PubMed Health⌕ Search

Biomedical subjects

A Lewandowska

Publications and source records attributed to A Lewandowska.

At least 19 recordsLinked to original sources
PubMed1994

Neurohypophysial response to peptides of the cholecystokinin family: in vivo and in vitro studies.

I.c.v. injection of CCK-8 (50 ng/day) to euhydrated rats significantly decreased vasopressin and oxytocin content in the hypothalamo-neurohypophysial system. In rats drinking hypertonic saline and simultaneously treated with CCK-8, the decrease of vasopressin content was more marked in hypothalamus but somewhat restrained in the neurohypophysis. The decrease of hypothalamic and neurohypophysial oxytocin content (as brought about by the salt load) was significantly less marked in animals treated simultaneously with CCK-8. Incubation of neurointermediate lobes in medium enriched with CCK-33/CCK-39 or CCK-8 did not change significantly the vasopressin and oxytocin release from the neurointermediate lobes both under basal conditions and during potassium stimulation. It is suggested that afferent impulses of osmoreceptor origin may modify the response of vasopressinergic and oxytocinergic neurons to CCK-8. The events, related to the influence of CCK peptides on vasopressin or oxytocin release, do not seem to be localized at the neurohypophysial level.

Animals↗
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↗
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↗
PubMed1981

The influence of rolipram on the central serotoninergic system.

The influence of rolipram, a potential psychotropic drug, on the central serotoninergic system was studied. Rolipram was found to elicit the head twitch reaction in rats but not in mice. This effect was abolished by phenoxybenzamine, clonidine and morphine but not by cyproheptadine, metergoline and pizotifen. The antagonistic action of morphine was reversed by naloxone. Rolipram stimulated the flexor reflex of the hind limb in the spinal rat but this effect was blocked neither by cyproheptadine and pizotifen, nor by phenoxybenzamine. In rats kept at a high ambient temperature, rolipram induced slight hypothermia and did not affect the hyperthermia induced by fenfluramine. Rolipram produced also slight hypothermia in rabbits. Our results indicate that rolipram does not affect the central serotoninergic transmission but in some of its central effects (the head twitch reaction) the noradrenergic system and the opiate receptors seem to be involved.

Animals↗
PubMed1979

The effect of etoperidone, a new potential antidepressant drug, on the central serotonin system.

The effect of etoperidone--a non-tricyclic potential antidepressant drug--on the central serotonergic system was studied. It was demonstrated that this compound inhibited the head twitch reaction induced by 5-HTP in mice and rats (ED50 values amounted to 2.89 and 2.29 mg/kg i.p. respectively). In the flexor reflex preparation in spinal rats etoperidone used in doses lower than 1 mg/kg i.v. produced no effect, while doses of 1 mg/kg i.v. and higher had a stimulating action which occurred 10--15 min after injection. This stimulating action was abolished by 5-HT antagonists (cyproheptadine, danitracen) and by the drug metabolism inhibitor SKF-525A, but not by the 5-HT uptake inhibitor clomipramine. Etoperidone given in a dose of 0.5 mg/kg i.v. had no effect on the stimulating action of serotoninmimetics (LSD, quipazine, fenfluramine) on the flexor reflex, but it abolished the effect of LSD in rats pretreated with SKF-525A. The above findings indicate that etoperidone has a biphasic action on the serotonergic transmission, revealing characteristics of the 5-HT antagonist and agonist. The agonistic action is probably connected with the formation of a metabolite.

Animals↗
PubMed1979

Central antiserotonin action of amitriptyline.

Amitriptyline (AMI) was studied in rats snd mice in order to find out whether it had a central antiserotonin activity, previously demonstrated for doxepin - a compound chemically related to AMI. It was observed that AMI at low doses antagonized the head twitch response to L-5-hydroxytryptophan or 5-methoxytryptamine, as well as tryptamine-induced convulsions. In the hind limb flexor reflex preparation of the spinal rat AMI acted as a serotonin antagonist: when administered alone, it did not change the flexor reflex but prevented its stimulation induced by serotoninmimetics (LSD, quipazine, fenfluramine) not affecting that one evoked by noradrenalinemimetics (clinidine). At higher doses, AMI revealed a noradrenolytic activity. The results indicate that AMI, similarly as doxepin, has a central antiserotonin activity.

5-Hydroxytryptophan↗