[Studies of the part played by angiotensin in the transport and metabolism of isonicotinic acid hydrazine (INH)].
Explore the source record for details and available documents.
Angiotensin II↗
Biomedical subjects
W Buczko
Publications and source records attributed to W Buczko.
The influence of somatotropin on the chlorpromazine distribution in rat tissues.
Explore the source record for details and available documents.
Animals↗
[Use of liver perfusion in rats for the evaluation of metabolism and transport of drugs].
Explore the source record for details and available documents.
Animals↗
Influence of fibrinogen degradation products on the action of amphetamine in the central nervous system.
Fibrinogen degradation products (FDP) in a dose dependent manner potentiated the action of amphetamine in the tests for locomotor activity (Knoll's motimeter) and stereotypy. They also antagonized the haloperidol-induced catalepsy. FDP increased the level of amphetamine 90 min after the drug administration, and depressed it 120 min after the treatment. FDP slightly depressed the level of dopamine, and increased that of homovanillic acid in the striatum. They also potentiated the accumulation of noradrenaline in the hippocampus, produced by amphetamine, but did not affect the concentrations of dopamine and serotonin. It is suggested that the change in action of amphetamine under the influence of FDP depends on the direct effect of the peptides on amphetamine level in the brain, and on the level of some neuromediators.
Amphetamine↗
Interaction of fibrinopeptides A and B with dopaminergic receptors in central nervous system.
The effect of fibrinopeptides A and B (FAB) on the action of compounds affecting the dopaminergic receptors in central nervous system (CNS) of rats was investigated. These peptides given intraperitoneally (ip) or intraventricularly (ivc) exerted dose-dependent stimulatory effects on the CNS: Enhanced the apomorphine and amphetamine-induced stereotypies and reduced the catalepsy induced by haloperidol. FAB depressed the dopamine level, especially when given together with alpha-MT, and elevated the level of homovanillic acid in the striatum. The results suggest that the stimulatory effects of FAB depend on their interaction with dopaminergic receptors in the CNS.
Amphetamine↗
The role of some prostaglandins in the interaction of fibrinogen degradation products (FDP) with central dopamine receptors of rats.
Indomethacin and fibrinogen degradation products (FDP) augmented amphetamine and apomorphine-induced stereotypies. In contrast, PGE1 and PGE2 decreased the stereotypies in rats, while PGF2 alpha enhanced amphetamine-induced stereotypy. Indomethacin given in combination with the peptides did not change their effect, whereas prostaglandins diminished the stimulatory effect of FDP on the amphetamine or apomorphine-induced stereotypy. Indomethacin and studied prostaglandins did not influence inhibitory action of FDP on haloperidol-induced catalepsy. It is concluded that prostaglandins do not play any essential role in the interaction of FDP with dopaminergic system in the CNS.
Amphetamine↗
Some pharmacological and biochemical effects of fibrinopeptides A and B in the circulatory system of rats.
Human fibrinopeptides A and B (FAB) increased the arterial blood pressure, accelerated the heart rate and elevated permeability of capillaries, produced a vasodilatory effect, evoked positive chronotropic and inotropic action on the isolated heart and did not affect the coronary flow. They lowered the content of glycogen in the heart muscle. They did not affect the concentration of glucose and elevated the content of lactic acid and free fatty acids (FFA) in the blood. As FAB are present in large quantities in the blood during disseminated intravascular coagulation, they may play an essential role in pathology of the circulatory system of mammals.
Animals↗
Studies on the role of catecholamines in the action of fibrinopeptides A and B in the circulatory system of rats.
Effects of fibrinopeptides A and B (FAB) in the rat circulation were examined after stimulation or inhibition of catecholamine system. FAB did not change the effects of noradrenaline and isoprenaline and increased the hypertensive action of dopamine. The effects of FAB on heart rate and blood pressure were absent in rats pretreated with propranolol and haloperidol respectively. Reserpine, alpha-methyl-p tyrosine and disulfiram diminished or abolished the effects of FAB. Apparently FAB can modify the function of adrenergic system in circulation either directly or indirectly.
Animals↗
Effect of fibrinogen degradation products (FDP) on heart rate and some metabolic parameters in the rat.
Investigations were carried out in vitro and in vivo on the effects of FDP on the rat heart. It was found that FDP have a positive chronotropic and inotropic effect. In in vivo investigations it was shown that the peptides raise the activity of phosphorylase a in the heart and increase slightly blood FFA and lactate levels decreasing glycogen content in the myocardium. The effects of the examined peptides are blocked partly by propranolol and reserpine, while phentolamine failed to change the FDP action. These data suggest that FDP exert chronotropic and inotropic effects through their action on the beta-adrenergic receptors in the myocardium.
Animals↗
[Value of leukotriene C4 in human subretinal fluid].
Concentration of leukotriene C4 (LT C4) in subretinal fluid and plasma of 12 patients with idiopathic retinal detachment has been studied. In 10 cases the subretinal fluid contained LT C4 (0.34 +/- 0.24 ng/ml) and concentration of this substance was about 10 times lower than that observed in plasma (4.05 +/- 0.83 ng/ml). The presence of LT C4 in subretinal fluid may result from retinal damage and it can be considered as an important prognostic factor.
Adolescent↗
Influence of acetaldehyde on some serotonergic mechanisms in rat blood platelets.
Acetaldehyde (ACT), both, ex vivo and in vitro did not change the ADP-induced rat platelet aggregation and the potentiating action of serotonin. The whole blood serotonin content was decreased only when ACT was used in doses of 20 and 30 mg/kg, i.v. and the platelet serotonin content remained unchanged. Ex vivo, ACT had no influence on the labeled serotonin uptake, whereas in experiments in vitro it inhibited the amine uptake and augmented the serotonin release from blood platelets in a dose dependent manner. The results indicate that all the changes in the platelet serotonergic mechanisms appear only after high concentrations of ACT. They may be of significant importance in the circulatory system or hemostasis only during disulfiram or calcium carbamide therapy.
Acetaldehyde↗
Effect of fibrinogen degradation products on the rat blood vessels.
Effect of fibrinogen degradation products on the rat blood vessels. Acta Physiol. Pol. 1977, 28 (2): 153--159. It was found that fibrinogen degradation products (FDP) exert a slight hypotensive effect and increase the flow of Tyrode's solution through isolated hindpaw of rat. The investigated peptides failed to change significantly the action of noradrenaline and had an additive effect with isoprenaline. Propranolol reduced the effects of FDP and isoprenaline. It is suggested that the described effects may be due to stimulation of the vascular beta-adrenergic receptors by FDP.
Animals↗
Influence of captopril on the serotonin-induced vasopressor effect in tail artery isolated from two-kidney, one-clip renal hypertensive rats.
The influence of captopril and ritanserin (5-HT2 receptor antagonist) on the serotonin-induced contraction of isolated tail artery of two-kidney, one clip hypertensive (2K, 1C-RHR) and normotensive rats was studied. Captopril, administrated in a single dose of 100 mg/kg, po or in a dose of 30 mg/kg/day, po for one week, diminished the systolic blood pressure in both groups of rats. Ritanserin (0.01 mg/kg/day, sc for one week) administrated alone or in combination with captopril (30 mg/kg/day) evoked such effect only in 2K, 1C-RHR. The reactivity of rat tail artery isolated from 2K, 1C-RHR to serotonin was significantly higher than that obtained from normotensive ones. Captopril given in a single dose or chronically did not change the serotonin-induced contraction of rat tail artery in normotensive rats. The attenuation of serotonin contractile effect was registered in hypertensive rats pre-treated with captopril. Administration ritanserin with or without captopril also inhibited the response to serotonin in both groups. The stronger effect was observed after administration of ritanserin with captopril in 2K, 1C-RHR than in control group. Our results indicate, that in 2K, 1C-RHR the reactivity of rat tail arteries to serotonin is enhanced and this effect can be reduced by chronic captopril administration.
Angiotensin-Converting Enzyme Inhibitors↗
Effects of drugs affecting the renin-angiotensin system on venous thrombosis in normotensive rats.
The aim of this study was to compare the potential antithrombotic action of captopril (angiotensin converting enzyme inhibitor) and losartan (a selective AT1 receptor antagonist) after their chronic administration in a model of venous thrombosis in rats. Captopril significantly reduced the incidence of venous thrombosis (67% vs 14%; p < 0.05) and both drugs markedly reduced the weight of thrombus. At the same time the platelet aggregation was reduced only in rats treated with losartan (100 +/- 7% vs 52 +/- 11%; p < 0.001). The mean blood pressure dropped only after losartan administration. We observed no changes in "transection" bleeding time after both drugs administration. In conclusion, captopril and losartan exerted an antithrombotic effect in venous thrombosis model in rats. The precise mechanism of this action should be established.
Animals↗
Antithrombotic effect of enalapril, an angiotensin-converting enzyme inhibitor, on venous thrombosis in rats.
The aim of the study was to investigate the potential antithrombotic action of enalapril in comparison with captopril after their acute and chronic administration in an experimental model of venous thrombosis in rats. Chronic treatment with captopril but not enalapril significantly reduced the incidence of venous thrombosis (67% vs 11%; p < 0.05). Both drugs markedly reduced the weight of thrombus. At the same time the platelet aggregation was reduced in rats acutely treated with both captopril and enalapril to 50 +/- 13% and 53 +/- 18%, respectively. The mean blood pressure dropped only after acute ACE-Is administration. No changes were observed in "transection" bleeding time. In conclusion, captopril and enalapril were able to inhibit the growth of thrombus in rats. Their antithrombotic effect seems to be independent from hypotensive action and influence on platelet aggregation.
Angiotensin-Converting Enzyme Inhibitors↗
Comprehensive study on platelet function, hemostasis, fibrinolysis, peripheral serotonergic system and serum lipids in nephrotic syndrome.
A comprehensive study on platelet aggregation, hemostasis, fibrinolysis and serum lipids in relation to peripheral serotonergic system has been performed on 41 nephrotic patients. Enhanced platelet aggregatory responses in both whole blood and in platelet rich plasma (PRP) were found upon stimulation with different agonists when compared to healthy volunteers. Increased levels of fibrinogen, fibrin monomers, and protein C activity were observed in nephrotic patients. Euglobulin clot lysis time was significantly prolonged in nephrotic patients. Activity of tissue plasminogen activator (tPA) inhibitor was higher in nephrotic syndrome, whereas tPA activity was significantly lower in these patients when compared to controls. Urokinase concentration, lipoprotein (a), cholesterol, LDL and VLDL levels were significantly higher in nephrotic patients over controls. Whole blood serotonin was significantly lower, whereas plasma serotonin was significantly higher in nephrotic patients relative to controls. Serotonin uptake and its release from platelets were markedly diminished in patients with nephrotic syndrome. Disequilibrium in the coagulolytic system, platelet hyperactivity, hyperfibrinogenemia, disturbances in peripheral serotonergic system together with lipid abnormalities may contribute to the progression and development of atherosclerosis and an enhanced risk of thromboembolic complications in nephrotic syndrome.
Adenosine Diphosphate↗
Cyclosporine A affects serotonergic mechanisms in uremic rats.
The aim of this study was to investigate the mechanism of cyclosporine-induced hypertension in respect to its action on blood serotonergic system. The experiment was carried out on healthy rats and animals with experimental chronic renal failure. Cyclosporine A (CsA) injected into the healthy and uremic rats caused an increase in systolic blood pressure. This effect was completely abolished by ketanserin, an antagonist of 5-HT2 receptors. Concomitantly a rise in blood and platelet serotonin concentration was observed. It is concluded that serotonin may play a role in the development of hypertension caused by CsA. Moreover, ketanserin may serve as a drug for pharmacological protection of CsA-induced rise of blood pressure in uremia.
Adenosine Diphosphate↗
Lack of the specific influence of histamine and histamine H1, H2 and H3 receptor ligands on the serotonin uptake and release in rat blood platelets.
This work was designed to investigate the influence of histamine, and H1 receptor agonist 2-(2-thiazolyl)ethylamine, H2 receptor agonist dimaprit and H3 receptor agonist R-(-)-alpha-methylhistamine on the serotonin uptake and release in rat blood platelets. Histamine and R-(-)-alpha-methylhistamine (up to 1 mmol/l), 2-(2-thiazolyl)ethylamine (up to 10 mumol/l) and dimaprit (up to 1 mumol/l) failed to affect the serotonin uptake. The concentration-dependent inhibitory effects of higher concentrations of 2-(2-thiazolyl)ethylamine and dimaprit (up to 1 mmol/l) were not diminished by the H1 receptor antagonist dimetindene and the H2 receptor antagonist ranitidine (1 and 100 mumol/l each), respectively. Histamine, 2-(2-thiazolyl)ethylamine, dimaprit and R-(-)-alpha-methylhistamine (up to 10 mumol/l) did not change the serotonin release from rat blood platelets. Our results demonstrate that histamine and histamine H1, H2 and H3 receptor agonists do not affect in a specific manner the serotonin uptake and release in rat blood platelets.
Animals↗