Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.1.8 (cholinesterase)
 12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the effects of eserine and ouabain on the permeability of the blood-brain barrier (B.B.B.) as related to the febrile response induced with LPS in rabbit. Results are as follows; The febrile response induced by LPS (0.02 and 1.0 mug/kg) i.v. was suppressed by administration of ouabain (0.06 mg/kg, i.v.). Contrary to the febrile response of LPS given i.c. (10(-4) and 10(-3) mug/kg), the febrile response was not suppressed with the same dose of ouabain. The pyrogenicity of cerebrospinal fluid (CSF) withdrawn at two hours after rabbits had been injected with LPS (25 mug/kg) was suppressed by ouabain (0.06 mg/kg, i.v.). Pyrogenic response was enhanced by pretreatment with eserine (0.5 mg/kg, s.c.) given one hr before LPS (1 mug/kg, i.v.). The pyrogenicity of CSF was also potentiated to a greater extent by pretreatment of eserine than with LPS alone. In the eserinized rabbit (0.5 mg/kg, s.c.), the pyrogenicity of CSF was potentiated to a greater extent by ACh (10 mug/kg, i.v.) than by LPS (1 mug/kg, i.v.) alone. From these data, it is concluded that the inhibition of Na, K-ATPase by ouabain decreases the pyrogenicity of LPS, while the inhibition of cholinesterase by eserine enhances the pyrogenicity.
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PMID:[Effects of eserine and ouabain on the febrile reaction induced by lipopolysaccharide]. 103 14

1. Longitudinal muscle strips of the guinea-pig ileum were incubated in Tyrode solution containing either DFP or physostigmine as cholinesterase inhibitor. After a 90 min preincubation period the acetylcholine resting release into the medium was determined. Acetylcholine was estimated by gas chromatography. 2. The resting release was 0.39 nmol/g times min irrespective of the cholinesterase inhibitor used. In the presence of hexamethonium, or after omission of external calcium, the resting release fell by 50 and 55 per cent, respectively. 3. Oxotremorine (10-5 and 10-4M) significantly inhibited the resting release of acetylcholine by 25 and 33 per cent, respectively. The inhibitory effect of oxotremorine was completely reversed by atropine (3 times 10-7 M). Oxotremorine did not reduce the spontaneous release of acetylcholine that occurred either in the presence of hexamethonium or in the absence of external calcium. 4. The acetylcholine content of the muscle strips was approximately doubled during the preincubation with a cholinesterase inhibitor. The subsequent incubation with oxotremorine did not lead to a further increase in the endogenous acetylcholine content. However, incubation of the muscle strips with oxotremorine in the absence of a cholinesterase inhibitor led to a rise in the endogenous acetycholine concentration. In in vivo experiments, oxotremorine also caused an increase in the acetylcholine content of the muscle strips. The possibility is discussed that the rise in the acetylcholine concentration following the administration of oxotremorine is a consequence of the decreased release. 5. It is concluded that oxotremorine inhibits the resting release of acetylcholine by activation of neuronal muscarinic receptors. The inhibitory effect of exotremorine is linked to that fraction of the acetylcholine resting release that is calcium-dependent and that arises from propagated activity in cholinergic neurones. The results are consistent with the hypothesis of a feed-back control of acetylcholine release mediated by inhibitory muscarinic receptors.
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PMID:Inhibition by oxotremorine of acetylcholine resting release from guinea pig-ileum longitudinal muscle strips. 111 41

1 The observations which Paton (1957) interpreted as 'acute tolerance' and 'dependence' have been confirmed for coaxially stimulated segments of guinea-pig ileum and extended to the contractions evoked by field stimulation in the myenteric plexus-longitudinal muscle preparation. Evidence is adduced that the morphine receptors of the myenteric plexus are not involved in the two phenomena. 2 The contraction of the longitudinal muscle depressed by low concentrations of morphine, or levorphanol, can be restored to control level not only by high concentrations of morphine but also by levorphanol and equally well by its (+)-isomer, dextrorphan, which does not fulfil the stereospecific requirements of the morphine receptor. Acetylcholine output was not increased. 3 When, after restoration of the twitch by high concentrations of morphine, the drug is washed out, contractions become depressed. This effect cannot be due to 'dependence' because either morphine or its antagonist, naloxone, restore the twitch again. 4 In the concentrations used, morphine, levorphanol and dextrorphan inhibit the cholinesterase of homogenates of the myenteric plexus-longitudinal muscle preparation by 10-15%. Since a concentration of physostigmine which causes a similar inhibition also restores the twitch, it is concluded that the described phenomena are best explained by the anticholinesterase effects of the drugs.
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PMID:An analysis of the phenomenon of acute tolerance to morphine in the guinea-pig isolated ileum. 112 85

The effect of reserpine on acetylcholine synthesis, choline acetylase and cholinesterase activity. Acta Physiol. Pol. 1975, 26 (1): 55-61. Reserpine-induced changes in ACh content in various tissues of white rats (cerebral cortex and brain stem, stomach, lungs, heart, spleen) and the effects of reserpine on the synthesis, enzymatic breakdown of ACh, and ChAc activity were studied. Reserpine administered subcutaneously caused a singificant rise in ACh content of the cerebral cortex and insignificant rise in the heart and spleen. Reserpine (in a concentration of 0.25 mug/ml) had no effect on ACh synthesis in vitro. Reserpine in vivo increased significantly ACh synthesis in the brain. No effect of reserpine on ChAc and AChE activity was demonstrated.
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PMID:The effect of reserpine on acetylcholine synthesis, choline acetylase and cholinesterase activity. 113 Feb 19

Developmental changes in sensitivity of the isolated expansor sedumdariorum muscle of posthatching chicks to noradrenaline (NA), Acetylcholine (ACh) and some other drugs were investigated. This muscle responded to both NA and ACh in early life. The sensitivity to ACh decreased progressively with increasing age and disappeared on day 40 after hatching, however, a corresponding elevation of cholinesterase activity was not observed. The sensitivity to NA remained at the same level during the period of 2-60 days after hatching. The Contractile action of ACh on this muscle was not affected by d-tubocurarine, hexamethonium or phentolamine, but was completely abolished by atropine. These results suggest that there are at least two kinds of responsive sites on the expansor secumdariorum muscle in the new-born chick and that the sites sensitive to ACh degenerate progressively during the developmental processes. The cholinergic sensitive sites of this muscle in the new-born chick may be muscarinic.
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PMID:Changes in acetylcholine and noradrenaline sensitivity of chick smooth muscle wholly innervated by sympathetic nerve during development. 117 90

The inhibition of cholinesterase by 50 mg/kg/5 ml, p.o., dichlorvos and subsequent recovery of enzyme activity was uniform in all brain regions studied. This uniformity was not observed in liver, erythrocytes and plasma. Acetylcholine levels were elevated in brain areas from 48 to 171% at 15 minutes after treatment. However, a biphasic effect was seen on choline metabolism in the brain. The cortex was found to be more cholinergic than the striatum in terms of per cent increase in acetylcholine and choline.
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PMID:Dichlorvos and the cholinergic system: effects on cholinesterase and acetylcholine and choline contents of rat tissues. 119 Sep 24

Activation of olivocochlear (OC) efferent fibers has been suggested to alter micromechanical events occurring within the cochlear partition, possibly through an effect of the efferent neurotransmitter (acetylcholine; ACh) on outer hair cells (OHCs). Based on the widely-accepted assumption that otoacoustic emissions reflect OHC activity, we investigated the in vivo influence of ACh on OHCs by studying alterations in emission amplitude with local ACh application. Distortion product otoacoustic emissions (DPOAEs) were measured in anesthetized guinea pigs before, during, and after intracochlear application of ACh (250 microM) with the cholinesterase inhibitor, eserine (20 microM). Perfusion of ACh/eserine was associated with a desensitizing reduction in DPOAE amplitude of approximately 4.4 dB. This reduction was intensity-dependent, with greater and more consistent reductions observed for DPOAEs elicited by low- than by moderate-intensity primaries. The response reduction was not seen during consecutive ACh perfusions performed without an intervening artificial perilymph wash, and was effectively blocked in the presence of pharmacologic antagonists of OC efferent activity (curare, 50 microM; strychnine, 50 microM). Finally, a similar alteration in DPOAE amplitude was never seen during perfusion of the control (artificial perilymph) solution alone. It is argued that these results support the hypothesis that OC efferent activation can alter sound-induced cochlear mechanical events.
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PMID:Intracochlear application of acetylcholine alters sound-induced mechanical events within the cochlear partition. 132 4

The use of cholinesterase (CHE) inhibitors provided valuable information about the mechanism(s) of neuromuscular transmission, but questions on side effects at the level of ACh-activated channels were raised. Patch-clamp recording was used to study the effects of prostigmine (PST) and methanesulfonyl fluoride (MSF), a reversible and an irreversible cholinesterase inhibitor, respectively, on ACh-activated channels. We found that these drugs diminish the average dwell time of elementary currents from around 5 msec (control) to less than 1 msec in the presence of PST (20 microM) or MSF (5 mM) (at room temperature). With MSF the ACh-activated channel conductance of the most frequently observed amplitude class decreased from 45 pS (control) to 30 pS, but not in the presence of PST. In control conditions there were also amplitude classes of 60 and 24 pS, with probabilities of occurrence less than 10%. In the presence of 1.5 mM MSF, where current dwell time was not affected, additional subconductance states of 19 and 36 pS were observed and may be due to partial blockade of the open channel. We conclude that the drug of choice to be used in studies on the role of CHE in the neuromuscular transmission is MSF, because at 20 microM PST, where blockade of ACh-activated channels is significant, cholinesterase was reported to be partially inhibited, whereas at 1 mM MSF it is fully inhibited and the dwell time of ACh-activated channels is not affected.
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PMID:Effects of irreversible and reversible cholinesterase inhibitors on single acetylcholine-activated channels. 137 11

Several cholinergic processes were demonstrated and partially characterized in rabbit kidney cortical minces: choline uptake, acetylcholine synthesis and calcium-dependent release. Minces took up labelled choline, acetylated it, and stored it in a pool that was not readily accessible to physostigmine-sensitive cholinesterase activity. [3H]Acetylcholine synthesis but not [3H]choline uptake was inhibited by the removal of sodium ions or incubation at 0 degrees C. The release of newly synthesized [3H]acetylcholine was increased by 300 mOsmol urea in a calcium-dependent manner, but not by potassium depolarization (300 mOsmol), vasopressin (10 microM), or bradykinin (10 microM). These results suggest that acetylcholine may be synthesized by non-neuronal rabbit kidney cortical cells and that this transmitter may be released in response to physiological levels of urea.
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PMID:Synthesis and release of acetylcholine in the rabbit kidney cortex. 143 79

The effects of muscarinic receptor antagonists on ACh release were studied in the absence or presence of cholinesterase (ChE) inhibition using the isolated perfused chicken heart. Presynaptic inhibitory muscarinic autoreceptor were characterized by determining the potency of various antagonists to enhance [3H]-ACh release evoked by field stimulation (3 Hz, 1 min). The order of potencies was: (+/-)-telenzepine > atropine > 4-DAMP > silahexocyclium > pirenzepine > hexahydro-siladifenid-ol > AF-DX 116. The comparison with known pA2 values for M1-, M2- and M3-receptors revealed that the presynaptic autoreceptor meets the criteria of an M1-receptor. Basal, not electrically evoked overflow of unlabelled ACh into the perfusate was caused by 'leakage' release (non-exocytotic), as it was independent of extracellular Ca2+. Muscarinic receptor antagonists failed to enhance basel overflow. In contrast, when ChE activity was inhibited by 10(-6) M tacrine or pretreatment with 10(-4) M DFP, the ACh overflow was partially Ca(2+)-dependent and was reduced by tetrodotoxine. Moreover, block of the inhibitory muscarinic autoreceptors by (+/-)-telenzepine or pirenzepine caused a several-fold enhancement of the ACh release. The potencies of these antagonists were identical to those found for the electrically evoked [3H]-ACh release. The rate of ACh release enhanced by ChE inhibition plus telenzepine corresponds to about 12% of the total ACh pool per min, which is about the maximum amount of ACh that is available for any kind of stimuli. The release was dependent on the presence of exogenous choline. Hence elevation of ACh release led to a correspondingly enhanced ACh synthesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibitory and excitatory muscarinic receptors modulating the release of acetylcholine from the postganglionic parasympathetic neuron of the chicken heart. 143 22


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