PubMed Health⌕ Search

Biomedical subjects

I Zebrowska-Lupina

Publications and source records attributed to I Zebrowska-Lupina.

At least 19 recordsLinked to original sources
PubMed2001

Brain monoamine receptors in a chronic unpredictable stress model in rats.

Antidepressant drugs are devoid of mood-elevating effects in normal (non-depressed) human subjects, thus, it is necessary to evaluate the antidepressant property of compounds (drugs) in animal models of depression. Several animal models of depression have been introduced, however, only a few have been extensively validated. In the present study we report the results of investigations into monoaminergic receptors in the brain of rats subjected to chronic unpredictable stress (CUS) procedure (one of the well validated animal models of depression). We have examined the dopaminergic (D-1, D-2), adrenergic (alpha-1, beta-1) and serotonergic (5HT-1A, 5HT-2A) receptors in different brain regions by a saturation radioligand binding method in rats subjected to CUS paradigm and control animals. CUS procedure resulted in a significant 29% increase in the D-1 receptor density in the limbic system and 52% increase of the density of 5HT-2A receptors in the cerebral cortex. The present data indicate that the increase of the density of brain D-1 and 5HT-2A receptors of rats subjected to CUS might be involved in the pathophysiology of "animal depression" (since chronic antidepressant treatment produced opposite changes i.e. decrease in the density of these receptors) and thus in pathophysiology of human depression.

Adrenergic Agonists↗
PubMed1997

ACTH 4-9 analogue facilitates the antiimmobility effect of antidepressants and dopamine agonists in swimming rats.

Evidence exists that the 4-10 or 4-9 fragments of adrenocorticotropic hormone (ACTH) produce some behavioral effects in animals and in humans. The present study was designed to investigate whether ACTH 4-9 interferes with the effects of antidepressants: fluoxetine (FLU), fluvoxamine (FOX), selegiline (SEL) or dopamine agonists: piribedil (PRB) or quinpirol (QPR) in forced swimming test and in open field in rats. ACTH 4-9 was given in a single dose (25, 50 or 100 micrograms/kg) or for 7 days (50 micrograms/kg/day), alone or together with antidepressants or dopamine agonists. It was shown that ACTH 4-9 alone did not influence the behavior of rats. However, when given in a single dose, ACTH 4-9 potentiated the antiimmobility effect of all antidepressants and dopamine agonists. ACTH 4-9 given for 7 days, facilitated only the effect of selegiline. The results suggest a functional interaction of ACTH 4-9 with serotonergic and dopaminergic brain mechanisms of drugs action.

Adrenocorticotropic Hormone↗
PubMed1994

[Concentrations of kininogen and prekallikrein in plasma and activity of plasma renin depending on the type of blood pressure response to captopril in patients with arterial hypertension].

The dynamics was analysed of changes of arterial blood pressure, plasma kininogen and prekallikrein concentrations and plasma renin activity (PRA) in 50 patients with arterial hypertension, in relation to the type of blood pressure response to captopril. It was shown that after three weeks of treatment with captopril 150 mg daily, in 23 patients (46%) normalization of systolic and diastolic blood pressure occurred, and in 27 patients (54%), despite a significant reduction, blood pressure normalization was not achieved. In both groups of patients a significant decrease of plasma kininogen concentration and an increase of plasma prekallikrein level were found, indicating kininogenase activation and PRA increase. However, only in patients with arterial blood pressure normalization, a return of kininogen concentration to normal value was observed and a twofold increase of PRA in relation to the initial value was noted. Our studies indicate that in patients with arterial hypertension treated with captopril a correlation appears between the changes of plasma kinin system and PRA which determines the mode of blood pressure reaction to captopril.

Adult↗
PubMed1992

[Effect of hydrochlorothiazide on various components of the kinin system and plasma renin activity in patients with arterial hypertension treated with captopril].

Combined hypertension treatment with inhibitors of the converting enzyme (ICE) and diuretocs gives manifold advantages, the most important of them is a synergistic action of both drugs resulting in blood pressure decrease and prevention of hypokaliaemia. The purpose of the present study was assessment of the effect of hydrochlorothiazide in 50 mg daily doses on blood levels of kininogen and prekallikrein and on plasma renin activity (PRA) in hypertensive patients treated during captopril 150 mg daily alone during 3 weeks, without success. The study was carried out on 15 patients with essential hypertension stage III after WHO. A control group comprised 18 healthy subjects. The determinations were done three time: before treatment, after 3 weeks on captopril, and after 2 weeks of combined treatment with captopril and hydrochlorothiazide. It was found combined treatment with captopril and hydrochlorothiazide produced blood pressure normalization in patients insufficiently responding to captopril alone. During the combined treatment normalization of blood pressure was associated with a higher fall of kininogen concentration, higher rise of prekallikrein and PRA in relation to the values obtained with captopril alone. This evidenced a more pronounced reaction of the kinin system and the renin-angiotensin-aldosterone system to the combined treatment as compared with the response of both systems to captopril alone.

Adult↗
PubMed1991

Chronic stress reduces fighting behavior of rats: the effect of antidepressants.

The effect of chronic stress (14 various unpredictable stressors over 16 days) on electric footshock-induced fighting behavior of pairs of male Wistar rats was studied. The influence of antidepressant drugs (imipramine, desmethylimipramine, nomifensine, clomipramine, mianserine and doxepine) administered chronically (1 h before the stressor) on the aggressive behavior was also investigated in control and in stressed rats. Moreover, the effect of chronic stress on noradrenaline (NA) utilization in the brain was estimated in control and in antidepressant-treated rats. It was demonstrated that, in rats submitted to repeated unpredictable stress, the fighting behavior was significantly reduced 48 and 72 h after the last stressor. NA utilization in the brain was decreased 72 h after the stress termination. Prolonged treatment with antidepressant drugs restored the intensity of fighting behavior in stressed rats to control value as well as normalized NA utilization in the brain. It is suggested that antidepressant drugs may counteract the affective aggression deficit induced by chronic stress.

Aggression↗
PubMed1989

[Effect of captopril on various components of the kinin system and plasma renin activity in patients with idiopathic arterial hypertension].

Authors studied effect of captopril on serum kininogen and prekallikrein concentrations, as well as on plasma renin activity (PRA) in patients with primary hypertension. The control group consisted of 18 healthy persons, 5 patients were in I, 12 in II and 8 in III WHO class. Monotherapy with 150 mg per day of captopril had been performed for 3 weeks. Patients were 3 times examined: 1--before therapy, 2--after 24 hours of treatment, 3--after 3 weeks of captopril therapy. It was proved, that captopril lowers arterial pressure with coexisting PRA increase and induces changes in kinins system such as: decrease of kininogen+ concentration and increase of serum prekallikrein level in comparison with their pretreatment values. Maximum PRA increase and blood pressure decrease were observed after 24 hours of captopril administration, whereas changes in kinins system were taking place during the whole observation period. Presented studies indicate that antihypertensive action of captopril is related to Renin-Angiotensin-Aldosterone System as well as to plasma kinins one.

Adult↗
PubMed1983

Studies on the participation of the dopaminergic system in the central effects of chronically administered antidepressant drugs.

Spontaneous locomotor activity, sedative and stereotypic action of apomorphine, and utilization of noradrenaline and dopamine in the brain of rats treated chronically for 3 weeks with imipramine, amitriptyline, doxepine, and nomifensine ip were tested 1, 24, 48 and 72 h after the last administration of the drugs. The treatment did not change the locomotor activity, producing only slight sedation after 1 h, counteracted the sedation and potentiated the stereotypy induced by apomorphine, and increased the utilization of noradrenaline and dopamine after 48 h. It also antagonized the depressant action of apomorphine on dopamine utilization after 72 h. The results indicate the participation of dopamine in the mechanism of action of all investigated antidepressant drugs. They also suggest the depression of sensitivity of presynaptic dopamine receptors in the brain 48-72 h after cessation of antidepressant treatment.

Animals↗
PubMed1980

Presynaptic alpha-adrenoceptors and the action of tricyclic antidepressant drugs in behavioural despair in rats.

The influence of the alpha-adrenolytics, yohimbine and phentolamine, given in low doses thought to block presynaptic alpha-adrenoceptors, on the action of the tricyclic antidepressants imipramine, nortriptyline and amitriptyline in the behavioural despair test was investigated in Wistar rats. Antidepressant drugs given in a single dose or for 2 weeks reduced immobility in rats. Yohimbine potentiated the effect of nortriptyline or amitriptyline administered in a single dose and the effect of imipramine and amitriptyline given for 2 weeks. The potentiating effect of phentolamine was observed only in rats receiving a single dose of nortriptyline. Yohimbine given chronically for 3 weeks together with antidepressants counteracted the effect of imipramine and nortriptyline on behavioural despair. Similarly clonidine abolished the reduction of immobility induced by antidepressants given in a single dose. It is concluded that the despair test is a behavioural model which is sensitive to the noradrenergic component of the drugs and that the blockade of presynaptic alpha-adrenoceptors facilitates the action of tricyclic antidepressants in this test.

Adrenergic alpha-Antagonists↗
PubMed1977

Clonidine-induced locomotor hyperactivity in rats. The role of central postsynaptic alpha-adrenoceptors.

The alpha-adrenergic agonist, clonidine, causes sedation in normal rats. The present study demonstrates that clonidine evokes strong locomotor stimulation in rats pretreated with 6-hydroxydopamine plus reserpine. Similar, but less intensive hyperactivity is observed in rats given clonidine after combined pretreatment with 6-hydroxydopamine plus p-chlorophenylalanine plus alpha-methyl-p-tyrosine, or with reserpine plus low doses of yohimbine. The aplha-adrenolytic drugs, phenoxybenzamine, phentolamine and aceperone, as well as high doses of yohimbine, antagonise the clonidine-induced locomotor stimulation; in contrast, the dopamine receptor blocking agents, pimozide and spiroperiodol, exert no antagonistic effect. The results indicate that in the brain of normal animals, clonidine predominantly activates presynaptic alpha-adrenoceptors on noradrenergic neurones and thereby induces sedation. After destruction of the noradrenergic fibres by 6-hydroxydopamine plus reserpine, activation of postsynaptic alpha-adrenoceptors prevails so that hyperactivity results.

Adrenergic Agents↗
PubMed1976

Behavioral effects of phenoxybenzamine administered intraventricularly in rats.

Phenoxybenzamine (PNB) injected into the lateral ventricle of the brain weakens spontaneous motility of rats and antagonizes hyperactivity induced with noradrenaline, amphetamine and caffeine. Body temperature rises briefly, sleep induced with chloral hydrate is shortened, and high doses enhance amphetamine-induced stereotypy. PNB injected intraventricularly intensifies turnover of noradrenaline but it has no effect on turnover of dopamine in rat brains. The results confirm a blocking influence of PNB on the cerebral noradrenaline receptors.

Animals↗