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Biomedical subjects

K Wiśniewski

Publications and source records attributed to K Wiśniewski.

At least 73 records · Page 4Linked to original sources

Effect of angiotensin II and vasopressin on acquisition and extinction of conditioned avoidance in rats.

The effect of angiotensin II on the acquisition and extinction of a conditioned avoidance response was examined in rats. Angiotensin II, 1 and 2 micrograms, given intracerebroventricularly facilitated acquisition of the conditioned avoidance response but did not influence extinction. [Sar1, Ile8]-angiotensin II (1 microgram), a specific antagonist of angiotensin II receptors, unexpectedly produced an effect quite similar to that of angiotensin II. Vasopressin (1 microgram) did not influence the rate of acquisition of the conditioned avoidance response but it markedly delayed its extinction. The data are discussed in terms of learning and memory facilitating properties of angiotensin II. This action seems to be independent of an interaction of angiotensin II with its known receptors or of release of vasopressin caused by the peptide.

Angiotensin II↗

Examinations on contribution of bradykinin in the action of dopamine in circulatory system of rats. II. Influence of bradykinin in the action of dopamine on the vessel perfusion of the isolated hindpaw of rats.

The influence of different doses of bradykinin (0.1 micrograms, 1.0 micrograms/0.1 ml) and dopamine (0.1, 0.25, 0.5 micrograms/0.1 ml) on the flow through vessels of the isolated hindpaw of rat was estimated. Dopamine in small doses did not change and in the highest doses decreased the vascular flow. Bradykinin decreased the vascular flow and the effect was dose-dependent. This peptide administered together with dopamine in the smallest dose, evoked the same effect as dopamine itself in the highest dose and decreased the effect of dopamine introduced into the organism in the highest dose. Administration of phentolamine and propranolol decreased the vascular flow. The vasodilating effect of dopamine was seen after administration of drugs blocking the adrenergic receptors and the vaso-constricting effect of dopamine administered in the highest dose was not observed. Bradykinin decreased the vascular flow and when administered together with dopamine evoked effect similar to that after administration of the peptide with phentolamine and propranolol. The authors suppose that except the modifying influence of bradykinin on the action of dopamine, the role of the peptide receptor in this action cannot be excluded.

Animals↗

The effect of fibrinopeptides A and B on the circulatory action of dopamine.

Fibrinopeptides A and B potentiate the hypertensive action of dopamine in the rat and potentiate its hypotensive effects after alpha- and beta-adrenergic blockade. Dopamine receptor blockade with haloperidol completely abolished the effects of FAB. The possible mechanism of the observed effects is discussed.

Animals↗

Examinations on contribution of bradykinin in the action of dopamine in circulatory system of rats. I. Influence of bradykinin in the action of dopamine on arterial blood pressure of rats.

The influence of different doses of bradykinin (2.5 micrograms, 5 micrograms/kg i.v.) and dopamine (0.5 micrograms - a small dose and 25 micrograms, 250 micrograms/kg i.v. - a big dose) administered into the rat femoral artery on the blood pressure was estimated. Dopamine evoked hypotension (the small dose) or hypertension (the big dose). Bradykinin evoked dose-dependent decrease of the blood pressure. Bradykinin (2.5 micrograms/kg i.v.) administered in the 45th sec of the dopamine action enhanced the hypertensive effect and decreased the hypotensive effect of dopamine. Dopamine administered in the big dose after phentolamine and propranolol evoked hypotension. This effect was stronger after administration of dopamine (25 micrograms/kg i.v.). The hypotensive action of bradykinin persisted in spite of phentolamine and propranolol application but this peptide did not change the hypotensive effect of dopamine under these conditions. The authors discuss hypothetical mechanism of action of the observed influence of bradykinin on the effect of dopamine in the circulatory system.

Animals↗

Examinations of contribution of bradykinin in the action of dopamine in circulatory system of rats. III. Influence of bradykinin on chosen metabolic effects of dopamine.

The influence of bradykinin on the action of dopamine in the biochemical examinations (the activity of phosphorylase "a" in the heart muscle, the level of free fatty acids and the level of lactic acid in blood) were estimated. It was shown that dopamine (250 micrograms, 500 micrograms, 750 micrograms/kg i.v.) increased and bradykinin (2.5 micrograms, 5 micrograms/kg i.v.) did not change the examined biochemical parameters. Bradykinin applied in the smaller dose simultaneously with dopamine in the smallest dose intensified the amine action. The peptide introduced into the organism in the higher dose increased the stimulatory action of dopamine as estimated by the of phosphorylase "a" activity in the heart muscle and diminished the amine effect as estimated by the free fatty acids and lactic acid in blood. Administration of bradykinin with dopamine in the highest dose - 500 micrograms/kg i.v., did not change the stimulatory action of the catecholamine. But application of bradykinin with dopamine in the highest dose diminished the stimulatory effect of the dopamine. Therefore, bradykinin modified the action of dopamine as it was demonstrated by the estimation of the metabolic effects.

Animals↗

The effect of strenuous exercise on the reactivity of the central dopaminergic system in the rat.

In rats subjected to physical strain the action of dopamine receptor agonists, amphetamine and apomorphine, was enhanced, but the effects of an antagonist, haloperidol, remained unchanged. The levels of biogenic amines in several brain regions were changed after the exercise. The results indicate that physical strain changes the functions of the central dopaminergic system in the rat.

Amphetamine↗

Reactivity of the central nervous system in the disseminated intravascular coagulation in rats.

The reactivity of the central nervous system in the disseminated intravascular coagulation was studied. In this state the action of pentylenetetrazol and thiopental were decreased. Also shortening of tonic phase of electric convulsions was observed. No changes were noted in the contents of noradrenaline and serotonin, whereas slight increase in dopamine level in some regions of brain was found. It seems that observed effects are connected with other mechanisms than interaction with central mediators.

Animals↗

The effect of apomorphine and bradykinin on uptake and release of dopamine in vitro by striatal synaptosomes of the rat.

Apomorphine (APO), 10(-5) and 10(-4) M, inhibited 3H-dopamine (DA) uptake by rat striatal synaptosomes. Bradykinin (BRS) produced a biphasic effect: at low concentration (1.6 x 10(-7) it potentiated, while in higher (1.6 x 10(-5) inhibited DA uptake. Only the low concentration of BRS potentiated the already weak effect of APO, 10(-5) M, on DA uptake. In concentrations 10(-5) and 10(-4) M, APO facilitated the release of radioactivity from synaptosomes preincubated with 3H-DA. BRS potentiated this effect, particularly that evoked by the high concentration of APO. The results indicate that BRS may potentiate the action of APO on the uptake and release of dopamine by rat striatal synaptosomes in vitro.

Animals↗

Effect of increased fibrinolytic activity of rats blood on the action of some centrally acting drugs.

The action of some centrally acting drugs during high fibrinolytic activity of blood was studied. In these state the action of amphetamine increases and the action of thiopental and pentetrazol decreases. The observed changes may depend either on the altered pharmacokinetics of the compounds examined or on the neurohormonal background of the nervous tissue, changed under the influence of physical strain.

Amphetamine↗

Prostaglandins /PGs/ and peristalsis.

The effect of some inhibitors of PG-synthesis /Aspirin, Indomethacin and Suprofen/ on the small intestine peristalsis and the PG-like activity in mice was investigated. It was found that the three drugs examined in the applied doses did not affect the small intestine peristalsis but they significantly decreased the PG-like activity. The role of PGs in the physiological peristalsis of the small intestine is discussed.

Animals↗

Further studies on the effect of fibrinopeptides A and B on the central nervous system.

Fibrinopeptides A and B (FAB) given intraperitoneally increased general activity of rats without affecting motor coordination. FAB depressed thiopental-induced sleeping time, prolonged the latency of pentetrazol convulsions, shortened the tonic phase of electrogenic convulsions. The peptides depressed the dopamine level in investigated brain areas of rats and increased the level of homovanillic acid. FAB accelerated the disappearance of dopamine after alpha-methyl-p-tyrosine injection. The data indicate tha FAB stimulate the central nervous system and this seems to be related to their interaction with the central dopaminergic system.

Animals↗

The influence of bradykinin in vitro on uptake and release of dopamine by rat striatal synaptosomes.

Bradykinin differently affected the uptake of 3H-dopamine (assayed in synaptosomes separated by two methods: centrifugation and filtration) under various conditions of amine and investigated peptide concentration. 3H-dopamine uptake (assayed with the method of centrifugation) was depressed by cocaine, and bradykinin potentiated this effect. Similarly ouabain inhibited the dopamine uptake and this effect was potentiated by bradykinin. Bradykinin did not influence or potentiated the release of tritium from synaptosomes previously incubated with 3H-dopamine. The results indicate that bradykinin modifies the uptake and release of dopamine in rat striatal synaptosomes.

Animals↗

The influence of kinins on the action of circulatory drugs. I. The influence of kinins on hypertensive and hypotensive effects of selected drugs.

The influence of bradykinin and kallikrein on the action of norepinephrine, epinephrine, isoprenaline, phentolamine, propranolol, aminophylline and theophylline on blood pressure was studied. The kinins potentiated the hypertensive action of norepinephrine and epinephrine, weakened the hypotensive action of isoprenaline, potentiated the hypotensive action of propranolol, and had no effect on the action of phentolamine, aminophylline and theophylline.

Aminophylline↗

Kinins and central effects of the acetylcholine.

The interaction between kinins formed in central nervous system and acetylcholine was studied. Endogenous ACh in excess acted psychodepressively on the animal's behavior as evaluated with Lat's test. This effect was more intense in those rats in which the activity of kinin-forming enzymes in the nervous tissue had been increased with either kallikrein or bradykinin. Both kallikrein and bradykinin intensified the psychodepressive action of exogenous ACh given into the brain ventricle. Results show that kinins can enhance the inhibitory central action of ACh.

Acetamides↗