Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of ethylenediamine in different regions of the rat and guinea-pig small intestine were investigated pharmacologically using isolated gut-bath preparations. In the guinea-pig, ethylenediamine caused concentration-dependent neurally mediated contractions or biphasic responses (contraction followed by relaxation). The contractions could be prevented by muscarinic and GABAA receptor antagonists. Ethylenediamine-evoked relaxations and depression of electrically evoked cholinergic twitch responses were blocked by desensitization to baclofen. However, in the rat intestine, the primary response to applied ethylenediamine was a concentration-dependent, non-desensitizing relaxation, evidently due to a direct action of ethylenediamine on the muscularis since it was unaffected by tetrodotoxin or GABAergic blockade.
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PMID:Differences in the effects (in vitro) of ethylenediamine on the guinea-pig and rat intestine. 234 Aug 58

Theophylline overdosage can cause life-threatening symptoms, that include seizures and cardiac arrhythmias, and can be fatal. Neither the onset of toxicity nor the severity of symptoms is well predicted by serum theophylline concentrations. Since depressed vitamin B6 plasma levels can occur in patients receiving theophylline, we explored a B6-theophylline interaction in a rabbit model. Administration of theophylline preparations intraperitoneally (aminophylline) or orally (sustained release anhydrous theophylline) resulted in a 47% depression of plasma pyridoxal 5'-phosphate (PLP) levels. The 87% increase in PLP with pyridoxine administration was only 18% when aminophylline was also given. The mechanism of the theophylline-B6 interaction is obscure. Ethylenediamine in some theophylline preparations binds directly to PLP, potentially increasing the less direct theophylline effect. Pyridoxine supplementation resulted in higher average PLP levels but did not prevent death in animals with profoundly low PLP levels. If these data apply to humans, B6 deficiency may contribute to chronic theophylline toxicity; however, pyridoxine administration in the dosage used may not prevent toxicity. Larger doses may prove beneficial after further investigation.
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PMID:Depression of vitamin B6 levels due to theophylline. 236 33

gamma-Aminobutyric-acid (GABA)-mimetic responses were induced by ethylenediamine (EDA) in the isolated ileum of the guinea-pig maintained in bicarbonate buffered Krebs-Henseleit (KBC) solution, pH 7.4, 37 degrees C, the responses consisting of a contraction followed by a relaxation. There were no such responses to EDA in bicarbonate-free phosphate buffered (KPO) or HEPES buffered (KHO) Krebs solution, gassed with 100% O2, pH 7.4, 37 degrees C, yet the ileum responded to GABA in bicarbonate-free Krebs solution. Similar GABA-mimetic responses were induced by EDA in the isolated ileum maintained in bicarbonate-free KPO or KHO modified Krebs solution, gassed with O2, if HCO3- (5mM) was first added immediately before the test dose of EDA (0.1-1 mM), the threshold [HCO3-]being 2 mM for EDA-induced responses in these preparations. However, ileal GABA-mimetic responses were induced in bicarbonate-free KPO or KHO solutions by EDA that had been pretreated with carbon dioxide, where the final [HCO3-]in the bath did not exceed 25 microM. Ethylenediamine monocarbamate (synthetic EDAC) released [3H]-GABA from preloaded segments of ileum maintained in bicarbonate-free KPO or KHO solution containing amino-oxyacetic acid and beta-alanine, the release being sensitive to 3-mercaptopropionic acid which prevents GABA release. EDA itself did not evoke any such release in the absence of bicarbonate, but released [3H]-GABA from segments maintained in KBC solution. 4 GABA-mimetic responses were induced by EDAC in the isolated ileum maintained in bicarbonate-free KPO solution, as was a delta-aminovalerate-sensitive depression of ileal twitch responses elicited by transmural stimulation, all of which were also sensitive to 3-mercaptopropionic acid. 5 It is concluded that GABA-mimetic responses to EDA in the isolated ileum of the guinea-pig, maintained in normal Krebs bicarbonate medium, result from the release of endogenous GABA by ethylenediamine monocarbamate formed through the rapid reaction of EDA with the carbon dioxide of bicarbonate buffered Krebs solution. Furthermore, in the ileum, HCO3 ions per se are not necessary for this GABA-releasing property of EDA if the latter is first converted to the monocarbamate, since syntheticethylenediamine monocarbamate elicits ileal GABA-mimetic responses in the total absence of bicarbonate.
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PMID:Bicarbonate-dependence of responses to ethylenediamine in the guinea-pig isolated ileum: involvement of ethylenediamine-monocarbamate. 358 Jul 7

Ethylenediamine (EDA) released [3H]-gamma-aminobutyric acid ([3H]-GABA) in a dose-dependent manner from the isolated preloaded ileum of the guinea-pig maintained in Krebs-bicarbonate solution (pH 7.4, 37 degrees C), in the presence of beta-alanine and amino-oxyacetic acid (AOAA) to prevent GABA uptake into glial cells and catabolism. This release was reversibly prevented by 3-mercaptopropionic acid (3-MPA), also in a dose-dependent manner. In the isolated ileal preparations of the guinea-pig maintained in Krebs-bicarbonate solution, EDA induced a dose-dependent transient, cholinergic contractile response (GABAA-receptor-mediated effect), followed by an 'after-relaxation' (GABAB-receptor-mediated effect). EDA also induced a transient contraction superimposed on repetitive twitch responses to electrical transmural stimulation of the cholinergic neurones, followed by a depression of the twitch contractions. This GABAA-receptor-mediated contraction was antagonized by bicuculline methochloride and picrotoxinin, whilst the GABAB-receptor-mediated 'after-relaxation', and depression of cholinergic twitch contractions, was susceptible to antagonism by delta-aminovaleric acid. The pA2 value for bicuculline methochloride antagonism of EDA was estimated to be 5.8, identical with that for GABA. 3-Mercaptopropionic acid also prevented these pharmacological actions induced by EDA without affecting responses to GABA, 3-aminopropranesulphonic acid, muscimol, baclofen or the twitch responses to transmural stimulation. It is concluded that EDA releases both [3H]-GABA and endogenous GABA in the guinea-pig ileum, thus providing further evidence that GABA is a transmitter in the enteric nervous system.
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PMID:Evidence that ethylenediamine acts in the isolated ileum of the guinea-pig by releasing endogenous GABA. 648 87

1 The effects of gamma-aminobutyric acid (GABA), ethylenediamine, 3-aminopropane sulphonic acid and (+/-)-baclofen have been examined on the responses to stimulation of the adrenergic excitatory and non-adrenergic non-cholinergic inhibitory innervation of the rat anococcygeus muscle in vitro. 2 GABA produced a dose-related depression of the contractile responses to field stimulation. Ethylenediamine and baclofen also depressed the contractile responses, though they were less potent than GABA. 3-Aminopropane sulphonic acid was almost inactive. The inhibitory action of GABA was not modified by phentolamine, propranolol or bicuculline methylbromide. 3 GABA did not affect the contractile responses of the anococcygeus muscle to noradrenaline, phenylephrine or carbachol in untreated muscles or those treated with 6-hydroxydopamine in vitro. 4 In preparations in which tone was raised by continuous perfusion with carbachol in the presence of phentolamine, field stimulation relaxed the muscle. GABA had no effect on this inhibitory response, and did not itself produce any relaxation. 5 It is concluded that GABA exerts a presynaptic inhibitory action on the excitatory adrenergic but not on the inhibitory innervation of the anococcygeus muscle, and that the GABA receptor involved exhibits properties of the previously described GABAB site.
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PMID:Inhibitory action of gamma-aminobutyric acid on the excitatory but not inhibitory innervation of the rat anococcygeus muscle. 715 Aug 75

Aminophylline, theophylline, etamiphylline and diprophylline have been tested as antagonists of neuronal inhibition produced by microiontophoretically applied adenosine, when ejected as cations or anions. Aminophylline proved to be an effective adenosine antagonist when ejected as an anion, especially from alkaline solution. Anionic theophylline was also effective but less so, and on a smaller proportion of neurones. Ethylenediamine and hydroxyl ions had no effect on adenosine responses. GABA depressions were unaffected by any of the methylxanthines at the time of adenosine blockade. Cationic ejection from aminophylline or ethylenediamine barrels produced a depression of unit firing on about one third of the cells tested, but no antagonism of adenosine was observed. It is concluded that the anionic ejection of aminophylline from alkaline solution, or of etamiphylline of diprophylline, yields potentially useful antagonists of adenosine for iontophoretic experiments.
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PMID:Aminophylline and theophylline derivatives as antagonists of neuronal depression by adenosine: a microiontophoretic study. 743 27