[The use of Hungarian medical terminology].
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History, 19th Century↗
Biomedical subjects
L György
Publications and source records attributed to L György.
[The ipriflavone story].
Ipriflavone is an original molecule. Its introduction took a complicated course first in veterinary use as a fodder additive then after checking out its antianginal effects it was registered and launched as an effective osteoporotic agent first in Japan 1988 nineteen years after the elaboration of the synthesis of the active ingredient. Dr. László Feuer who started and managed the research died after a short sickness in 1984 and so didn't live to see the success of ipriflavone.
Angina Pectoris↗
[Various problems of environmental hygiene in Hungary].
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Environmental Pollutants↗
Evidence that serotonin receptors are involved in the anticonvulsant effect of yohimbine in mice.
The threshold of seizures induced by electroconvulsive shock (ECS) was determined in mice and the effects of alpha 2-adrenoceptor antagonists (yohimbine, rauwolscine, idazoxan), alpha 2-adrenoceptor agonists (clonidine, B-HT 920), serotonin antagonists (methysergide, metergoline) and a serotonin agonist (quipazine) were studied. The interaction of yohimbine with clonidine, methysergide, metergoline and quipazine was also examined. It was found that yohimbine and rauwolscine elevated the seizure threshold, while idazoxan was ineffective. Clonidine and B-HT 920 were also ineffective, but quipazine elevated the seizure threshold. Methysergide and metergoline did not change the seizure threshold alone, but both of them antagonized the anticonvulsant effect of yohimbine. Clonidine failed to antagonize yohimbine's effects. Quipazine potentiated yohimbine's action. These results suggest that, in mice, the protective effect of yohimbine against ECS-induced seizures may be mediated via serotonin receptors and not via alpha 2-adrenoceptors.
Adrenergic beta-Agonists↗
Synthesis and pharmacological evaluation of some new tetrahydroisoquinoline derivatives inhibiting dopamine uptake and/or possessing a dopaminomimetic property.
As shown by structure-activity relationship studies in 8-(substituted-amino)-4-aryl-2-methyl-1,2,3,4-tetrahydroisoquinolines, the most important structural requirement for a marked antidepressant action is the presence of an ureido, (alkoxycarbonyl)amino, or [(alkylamino)acyl]amino group attached to the isoquinoline skeleton in position 8. In one of the biological tests a significant difference was found between 8-amino-4-phenyl-2-methyl-1,2,3,4-tetrahydroisoquinoline (nomifensine) and the new compounds synthesized. Nearly all compounds substituted in the amino group either decrease the spontaneous motility in mice or exert no effect on it. Two syntheses have been elaborated for the preparation of the compounds represented by the general formulas II-V where R1 = hydrogen, halogen, or methyl; Y = CONHR, OCOR, or CO(CH2)nNHR, in which R = alkyl or aralkyl or NHR = cyclic amine and n = 1-2. The syntheses start either from the corresponding 8-amino-4-aryl-2-methyl-1,2,3,4-tetrahydroisoquinolines or from the corresponding noncyclized amino alcohols. Of the compounds, 4-(p-chlorophenyl)-8-[(ethoxy-carbonyl)amino]-2-methyl-1,2,3,4- tetrahydroisoquinoline was found to possess the highest activity.
Animals↗
Yohimbine can not exert its anticonvulsant action in genetically audiogenic seizure-prone mice.
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Acoustic Stimulation↗
Some central effects of angiotensin II. Interactions with dopaminergic transmission.
The effects of angiotensin II (AT II) administered intracerebroventricularly (i.c.v.) on some behavioural reactions were studied. AT II increased the electroshock convulsive-seizure threshold in mice. Sulpiride antagonized this effect of AT II. AT II increased the exploratory behaviour of rats in open field. This effect was potentiated by nomifensine (a dopamine uptake blocker) and was blocked by haloperidol. AT II increased apomorphine stereotypy and the effect was antagonized by saralasin and haloperidol and partly by alpha-methyl-para-tyrosine (alpha-MpT) (an inhibitor of dopamine synthesis). AT II decreased the locomotor activity of mice. At doses of 0.5 and 1 microgram per mouse AT II did not change haloperidol (5 mg/kg)- or tetrabenazine (25 mg/kg)-induced catalepsy. It is assumed that the behavioural effects of AT II are realized through angiotensin receptors and through interactions between these receptors and dopaminergic transmission in the brain structures involved in the behavioural reactions studied.
Angiotensin II↗
Dopaminergic influence on the effects of angiotensin II in behavioural reactions.
Using a neuropharmacological approach we studied the dopaminergic influence on the effects of angiotensin II (ATII) in some behavioural reactions. Haloperidol reduced the exploratory behaviour-increasing effect of ATII in the open field. Haloperidol also reduced the apomorphine stereotypy-increasing effect of ATII. Sulpiride tended to overcome the locomotor activity-decreasing effect of ATII. Seven resp. 21 days after withdrawal of pimozide (applied for 14 days) the convulsive-seizure thresholdincreasing effect of ATII was enhanced. Haloperidol impaired the retention-facilitating effect of ATII in rats performing a shuttle-box active avoidance task. The results suggest close interactions between central DA-ergic transmission and ATII in the realization of the ATII effects on behaviour.
Angiotensin II↗
The effect of dopamine, apomorphine and piribedil on the mesenterial blood flow of the cat.
Responses to i.v. administration of dopamine, apomorphine, piribedil and bromocriptine were investigated in the feline mesenteric vascular bed. Dopamine increases the mesenterial flow in doses of 0.3 to 30 micrograms/kg; its effect can be inhibited by 1 to 3 mg/kg of sulpiride. Apomorphine and piribedil also increased the blood flow, but only in 20 to 200 times higher doses; they show a tachyphylaxis phenomenon and their maximal activity is 32 and 59 per cent, respectively, that of dopamine. Apomorphine is a partial agonist of dopamine and can inhibit the activity of the transmitter amine. Bromocriptine has no activity on the feline mesenterial flow. The postsynaptic dopamine receptors of the cat can be characterized by the following: strong efficacy of dopamine and lower ones of apomorphine, piribedil and of sulpiride. The presynaptic dopamine receptors are involved mostly in the hypotension, they are activated by low doses of apomorphine, and piribedil and by higher doses of dopamine; sulpiride reacts with these receptors in much lower doses than with the postsynaptic ones.
Animals↗
The inhibitory effect of dopaminomimetics on nerve stimulation-induced vasoconstriction of the cat's carotid artery.
The experiments were carried out in cats anaesthetized with chloralose and urethane. The preganglionic sympathetic nerve was stimulated and blood flow in the common carotid artery and the contractions of the nictitating membrane were recorded. Three intravenously given dopaminomimetics inhibited the vasoconstriction and nictitating membrane contractions induced by nerve stimulation. The rank order of the drugs was: bromocriptine greater than apomorphine greater than piribedil. The relative potencies on carotid blood flow were 100:30:3.1, respectively. The presynaptic site of activity was discussed.
Animals↗
Effects of dopaminergic agonists on somato-autonomic reflexes.
In cats lightly anesthetized with urethane (600 mg/kg, i.p.) reflexes of the blood pressure (BP) and of the nictitating membrane (NM) were elicited by stimulation of the sciatic nerve (16 V, 0.3 ms, 1-128 Hz, 2 s or 2 min) prior to and after the administration of apomorphine (0.05-0.2 mg/kg, i.v.) or piribedil (0.4-1.0 mg/kg, i.v.). In case of short-train (2 s) stimulation, both dopaminergic agonists shifted the frequency-response curves of NM contractions to the right, i.e. depressed NM reflexes in the entire range of the stimulation frequencies applied. At the same time, BP reflexes were depressed only in the range of lower frequencies (1-4 Hz). At higher rates (32-128 Hz) BP reflexes were potentiated. The reactions of BP to sustained (2 min) stimulations displayed a flat pressor plateau in response to lower-frequency stimulation, and a two-component pattern (an initial pressor peak followed by a plateau) to the higher-frequency one. Compatibility with the effects seen to short-train stimulations, the dopaminergic agonists prolonged the rise-time and augmented the amplitude of the initial pressor peak to sustained stimulations with lower and higher frequencies, respectively. The plateau of the pressor response to higher frequencies was depressed by higher doses (greater than 0.4 mg/kg) of piribedil. Administration of haloperidol (0.05-0.2 mg/kg, i.v.) resulted only in a partial restoration of the reflexes of BP and NM. The manifold effects of dopaminergic agonists on the somato-autonomic reflexes studied support the thought than NM and BP reflexes are organized, at least partially, in different ways.
Animals↗
Influence of the dopaminergic agonists bromocriptine, piribedil and nomifensine on the sympathetic neural transmission in the nictitating membrane of the cat.
The effect of some dopaminergic drugs on the nictitating membrane contractions induced by cervical sympathetic nerve stimulation was investigated in cats. Bromocriptine and piribedil injected into the lingual artery inhibited the nerve stimulation-induced contractions but did not suppress the effect of noradrenaline. Both compounds caused a parallel shift of the frequency-effect curve to the right. Nomifensine (in high doses, after desipramine pretreatment) inhibited the contractions induced both by nerve stimulation and by noradrenaline. Haloperidol or sulpiride antagonized the inhibition due to piribedil. Sulpiride prevented the effect of bromocriptine. We suppose that these agonists have a specific inhibitory activity on the presynaptic dopaminergic receptors.
Animals↗
The influence of dopamine and dopaminergic agonists on the contractions of field stimulated rat vas deferens.
In isolated field stimulated rat vas deferens frequency-response curves were shifted to the right by noradrenaline, dopamine, apomorphine, bromocriptine and nomifensine. Piribedil was found to be inactive. Phentolamine antagonized the effect of each active drug. The inhibition due to dopamine and apomorphine was also counteracted by haloperidol and sulpiride, while that caused by bromocriptine and nomifensine only by sulpiride. On the basis of these results an interaction was suggested between the presynaptic alpha and dopaminergic receptors: in the rat vas deferens dopaminergic receptors might activate alpha 2 receptors. The agonists increased the slope of the frequency-response curves. The drugs had a reversible activity on the vas deferens, except for bromocriptine which could not be removed by repeated wash-outs from the organ.
Animals↗
Influence of dopamine and dopaminergic agonists on relaxation of isolated rabbit ileum induced by sympathetic nerve stimulation.
The inhibitory effect of noradrenaline, dopamine and four dopaminergic agonists on smooth muscle relaxation induced by nerve stimulation was compared in isolated rabbit ileum. All these compounds inhibit the relaxation evoked by nerve stimulation. Their activity decreased in the following order: bromocriptine, noradrenaline, nomifensine, dopamine, piribedil and apomorphine. Yohimbine inhibited the effect of noradrenaline and to a lesser extent that of dopamine, while the antidopamine agent sulpiride abolished the effect of dopamine, apomorphine and nomifensine. The presynaptic action of these compounds is discussed.
Animals↗
Dopaminergic--GABA-ergic interaction in the nigrostriatal system.
Unilateral electrolytic lesion at the level of the substantia nigra resulted in ipsilateral rotation after the administration of different dopaminergic agonists such as d-amphetamine (5 mg/kg), apomorphine (3 mg/kg) and piribedil (50 mg/kg) in rats. The influence of the alteration of the GABA level was investigated on circling behaviour induced either by the presynaptic DA-ergic agonist d-amphetamine or by the postsynaptic stimulant apomorphine. Aminooxyacetic acid (12.5 mg/kg) as a GABA-transaminase inhibitor, decreased the rotation elicited by d-amphetamine or apomorphine. Picrotoxin pretreatment (1.5 mg/kg) acted reversely on the circling behaviour elicited by the presynaptic DA-ergic agonist. Picrotoxin pretreatment showed a trend to decrease the rotation induced by the postsynaptic DA-ergic agonists apomorphine and piribedil. It is concluded that the action of GABA in this behavioural test might appear not only presynaptically but also postsynaptically in the nigrostriatal system and even in different forms.
Animals↗
Oxotremorine-tolerance: muscarinic blockade or homeostatic adaptation?
Tremorine pretreatment of mice induces tolerance to some effects of oxotremorine. In the state of tolerance even the highest doses of oxotremorine did not cause antinociception, this blockade being insurmountable. Oxotremorine decreased motility and amphetamine hypermotility, and both effects were diminished by tremorine pretreatment. Amphetamine hypermotility increased in the tolerance state. The increase of cerebral acetylcholine level due to oxotremorine was diminished by tremorine pretreatment. It is suggested that a special blockade of cerebral muscarinic receptors might play a role in the tolerance phenomenon, moreover it is possible that some excitation develops in the CNS. A homeostatic adaptation may be involved a role in this kind of tolerance.
Acetylcholine↗
Role of dopaminergic and GABA-ergic interactions in seizure susceptibility.
The seizure susceptibility to electroshock in mice is decreased by apomorphine and piribedil; the effect of the two dopaminergic agonists is reduced by haloperidol. The seizure susceptibility is not influenced, increased or reduced by the different doses of haloperidol. The seizure threshold is elevated by amino-oxyacetic acid; its effect is reduced by picrotoxin, haloperidol and reserpine, and not influenced by apomorphine. The interaction between dopaminergic and GABA-ergic systems has been established; however, its characteristics are different from the well known interaction in the nigrostriatal region.
Aminooxyacetic Acid↗
Effects of phenytoin on sympathetic reflex responses in the cat.
Phenytoin (DPH), in a low dose (2 mg/kg) was found to potentiate reflex elevations in blood pressure and responses of the nictitating membrane induced either by the electrical stimulation of the sciatic nerve or by intravenously applied pentetrazol in light anaesthetized cats. Pressor responses to carotid occlusion under chloralose anaesthesia were also potentiated. In contrast a high dose (20 mg/kg) of DPH exerted an inhibitory effect on these responses. These effects of DPH on sympathetic reflex responses proved to be long-lasting. Intravenously applied picrotoxin (0.05 mg/kg) or the same dose of ouabain, injected into the vertebral artery, partially reversed the inhibitory effect of DPH (20 mg/kg). Our data support the suggestion that DPH exerts its inhibitory action by effecting ionic fluxes in the CNS, mostly in inhibitory structures.
Animals↗