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At least 19 recordsLinked to original sources

PubMed1982

Pharmacological studies on supersensitization. VII. Inhibitory effect of dibenamine on cocaine-induced supersensitivity of isolated vas deferens of guinea pig.

Effects of dibenamine on cocaine-induced supersensitivity of isolated vas deferens of guinea pig were examined. Dibenamine at 1.0 x 10(-7)-1.0 x 10(-5) M attenuated the degree of cocaine-induced increase in sensitivity to acetylcholine without any effect on acetylcholine-contraction. The degree of dibenamine-induced inhibition was dependent on the concentration of dibenamine and inversely related to the concentration of cocaine. Dibenamine at the concentration capable of inhibiting the contractile response to norepinephrine did not affect the degree of the increase in sensitivity to norepinephrine induced by cocaine. Dibenamine diminished the degree of cocaine-induced increase in sensitivity to potassium in standard Tyrode solution and that in maximum response to calcium in partially depolarized vas deferens. Dibenamine at the concentration of 3.2 x 10(-7) M did not affect acetylcholine-contractions and attenuated potassium-contractions of the preparations exposed 5 min to calcium-free Tyrode solution, but the degree of cocaine-induced potentiation of contractile response in calcium-free Tyrode solution was not affected by dibenamine. These results suggest that cocaine-induced increase in calcium influx from extracellular fluid is selectively inhibited by dibenamine.

Acetylcholine↗

PubMed1975

Dibenamine blockade on gastric acid secretion in vitro and its protection by histamine antagonists.

Experiments to protect the histamine receptor against dibenamine blockade were carried out to elucidate the pharmacological characteristics of the H2-histamine receptor system for gastric acid secretion in isolated bullfrog gastric mucosa. Dibenamine alone (5 times 10-minus 5 g/ml) irreversibly blocked both basal and histamine-stimulated acid secretion. However, when the preparation was treated with dibenamine in combination with histamine (1 times 10-minus 5 g/ml) irreversibly blocked both basal and histamine-stimulated acid secretion. However, when the preparation was treated with dibenamine in combination with histamine (1 times 10-minus 5 g/ml), the acid secretory response to histamine was restored after washing out dibenamine. Burimamide, an H2-receptor antagonist, also protected the histamine sensitivity against dibenamine blockade in the concentration of 1 times 10-minus 4 g/ml. Diphenhydramine and pyribenzamine were also protected with histamine receptor against dibenamine blockade. The acid secretion induced by the action of histamine on the diphenhydramine-protected receptor was antagonized by diphenhydramine as well as burimamide.

Animals↗

PubMed1983

Pharmacological studies on supersensitization. XI. Inhibitory effect of dibenamine on tripelennamine-N,N-dimethyl-N',N'-dibenzylethylenediamine- and N,N-dibenzyl-N', N'-dimethyl-1, 2-propanediamine-induced supersensitivity of isolated vas deferens of guinea pig.

Effects of dibenamine on tripelennamine-, N,N-dimethyl-N',N'-dibenzylethylenediamine (DBED)- and N,N-dibenzyl-N',N'-dimethyl-1,2-propanediamine (DBPD)-induced supersensitivity of isolated vas deferens of guinea pig were examined. Dibenamine attenuated the degree of tripelennamine- and DBED-induced increase in sensitivity to acetylcholine and potassium in standard Tyrode solution, but did not affect the degree of DBPD-induced increase in sensitivity to acetylcholine. Dibenamine diminished the degree of tripelennamine-induced increase, but did not affect the degree of DBED-induced increase, in maximum response to Ca2+ of partially depolarized vas deferens. Dibenamine diminished the degree of tripelennamine- and DBED-induced augmentation of potassium-contraction in Ca2+-free Tyrode solution, but did not affect that of acetylcholine-contraction. These results suggest that dibenamine prevent tripelennamine- and DBED-induced increase in Ca2+-influx (including extracellular Ca2+-superficial Ca2+ exchange) induced by acetylcholine and potassium. It is also suggested that DBPD potentiates acetylcholine-contraction by dibenamine-insensitive mechanisms.

Acetylcholine↗

PubMed1983

Dibenamine enhancement of histamine-induced relaxation of the rabbit mesenteric artery.

Helically cut strips of rabbit mesenteric artery relax when exposed to histamine if their histamine H1 receptors are first blocked by 7 X 10(-6) M mepyramine. Relaxations are potentiated by 20 min pretreatment with 10(-6) M dibenamine. This dibenamine regimen also enhances relaxation of the strips to the selective H2 receptor agonist dimaprit, and to a lesser extent to papaverine which does not act on histamine receptors. This enhancement occurs both at 38 degrees and 22 degrees, and in mesenteric artery strips from rabbits reserpinized to deplete amine stores. Histamine has a greater relaxant effect on mesenteric artery strips at 22 degrees than at 38 degrees, normally. Dibenamine-treated strips do not relax more at the lower temperature, however. Thus, dibenamine nonselectively enhances relaxations of mesenteric artery and may enhance histamine-induced relaxations by an additional mechanism.

Animals↗

PubMed1976

Synthesis and adrenoreceptor blocking action of aziridinium ions derived from phenoxybenzamine and dibenamine.

Crystalline perchlorate salts of aziridinium ions derived from phenoxybenzamine and dibenamine were prepared. Both aziridinium ions were tested on the rat vas deferens and found to possess alpha-adrenergic potencies which were nearly identical with those of the parent compounds. The hydrolysis rates of phenoxybenzamine and dibenamine aziridinium ions (2a,b) in physiological medium were found to be 6.0 4 x 10(-4) and 8.35 x 10(-4) sec-1, respectively. The rates of cyclization of the parent amines to 2a and 2b in aqueous medium were 1.9 x 10(-2) and 7.2 x 10(-3) sec-1, respectively. The potencies and kinetic profiles indicate that the aziridinium ion is the only active species in alpha-adrenergic blockade. Moreover, differences in potency between phenoxybenzamine and dibenamine appear to be exclusively to a difference in receptor affinity rather than to a difference in intrinsic alkylating ability.

Adrenergic alpha-Antagonists↗

PubMed1969

Reversal by pronethalol of dibenamine blockade: a study on the seminal vesicle of the guinea-pig.

1. The guinea-pig seminal vesicle has been shown to be a very suitable test object for the study of mechanisms involving alpha-adrenoceptive receptors, because no beta-receptors were found in this preparation.2. Adrenaline, noradrenaline and phenylephrine were directly acting agonists, their ED50 values being 7.1 x 10(-6)M, 1.5 x 10(-5)M and 2.7 x 10(-5)M, respectively.3. Pretreatment with reserpine had no influence on the contractions caused by adrenaline, noradrenaline and phenylephrine but abolished or greatly reduced the contractions caused by dopamine. Cocaine enhanced the effects of adrenaline, noradrenaline and phenylephrine and reduced those of dopamine.4. Pronethalol (6.8 x 10(-5)M) reversed the alpha-receptor blockade by dibenamine, ergotamine and phentolamine of responses to adrenaline, noradrenaline and phenylephrine; it did not affect the blockade by dibenamine of responses to histamine.5. Reversal of the blockade by dibenamine was observed only when its concentration was such that it caused a parallel shift of the dose-effect curves of the agonists to the right; higher concentrations, which caused an unsurmountable depression of the maximal contraction, were not antagonized by pronethalol.6. It is assumed that the reversal is dependent on a direct action on alpha-receptors, "spare receptors" being probably involved.

Animals↗

PubMed1985

Inhibition of cholecystokinin response in the gallbladder by dibenamine and its protection by benzodiazepines.

The contractile response of the guinea-pig gallbladder to cholecystokinin (CCK) and acetylcholine (ACh) was irreversibly inhibited by 5 X 10(-5) M dibenamine, and the dibenamine-induced inhibition in the CCK response was prevented by 10(-4) M chlordiazepoxide (CDP) and diazepam (DZP), but not by 10(-2) M proglumide or 10(-6) M atropine. The dibenamine-induced inhibition in the ACh response was prevented by 10(-6) M atropine, but not by 10(-4) M CDP. These findings suggest that the binding of CCK to the CCK receptor can be inhibited by benzodiazepines.

Animals↗

PubMed1999

Schizophrenia - A disturbance of signal interaction between the entorhinal cortex and the dentate gyrus? The contribution of experimental dibenamine psychosis to the pathogenesis of schizophrenia: A hypothesis.

In addition to the existence of complex memory (similar to the implicit nondeclarative memory of Squire), the existence of a phylogenetically old apparatus of a memory of situations (SMA) is supposed, which is to some extent comparable with the declarative memory of Squire. During actual sensory information the SMA generates a general frame and forms a general 'mark', indicating whether a given information has its origin inside or outside the body, and whether it is new or known. The procedure of this marking process can be explained as the time-depending arrest of a copy of the actual original information-transporting signal 'shower'; this copy must last until the feedback from thalamocortical centers indicates the termination of the processing of the original signal showers. The arrest of the shower copies is the performance of neuronal networks of the entorhinal cortex (EC) and the gyrus dentatus (GD). The psychopathological and biochemical analyses of experimental dibenamine psychosis show a different effect of dibenamine on the noradrenaline (NA) receptors of the EC and GD, respectively: these effects are responsible for the repeated perception cycles of a single situation. N,N-Dibencylamine blocks the postsynaptic alpha(1)-receptors of the EC without influencing the beta-receptors of the GD. Thus the interaction between EC and GD is changed: instead of new scenes, perceptions that have just been experienced get repeated presence and the quality of familiarity. The prolonged arrest of shower copies simultaneously blocks the entrance of new signal showers from the EC to the GD. No information-transporting signal showers can come in as long as the arrest lasts. In case of a disturbance in NA-dependent actions within the EC and the GD, the duration of arrest of information-transporting signal showers is shortened. Thus the formal frame of experience receives the quality of novelty instead of familiarity, and in addition the qualities of uncertainty, vagueness, and alienity. These very changes in perception and experience represent the basic disturbance of schizophrenia. All the symptoms of schizophrenia may be explained by this basic disturbance. The analysis of biochemical aspects turns attention to the energetic situation of NA and N-methyl-D-aspartate systems. These considerations suggest a genetic background of the basic disturbance of schizophrenia: transmitter effects on membranes of neurons and possibly also on glial cells, and energy supply of these effects may be predetermined genetically. It may be assumed that the compensation of such membrane-dependent disturbances will be possible within wide areas of the neural network, except for the 'bottleneck' of the overlapping region of the iso- and allocortex.

Adult↗

PubMed1982

Antagonism with dibenamine, D-600, and Ro 3-7894 to estimate dissociation constants and receptor reserves for cardiac adrenoceptors in isolated rabbit papillary muscles.

In papillary muscles isolated from reserpinized rabbits, positive inotropic responses to the alpha (alpha)-adrenergic agonist, (-)-phenylephrine in the presence of 10(7) M timolol and the beta (beta)-adrenergic agonist. (-)-isoproterenol were antagonized with the irreversible alpha-adrenergic antagonist, dibenamine, the irreversible beta-adrenergic antagonist. Ro 3-7894, and the calcium blocker, D-600. D-600 was employed as a functional antagonist of both alpha- and beta-adrenoceptor responses. Dissociation constants (Ka values) for drug-receptor interactions were calculated by the method of Furchgott and used to estimate fractional receptor occupancy and agonist efficacies. Comparison of responses showed that the receptor reserve for cardiac beta-adrenoceptors was greater than for alpha-adrenoceptors. D-600 was an effective inhibitor of both cardiac alpha- and beta-adrenoceptor responses; however, estimates of KA and receptor reserves were similar to estimates using an irreversible antagonist for alpha-but not beta-adrenoceptors.

Animals↗

PubMed1976

[Action mechanism of dibenamine on the tonus and inhibition of drug-induced contraction of the isolated guinea pig ileum, with special reference to its relationship to Ca].

Dibenamine (DB) produced contraction due to influx and release of Ca in normal medium, whereas it produced relaxation of the K-induced contraction due to depression of the activity of the muscle cell membrane. DB inhibited active influx, passive influx and release of Ca induced by ACh in this order as the concentrations were increased and also inhibited the contraction by histamine selectively as compared with the contractions by ACh, K and Ba, the inhibition of the ACh-, K- and Ba-contractions being almost to the same degree. In addition, DB inhibited to much the same degree the phasic contraction(PC) and tonic contraction(TC) by histamine, whereas it inhibited TC in preference to PC induced by ACh, K and Ba. Irreversible inhibition by DB of ACh-, K- and Ba-induced contractions were protected by Ca, whereas those of histamine-induced contraction were selectively protected by histamine and antihistamine, but not by Ca. These results indicate that the antagonism of DB and its irreversibility against histamine may be due to blockade of the histaminergic receptor, whereas those against ACh, K and Ba may be due to inhibition of the Ca-site. Evidence has been obtained suggesting that the irreversible parallel shift to the right of the log concentration-action curve of histamine after washout of DB may be due to spare receptors, whereas that of ACh, K or Ba may be due to inhibition of the Ca-site.

Acetylcholine↗

PubMed1976

Influence of adrenaline, dibenamine and dopamine on acidosis, hemoconcentration and lethality in protracted anaphylactic shock of guinea-pigs.

Protracted anaphylactic shock of guinea-pigs was accompanied by a marked decrease in blood pH, and an increase in hematocrit. Death ensued in 58.3% of the animals within 3 hr of observation. Infusion of adrenaline (20 mug/kg/min), after eliciting anaphylaxis, intensified the acidosis, and increased the lethality to 100%. Pretreatment with dibenamine (5 mg/kg) reversed the effect of adrenaline. Dopamine, infused in amounts of 200 mug/kg/min, acted similarly to the combination dibenamine/adrenaline. Hemoconcentration was neither prevented nor intensified by adrenaline. Dopamine, however, reduced significantly the anaphylactic increase in hematocrit.

Acidosis↗

PubMed1977

[Phentolamine and dibenamine action on the carotid reflexes induced by lobeline].

On the carotid reflexogenic zone lobeline provoques : 1) a increase of amplitude and rate of respiratory movements with bradycardia and hypotension ; 2) a secondary decrease of amplitude and rate of breathing with tachycardia. Acting on the reflexogenic zone, phentolamine and dibenamine provoque a transitory weakening or disappearance of these reflexes. These effects are induced by a local action, because they are not observed by intravenous injection of the drugs and the lobeline reflexes starting from the carotid sinus of the other side are not affected.

Animals↗

PubMed1951