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I Zebrowska-Lupina

Publications and source records attributed to I Zebrowska-Lupina.

49 records · Page 3Linked to original sources

Involvement of alpha 2-adrenoceptors in the activation of kininogenesis by clonidine.

The effects of clonidine and alpha 2-adrenoceptor blocking agents, yohimbine and tolazoline on kininogen and prekallikrein levels in plasma and on blood pressure were investigated in male Wistar rats. Clonidine (0.5 mg/kg) decreased concentration of kininogen. Yohimbine (3 mg/kg) and tolazoline (5 mg/kg) counteracted this effect of clonidine and increased the kininogen level in plasma. Clonidine did not change the level of prekallikrein, however in rats receiving alpha 2-adrenoceptor blockers alone or together with clonidine kallikrein utilization was reduced, which indicated indirectly that the level of prekallikrein in plasma augmented. Yohimbine and tolazoline in the same doses (3 mg/kg and 5 mg/kg resp.) increased the blood pressure and counteracted the hypotensive action of clonidine, which indicated the presynaptic alpha 2-adrenoceptor blocking effect of the doses used. The data indicate that clonidine-induced activation of kininogenesis as well as its hypotensive effect are counteracted by yohimbine and tolazoline in doses blocking specifically presynaptic alpha 2-adrenoceptors. It can be suggested that alpha 2-adrenoceptors are involved in the kininogenesis-activating effect of clonidine.

Animals↗

Hypertensive drugs and plasma kinins in rats.

The influence of phenylephrine (PHE), methoxamine (MET) and ephedrine (EPH) on kininogen and prekallikrein level in plasma was investigated in male Wistar rats. Simultaneously the effect of these drugs on blood pressure was monitored. No changes in kininogenesis were observed during the hypertension period (2 h after ip injection). The significant decrease in kininogen level (by 20-30%) was found 4 h after PHE (5 mg/kg) or EPH (40 mg/kg) and 4-12 h after MET (40 mg/kg) injection. The reduction of kallikrein utilization, indicating an increase in prekallikrein level in plasma, was noted only after PHE (by 34%) or MET (by 44%) administration. Phentolamine (REG) in a dose of 20 mg/kg, which counteracted the hypertensive effect of investigated drugs, abolished the influence of these drugs on kininogen level. The results indicate that the hypertension induced by alpha-adrenoceptor agonists evokes the delayed activation of kininogenesis parallel to the secondary decrease in blood pressure. Such a reaction of kinin system seems to be related to primary alpha-adrenoceptor stimulation, not to the direct influence of hypertensive drugs on kinin system in rat plasma.

Adrenergic alpha-Agonists↗

Anticataleptic effect of taurine: interaction with antiparkinsonian agents.

The influence of taurine on cataleptogenic effect of neuroleptics was investigated in male Wistar rats. It was found that taurine 900 micrograms/rat icv reduced significantly haloperidol or fluphenazine-induced catalepsy. In rats receiving taurine in a dose of 450 micrograms, not influencing catalepsy, with low doses of anticholinergic antiparkinsonian agents (trihexyphenidyl and pridinol) strong anticataleptic effect was observed. The results suggest that taurine facilitates neurotransmission in nigrostriatal dopaminergic neurons.

Animals↗

Immobilization stress modifies locomotor response to catecholamine receptor agonists in rats.

The effects of dopaminergic (apomorphine, nomifensine, B-HT 920) and noradrenergic (methoxamine, clonidine, salbutamol) agonists on locomotor activity were investigated in rats submitted to acute (3 h) or repeated (3 h/4 days) immobilization stress. The stress-induced functional changes were monitored by the blood level of corticosterone and the number of lymphocytes as well as the brain utilization of NA and DA. The rats subjected to acute immobilization stress displayed 30 min later an enhanced locomotor activation after apomorphine, nomifensine, or methoxamine and reduced sedative effect of clonidine, salbutamol or B-HT 920. 24 h after the repeated stress only the locomotor responses to apomorphine, nomifensine, B-HT 920 and salbutamol were modified. Spontaneous locomotor activity was not significantly changed under the influence of stressful stimuli. Increased plasma corticosterone level, strong reduction of blood lymphocytes and enhanced NA and DA utilization in the brain of rats after acute stress, together with above mentioned results, suggest that short-lasting stress evokes (30 min later) significant functional changes not only in the blood but also in the brain: enhanced CA neurons activity as well as the increased alpha 1-adrenergic and DA-post-synaptic receptors responsiveness in parallel with reduced alpha 2 - and beta-adrenergic and DA-presynaptic receptors reactivity. On the other hand, 24 h after last session of repeated stress CA brain neurons activity was not changed, however DA and beta-adrenergic responsivity was farther modified. It is postulated that the stress conditions produce in NA and/or DA brain systems a state of readiness to locomotion activating stimuli.

Albuterol↗

Studies on the mechanisms of central action of alpha-adrenergic receptor blocking agents.

The article summarizes the results of experiments, partly published, on the central action of alpha-adrenergic receptor blocking drugs given systemically in rats. Phenoxybenzamine, phentolamine and aceperone increase utilization of noradrenaline (NA in whole brain and antagonise NA--stimulated formation of cyclic AMP in brain cortical slices. They also counteracts locomotor hyperactivity and flexor reflex stimulation induced by NA receptor agonists. The investigated alpha-adrenolytics do not antagonize brain dopamine (DA) or acetycholine (ACh) receptor stimulation, although they weakly reduce the effects of central serotonin (5-HT) system activation. It is concluded, that phenoxybenzamine, phentolamine and aceperone block directly central NA receptors. They do not block DA or ACh receptors in the brain but they are weak antagonists of 5-HT system stimulation. The investigated compounds decelerate utilization of DA and increase those of ACh in the brain, these effects seem to be secondary to NA system hypofunction.

Acetylcholine↗

The effect of alpha-adrenergic receptor stimulant drugs on amphetamine or apomorphine-induced stereotypy in rats.

Clonidine, xylometazoline and naphazoline given ip cause a transition from sniffing to licking or gnawing stereotypy induced by amphetamine or apomorphine. Methoxamine, phenylephrine and in a lesser degree noradrenaline (all given ivc) inhibit licking and gnawing stereotyped behavior. Biochemical results correlate with the depressant action of clonidine and naphazoline on central noradrenergic neurotransmission and also with the stimulant action of methoxamine and phenylephrine on noradrenergic system. The both groups of alpha-adrenergic agonists seem to modify both the central dopaminergic and noradrenergic system activity in the same direction. It is suggested that this action can play a role in observed modification by alpha-sympathomimetic drugs of responses to dopamine agonists. However, the influence of alpha-sympathomimetics on other brain systems must be also taken into consideration.

Adrenergic alpha-Agonists↗

The influence of alpha-adrenergic drugs on catalepsy induced by haloperidol or fluphenazine in rats.

Clonidine (ip) and methoxamine (ivc) inhibit the catalepsy produced by haloperidol or fluphenazine. Naphazoline and xylometazoline antagonize the catalepsy produced by haloperidol, but do not affect significantly that produced by fluphenazine. Phenylephrine did not affect the catalepsy produced by either neuroleptic. The results indicate that drugs stimulating central noradrenergic receptors antagonize the action of compounds blocking the central dopaminergic receptors.

Adrenergic alpha-Agonists↗

Interaction of antidepressants with antiparkinsonian agents in rats.

The influence of antidepressants: nomifensine, imipramine, amitriptyline and trazodone on the effect of antiparkinsonian agents: trihexyphenidil and L-DOPA + carbidopa mixture (sinemet) in the model of haloperidol catalepsy was investigated in rats. In some experiments deprenyl, a selective MAO-B inhibitor, was used. It was found that antidepressant drugs in doses not influencing haloperidol catalepsy enhanced significantly the anticataleptic effect of trihexyphenidil and L-DOPA + carbidopa. The most effective in the interaction with both antiparkinsonian agents was nomifensine. Imipramine and trazodone potentiated anticataleptic effect of L-DOPA + carbidopa more strongly than those of trihexyphenidil. The most potent anticataleptic effect was observed after combined treatment of rats with deprenyl and L-DOPA + carbidopa.

Animals↗

Interaction between antidepressants and alpha-adrenergic receptor blocking agents.

Yohimbine and phentolamine administered in doses regarded as blocking presynaptic alpha-adrenoreceptors counteracted locomotor sedation elicited in rats by antidepressant drugs (imipramine, nortriptyline and amitriptyline). The reduction of noradrenaline (NA) utilization in the brain evoked by a single dose of antidepressants and the increase of NA utilization induced by chronic treatment with imipramine or nortriptyline were prevented by yohimbine. The results indicate the role of presynaptic alpha-adrenoceptors in the influence of tricyclic antidepressants on NA neurons in the brain.

Adrenergic alpha-Antagonists↗

[Changes of components in the kinin system and plasma renin activity during different stages of hypertension in patients treated with captopril].

The authors aim was to evaluate if the changes in the components of the plasma kinin system on PRA, determined during 3-weeks period of treatment with captopril in daily doses of 150 mg, depend on the stage of arterial hypertension. Investigations were carried out in 40 patients with primary hypertension; 6 patients were in I, 20 in II and 14 in III WHO stage. The control group consisted of 18 healthy persons. All the parameters were examined 3 times: before therapy, after 24 h and after 3 weeks of therapy. It was proved that captopril as monotherapy, was effective in every stage of hypertension, however the normalisation of blood pressure was observed only in I and II WHO stage. The normalisation of the prekallikrein levels appeared after 3 weeks of treatment in all periods of hypertension, while the normalisation of the kininogen levels occurred only in patients of I and II WHO stage. Since changes of kininogen level in plasma occurred along with changes in blood pressure, therefore the estimation of kininogen seems to be better criterium of effectiveness of captorpil than the determination of prekallikrein. The changes of PRA were similar in all stages of hypertension, but they were significant only in the group of patients of II WHO stage and only after 24 h. Presented studies indicate that renin-angiotensin-aldosterone system as well as kinin system, participate in the mechanism of antihypertensive effect of captopril in every stage of hypertension.

Adult↗

Studies on the interaction of antidepressant drugs with adrenocorticotropic hormone or prednisone in rats.

The influence of adrenocorticotropic hormone (ACTH) and prednisone on the effects of amitriptyline (AMI), imipramine (IMI), mianserin (MIA) or nomifensine (NOM) was investigated in forced swimming and in open field tests. ACTH (50 I.U./kg) or prednisone (1 mg/kg) were given in a single dose or for 7 consecutive days alone or together with AMI (10 mg/kg), IMI (10 mg/kg), MIA (10 mg/kg) or NOM (2 mg/kg). It was found that neither ACTH nor prednisone administered alone in a single dose or for 7 days influenced the behavior of rats. ACTH co-administered with AMI or NOM in a single dose or with AMI, IMI or NOM for 7 days potentiated the antiimmobility effect of antidepressant drugs. Prednisone potentiated only antiimmobility effect of NOM in forced swimming test. ACTH as well as prednisone co-administered with NOM (but not with the other drugs), in a single dose as well as for 7 days, increased also locomotor activity in open field. Neither ACTH nor prednisone influenced the effect of MIA in both tests used. It was concluded that the specific synergism exists only between ACTH and tricyclic antidepressants (AMI, IMI). The observed behavioral interaction between ACTH and AMI or IMI does not seem to be mediated by adrenocorticoids (prednisone was without effect). The potentiation of NOM effects by ACTH as well as by prednisone and lack of any interaction with MIA seems to be related with different mechanism of action of those antidepressant drugs.

Adrenocorticotropic Hormone↗

Acute effect of dopamine agonists and some antidepressants in stress-induced deficit of fighting behavior.

The effect of dopamine (DA) agonists (apomorphine, quinpirole) and three antidepressants (selegiline, nomifensine, imipramine), given in a single dose, on the electric footshock-induced fighting behavior was investigated in the control and chronically stressed rats. It was found that 48 h after the last session of chronic stress (various stressors applied for 16 days) the number of shock-induced fighting attacks was reduced by 50-70% in comparison with the control value. The drugs (except for imipramine), given in a single dose, 48 h after the last session of chronic stress, increased the number of fighting attacks and restored it to the control or above the control value. The same drugs at doses used, changed neither the intensity of fighting in the control (unstressed) rats nor the exploratory activity in both groups of animals. It is concluded that the short-lasting dopaminergic activation facilitates the aggressiveness reduced by chronic stress and that this effect does not depend on the locomotor activity level.

Aggression↗

Prolonged treatment with beta-adrenoceptor antagonists counteracts the aggression deficit induced by chronic stress.

Chronic stress-induced behavioral disturbances have been used as experimental models of depression. One of them is the deficit of fighting behavior induced by 16-day application of various unpredictable stressors. In the present study we investigated the effect of beta-adrenoceptor antagonists (propranolol, pindolol, nadolol and acebutolol) on electric footshock-induced fighting behavior in chronically stressed (14 various stressors over 16 days) male Wistar rats. It was found that the number of fighting attacks was reduced by about 50-80% in the rats submitted to chronic stress. Prolonged, 14-day, but not acute, treatment with propranolol, pindolol or nadolol (but not acebutolol) counteracted the deficit of aggression induced by chronic stress. It is suggested that beta-adrenoceptor antagonists which penetrate the blood-brain barrier may prevent the behavioral changes induced by chronic stress.

Acebutolol↗