Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.1.7 (acetylcholinesterase)
28,390 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three patients with chronic obstructive lung disease (COPD) and myasthenia gravis whose pulmonary symptoms were worsened by therapy with cholinesterase inhibitors were improved by inhaled ipratropium bromide. Two had increases in FEV1 (19 percent, 35 percent) and specific conductance (106 percent, 81 percent) and reductions in dyspnea. The third had no change in airflow with ipratropium, but improved due to decreased bronchial secretions which had limited the use of cholinesterase inhibitors. In contrast, beta agonist bronchodilators had no effect in any of these patients. This experience suggests that ipratropium may be the bronchodilator drug of choice in patients with obstructive lung disease aggravated by cholinesterase inhibitors.
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PMID:Ipratropium in patients with COPD receiving cholinesterase inhibitors. 296 27

It is known that in normal subjects repeated administration of the growth hormone-releasing factor (GRF) induces a state of partial refractoriness of the somatotropes to GRF. Studies were conducted to verify whether the cholinergic system plays a role in the mechanism(s) underlying the reduced GH responsiveness to the neuropeptide. In five healthy men, the GH response to three consecutive injections of GRF (50 micrograms iv), administered at 2 h intervals, was considerably blunted after the second and third GRF bolus. Administration of the inhibitor of cholinesterase, pyridostigmine bromide (120 mg orally) 30 min before the second GRF bolus, not only restored but greatly potentiated the GH responsiveness to the second GRF bolus. The GH response to the third GRF bolus was not apparently influenced by pre-treatment with pyridostigmine. These data reinforce the view that cholinergic neurotransmission plays an important role in the control of GH secretion in human.
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PMID:Potentiation of cholinergic tone by pyridostigmine bromide re-instates and potentiates the growth hormone responsiveness to intermittent administration of growth hormone-releasing factor in man. 302 Aug 50

To throw light onto the mechanism(s) by which the cholinergic system influences growth hormone (GH) release, the effects of two muscarinic receptor blockers, pirenzepine and atropine, and of an acetylcholinesterase inhibitor, pyridostigmine bromide, on the GH response to GHRH-44 were studied in 19 normal volunteers. Moreover, the effects of pirenzepine administration on plasma GH levels both in basal conditions and after stimulation by GHRH-44 and TRH were studied in 9 acromegalics. Both pirenzepine (0.6 mg/kg i.v., 5 min before GHRH) and atropine (1 mg i.m., 15 min before GHRH) blunted the GH response to GHRH (1 microgram/kg i.v. bolus) (area under the response curve, AUC: 81.3 +/- 17.3 vs. 481.2 +/- 211.3 ng/ml/h for pirenzepine and 100.2 +/- 27.0 vs. 364.7 +/- 81.0 ng/ml/h for atropine; p less than 0.01). Pyridostigmine (120 mg orally, 30 min before GHRH) induced a variable but significant (p less than 0.02) rise in basal plasma GH levels and, furthermore, an unequivocal potentiation of the GH response to GHRH (AUC: 1044.6 +/- 245.3 vs. 481.2 +/- 211.3 ng/ml/h; p less than 0.01). In all but one acromegalics 0.6 mg/kg i.v. pirenzepine was unable to modify the basal GH levels whilst it showed a variable inhibitory effect on the GH response to GHRH. The GH response to TRH (200 micrograms i.v. bolus) was instead unmodified by pirenzepine. In conclusion, muscarinic receptor blockade inhibits while cholinergic potentiation seems to positively modulate the GH response to GHRH. Therefore, the cholinergic system seems to positively modulate the GHRH effect on somatotrophs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cholinergic involvement in the growth hormone releasing hormone-induced growth hormone release: studies in normal and acromegalic subjects. 309 9

Electron microscopical localization of non-specific cholinesterase activity was studied in the encapsulated part of rat hindlimb muscle spindles. After incubation of the muscle tissue in a medium containing butyrylthiocholine bromide as substrate and BW284c51 as the specific inhibitor of acetylcholinesterase, a distinct electron-dense precipitate corresponding to non-specific cholinesterase activity was found along the whole length of muscle spindles. The richest source of non-specific cholinesterase activity were the motor end-plates present in the polar and juxtaequatorial regions. Much smaller amounts of reaction deposits were found at the secondary sensory terminals in the juxtaequatorial zones. The primary sensory terminals in the equatorial zone contained only low amounts of the reaction product. A fine homogeneous reaction product was localized in the narrow spaces between Schwann cell processes or in gaps between the Schwann cell, and axonal and muscle membranes. A granular precipitate was localized on the basal lamina in the synapse region of motor terminals or covering Schwann cell processes and sensory terminals with adjacent intrafusal muscle fibres. Our results suggest that most of non-specific cholinesterase in muscle spindles is synthesized by the Schwann cells; but a small amount can also be synthesized by fibroblast-like cells forming the inner capsule of muscle spindles. Non-specific cholinesterase thus coexists with acetylcholinesterase at motor end-plates, but is single at sensory terminals. The function of non-specific cholinesterase in sensory receptors is still not clear. It seems most probable that non-specific cholinesterase in muscle spindles may play a role in the maintenance of the external milieu around nerve endings, especially in the sensory region.
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PMID:Ultrastructural localization of non-specific cholinesterase activity in rat muscle spindles. 312 47

(-)-N1-Benzylnorphysostigmine (4), prepared from synthetic (-)-O-methyl-N1-noreseroline (1) by N-benzylation, ether cleavage, and reaction of (-)-N1-benzylnoreseroline (3) with methyl isocyanate, was the intermediate used to prepare the title compounds. Catalytic debenzylation of 4 afforded (-)-N1-norphysostigmine (5), and (-)-eseramine (6) was obtained by reaction of 5 with methyl isocyanate. Reductive N-methylation of 5 gave (-)-physostigmine (9) while reaction of 5 with allyl bromide and phenethyl bromide afforded carbamates 7 and 8, respectively. Data on the in vitro potencies (IC50) and activities of certain of these compounds (4-8) as inhibitors of electric eel acetyl cholinesterase are reported. (-)-N1-Norphysostigmine (5) was found to be similarly potent against AChE as (-)-physostigmine (9).
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PMID:Synthesis and anticholinesterase activity of (-)-N1-norphysostigmine, (-)-eseramine, and other N(1)-substituted analogues of (-)-physostigmine. 319 22

An estimate of the amplitude of respiratory sinus arrhythmia (V) has been proposed as a noninvasive measure of parasympathetic activity. This experiment monitored V in response to a subclinical dose of pyridostigmine bromide (PYR) and a pharmacological challenge of atropine sulfate (ATR). Twelve male rhesus macaques received 200 micrograms/kg of PYR 30 min prior to an injection of 0, 14, 44, or 140 micrograms/kg ATR. The decrease in V after both the 44 and 140 micrograms/kg ATR doses was similar to the response to ATR alone in a previous experiment. The 14 micrograms/kg dose of ATR did not significantly decrease V in this experiment, which is in contrast with the large decrease of V after ATR alone in a previous experiment. Neither drug affected respiration. The dose of ATR which would be effective in causing a 30% decrease of V in the presence of PYR was estimated to be 18.3 micrograms/kg of ATR. This is twice the dose of ATR calculated to have the same effect without PYR. The attenuated response of V after a pharmacological challenge of ATR may be used to quantify the latent muscarinic effects from exposure to anticholinesterase agents. The attenuated response to ATR may also be useful for evaluating the return of normal cholinergic function after disruption by cholinesterase inhibitors.
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PMID:Quantifying the altered cardiac response to atropine following pyridostigmine in rhesus macaques. 324 15

Analogues of the potent inhibitor of choline acetyltransferase (CAT) (E)-4-(1-naphthylvinyl)pyridine methiodide were synthesized and evaluated for their ability to inhibit CAT and protect against nerve agent intoxication. Several compounds, notably (E)-1-(2-hydroxyethyl)-(1-naphthylvinyl)pyridinium bromide (3), (E)-1-methyl-4-(1-naphthylvinyl)-1,2,3,6-tetrahydropyridine hydrochloride (22), and (E)-1-methyl-4-(1-naphthylvinyl)piperidine hydrochloride (23), were found to afford significant protection against sarin in the mouse and against soman in the guinea pig. However, protection was apparently not related to CAT inhibition. Compound 23, our most effective compound in protecting against nerve agent, was without CAT inhibitory activity. Compound 22, which proved to be a potent CAT inhibitor, most likely owed this activity to being dehydrogenated back to the pyridinium quaternary salt by oxidative enzymes. Several of the (naphthylvinyl)pyridine quaternary salts, but not their tertiary amine analogues, were found to be effective in slowing the rate of aging of soman-inhibited acetylcholinesterase. Ability to slow the rate of aging was enhanced by introduction of methoxy substituents on the aryl moiety whereas the aging rate was actually accelerated by chloro substituents. To date, our most effective compound in slowing the rate of aging, (E)-4-[(4-methoxy-1-naphthyl)vinyl]pyridine methochloride (6), did not provide significant protection against soman in the mouse.
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PMID:Approaches to protection against nerve agent poisoning. (Naphthylvinyl)pyridine derivatives as potential antidotes. 335 60

The effects on vision of ingestion of the anticholinesterase pyridostigmine bromide (60 mg), assessed from pharmacokinetic data to provide at least 20% inhibition of blood cholinesterase over the 1 1/2-4 1/2 h experimental period, was compared with 60 mg lactose in a double-blind crossover protocol. Contrast sensitivity to stationary oscilloscope-generated gratings of 3-40 c/deg showed a small but significant increase of 7% which was consistent with a small reduction in pupil diameter, surmised to cause a small improvement in optical quality. This reduction in pupil diameter was, however, overshadowed by a larger though still non-significant reduction on the second visit to the laboratory compared with the first. Contrast sensitivities to laser interference fringes observed in the Maxwellian view, by which the effects of the optical media are essentially bypassed, thus providing an entirely neural assessment, were unchanged after pyridostigmine. It is concluded that pyridostigmine may be given as a prophylactic in anticipation of exposure to an organophosphorus anticholinesterase without a deleterious effect on stationary visual function.
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PMID:The effects of ingestion of 60 mg pyridostigmine bromide on contrast sensitivity in man. 341 Apr 84

A commercial preparation of water-soluble acetylcholinesterase from horse red cells has been purified to a specific activity of 2380 U/mg of protein (a 1660-fold purification) by a twofold affinity chromatography on the known sorbent of Sepharose-p-[NH-(CH2)5-C(O)NH(CH2)5C(O)NH-]-C6H4-N+(CH3)3 X Br- at pH 7.5. A selective elution of the enzyme was carried out from 10 mM of the phosphate buffer solution which contains 0.2% of triton X-100. Subsequent desorption of the enzyme proceeded with 5 mM of phenyltrimethylammonium bromide introduced into the buffer. Such effective preparations of acetylcholinesterase have not been previously produced. Effectiveness of the affinity sorbents considerably depends on the nature of the ligand which is covalent-linked with a Sepharose matrix and on the length of the attachment spacer arm ("insert") between them. A reversible inhibitory effect of certain ligands (tetramethylammonium, phenyltrimethylammonium) and their derivatives on acetylcholinesterase is estimated in comparison.
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PMID:[Purification of acetylcholinesterase from horse erythrocytes using affinity chromatography]. 360 28

In all mammals so far investigated the occurrence of ponto-geniculo-occipital (PGO) waves precedes the onset and maintenance of desynchronized (D) sleep. As unitary electrographic events, PGO waves provide an index for quantitative evaluation of physiological D sleep or the D sleep-like state evoked by centrally administered acetylcholinesterase inhibitors. The present study characterized PGO wave frequency and time course following central administration of neostigmine bromide (Neo). The results show that Neo produced a dose-dependent increase in PGO wave frequency and time course when injected into brainstem regions other than areas containing putative PGO wave generating neurons. These results support the concept that PGO waves and D sleep are generated by an anatomically distributed network of cholinoceptive neurons.
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PMID:Increased ponto-geniculo-occipital (PGO) wave frequency following central administration of neostigmine. 369


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