased vasopressin and oxytocin storage in the hypothalamo-neurohypophysial system. Following pineal removal, melatonin did not augment the pinealectomy-induced decrease of vasopressin and oxytocin in the neurohypophysis; the hypothalamic storage of both neurohormones was even higher when compared with vehicle-treated animals.

Animals↗
PubMed1988

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History, Modern 1601-↗
PubMed1987

The effects of beta-adrenergic blockade on the hypothalamic and neurohypophysial vasopressin and oxytocin content in pinealectomized male rats.

Pinealectomized (PX), sham-operated and non operated control rats were injected intraperitoneally (i.p.), once daily at 8.00 over five days, with: (a) 0.9% sodium chloride, (b) propranolol hydrochloride in a dose of 10 mg/kg (= 0.1 ml solution per 100 g b.w.). Three hours following the last injection the animals were decapitated and the content of vasopressin and oxytocin was bioassayed in the hypothalamus and neurointermediate lobe. PX was followed by known decrease of both vasopressin and oxytocin in the hypothalamus and neurohypophysis. In rats not-PX propranolol did not change the vasopressin and oxytocin content in the hypothalamus and neurointermediate lobe. In PX-rats, treatment with propranolol resulted in a distinct increase of the vasopressin in the neurohypophysis. It may be therefore supposed that the beta-adrenergic transmission is in some way involved in the regulatory mechanisms of pineal-neurohypophysial functional relationship.

Adrenergic beta-Antagonists↗
PubMed1987

The influence of desmethylimipramine on the hypothalamic and neurohypophysial vasopressin content in pinealectomized male rats.

The effect of desmethylimipramine (DMI) on the hypothalamic and neurohypophysial vasopressin content was investigated in normal and pinealectomized male rats. The vasopressor activity of the hypothalamus and neurohypophysis was bioassayed by the method of Dekański (1952). A single i.c.v. injection of DMI (20 micrograms; dissolved in 10 microliters of normal saline) decreased vasopressin content in the neurohypophysis of non-operated and sham-operated animals. In pinealectomized rats the vasopressin content in the neurohypophysis diminished and was not modified by an i.c.v. DMI injection. Repeated treatment with DMI (i.p.; 10 mg/kg, twice a day over five days) resulted in a distinct increase of the hypothalamic and neurohypophysial vasopressin in both normal and pinealectomized rats.

Animals↗
PubMed1987

The hypothalamic and neurohypophysial vasopressor and oxytocic activities in stressed rats treated with haloperidol.

A decrease of oxytocin and vasopressin content was observed in the hypothalamus and neurohypophysis of immobilized rats but not of those exposed to cold. In rats otherwise not treated, dopaminergic blockade due to haloperidol was followed by an increase of the vasopressin content in the neurohypophysis. In immobilized animals, the hypothalamic and neurohypophysial content of oxytocin decreased and could be further reduced by haloperidol. In contrast haloperidol prevented the decrease of the hypothalamic and neurohypophysial vasopressin under conditions of stress owing to immobilization. In cold-exposed animals, however, haloperidol did not affect the storage of neurohypophysial vasopressin and oxytocin. Thus, it may be supposed that the response of oxytocinergic and vasopressinergic neurones to stress is dependent on the kind of stressor; furthermore, the dopaminergic transmission seems to be involved in the functional regulation of these neurones under conditions of stress due to immobilization.

Animals↗
PubMed1986

The effects of prostaglandin synthetase inhibitor indomethacin on the hypothalamic and neurohypophysial oxytocin content in euhydrated and dehydrated male white rats.

Rats euhydrated or dehydrated up to eight days were given intraperitoneally indomethacin (IM) twice daily in a dose of 0.2 mg/100 g of initial body weight. A single dose of IM injected to euhydrated animals did not affect the neurohypophysial oxytocic activity but decreased that potency in the hypothalamus. When IM was administered repeatedly during four or eight days, the hypothalamic oxytocic activity did not differ from the respective controls; under such conditions the oxytocic activity in the neurohypophysis increased progressively. Under conditions of dehydration the known depletion of hypothalamic and neurohypophysial oxytocin storage was not affected by indomethacin. It is therefore suggested that impulses of osmoreceptor origin are of distinct importance in determining the function of oxytocinergic neurones under conditions of inhibited prostaglandin synthesis.

Animals↗