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PubMed1978

[Pharmacological studies on supersensitization. V. Augmentation of pressor response to catecholamine induced by N, N-dimethylethylenediamines (author's transl)].

Effects of N,N-dimethylethylenediamines on epinephrine-induced pressor response in pentobarbital-anesthetized rats were examined and 3 out of 12 compounds, i.e., tripelennamine, N,N-dibenzyl-N', N'-dimethylethylenediamine (I) and N1, N1-dibenzyl-N2, N2-dimethyl-1,2-propanediamine (II), were found to be more potent as potentiators to epinephrine. In pithed rats, tripelennamine, I, II and cocaine also augmented pressor response induced by epinephrine. In pentobarbital-anesthetized rats or in perfused hind paw of rats, the potentiation induced by cocaine and tripelennamine was more marked to norepinephrine than to epinephrine, but an inverse relation between norepinephrine and epinephrine was observed in the potentiation by I and II. In pentobarbital-anesthetized rats, tyramine-induced pressor responses were decreased or abolished by cocaine and tripelennamine, but these responses were increased by I and II. In pentobarbital-anesthetized rats, isoproterenol-, acetylcholine- and histamine-induced depressor responses were not influenced by cocaine, tripelennamine, I and II. Sensitivity of reserpinized rats to epinephrine was increased about eight times that seen in pentobarbital-anesthetized rats. In reserpinized rats, epinephrine-induced pressor responses were slightly increased by cocaine, tripelennamine and II, but these potentiations were not dose-dependent. These results indicate that one of the sites of action of cocaine, tripelennamine, I and II is localized in the peripheral portion of cardiovascular system. The principal mode of action of cocaine and tripelennamine appears to be the inhibition of amine-uptake mechanism at sympathetic nerve endings. The mode of action of I and II is apparently different from the actions of cocaine and tripelennamine.

Animals↗
PubMed1996

Effects of trepelennamine on brain monoamine turnover in morphine dependent and abstinent mice.

Previous studies have reported that the histamine H1 receptor blocker tripelennamine potentiates morphine withdrawal. In this paper, the in vivo effects produced by tripelennamine on the turnover of serotonin (5-HT), dopamine (DA) and noradrenaline (NA) in the whole brain, excluding the cerebellum, were studied in control, morphine-dependent (by SC implantation of a 75 mg morphine pellet) and morphine-dependent male CD1 mice just before naloxone-precipitated withdrawal. Tripelennamine (1-10 mg/kg) was administered SC 45 min. before the animals were killed. Serotonin, 5-hydroxyindole-3-acetic acid (5-HIAA), dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and noradrenaline were measured by high performance liquid chromatography coupled with electrochemical detection (HPLC-ECD) and 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG) was measured by HPLC coupled with fluorimetric detection. Ratios 5-HIAA/ 5-HT, DOPAC + HVA/DA and MHPG/NA were taken as an index of serotonin, dopamine and noradrenaline turnovers, respectively. Tripelennamine (1 and 10 mg/kg) significantly reduced serotonin turnover in control and morphine-dependent mice, and potentiated the serotonin turnover reduction when it was administered 30 min before naloxone injection. The dopamine turnover was diminished by tripelennamine (1 and 10 mg/kg) in the morphine-dependent group. Tripelennamine (10 mg/kg) reduced noradrenaline turnover during abstinence. These results suggest that the potentiation of opiate abstinence by tripelennamine could be related to its antiserotonergic profile.

Animals↗