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:3.1.1.8 (cholinesterase)
12,691 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1 The aim of this study was to examine the cholinoreceptor population in the rat costo-uterine muscle. 2 The nicotinic cholinoreceptor agonists nicotine and DMPP, and the ganglionic muscarinic cholinoreceptor stimulant McNeil A-343, had no effects upon isolated preparations of this tissue. 3 Acetylcholine was more potent than carbachol and approximately equipotent with methacholine (the mean EC50 values were 7.0, 6.3 and 6.7 respectively) in producing contractions of the preparation; each was a full agonist. The potencies of carbachol and methacholine were similar in preparations taken from animals in oestrus and in dioestrus. 4 Atropine competitively antagonised the effects of carbachol and methacholine, the pA2 values were 9.37 and 9.41 respectively. The pA2 value for pirenzepine with carbachol as the agonist was 6.69. 5 Pilocarpine produced phasic contractions of the tissue (EC50 value = 4.17), and competitively antagonised the effects of carbachol with a pA2 value of 5.26. The anticholinesterase, physostigmine, produced only a small potentiation of the effects of acetylcholine. 6 It is concluded that the cholinoreceptors which mediate contraction of the rat costo-uterine muscle are muscarinic, homogeneous in nature and unaffected by fluctuating levels of ovarian hormones occurring during the oestrous cycle. The consequences of inhibition of cholinesterase activity in isolated preparations of the tissue are minimal.
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PMID:Cholinoreceptors in the isolated costo-uterine muscle of the rat. 365 84

The relationship between physostigmine (Phy) concentration, acetylcholine (ACh), choline (Ch) and cholinesterase (ChE) activity was examined in whole rat brain after the administration of [3H]Phy (650 microgram/kg i.m.). Cholinesterase inhibition was found to be inversely related to Phy levels. Maximal inhibition (80%) was seen at 5 min and by 2 hrs ChE activity had returned to control levels. Acetylcholine levels in whole brain peaked at 30 min at a concentration (80 nmol/g) 2.3 times higher than controls (33 nmol/g). Choline levels were not significantly altered. The regional distribution of Phy concentration and ChE activity was studied in six areas of the brain following i.m. administration of three different dosages of ( 3H]Phy. Physostigmine concentration and ChE activity showed a dose dependency in each area examined except in SP (medial septum). Striatum (ST) showed the greatest relative increase of ACh up to 30 min, when compared to other areas. Choline levels were not changed in any area with the exception of ST at 5 min where a decrease was seen. There was a relationship between ChE activity, Phy concentration and ACh levels in all areas examined with exception of the medulla oblongata (MO). Our results indicate that even though ChE was inhibited practically uniformly in all brain areas, the percent increase with respect to control animals and the relative increase of ACh varied widely from area to area. This finding has clinical implications in cases in which cholinomimetic therapy is used to elevate ACh levels in specific brain areas which show a cholinergic deficit.
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PMID:Relation of brain regional physostigmine concentration to cholinesterase activity and acetylcholine and choline levels in rat. 374 73

Acetylcholine and choline acetyltransferase are found in high concentrations in the corneal epithelium of most species, although their function is unknown. We have measured the levels of each in different regions of the rabbit cornea and found that both are much more abundant in central than in peripheral cornea or conjunctival epithelium. Following abrasion of the cornea, epithelial cells from the surrounding cornea or conjunctiva move over rapidly and regenerate. We have assayed choline acetyltransferase and total protein after complete or incomplete abrasion of the corneal epithelium. Acetylcholine-synthesizing activity was not detectable in the regenerating cells until 14-21 days later (depending on the degree of abrasion). Like glycogen and oxidative enzymes, which are also much more abundant in corneal than conjunctival epithelium, choline acetyltransferase regeneration is complete about 28 days after abrasion. In contrast with acetylcholine and choline acetyltransferase, cholinesterase activity is low and its distribution relatively uniform over cornea and conjunctiva. The high ratio of acetylcholine synthesis to cholinesterase activity suggests that acetylcholine released from the corneal epithelium would be able to diffuse to more distant structures within the eye.
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PMID:Regional distribution of acetylcholine and associated enzymes and their regeneration in corneal epithelium. 375 22

Acetylcholine levels of whole blood from 80 healthy subjects were determined by pyrolysis-gas chromatography-mass fragmentography. Acetylcholine was extracted from 1.2 ml of venous blood in the presence of eserine, demethylated by pyrolysis, and assayed by selected ion-current monitoring using butyrylcholine as an internal standard. Inhibition of blood cholinesterase activity by eserine was essential to accurate measurement. The overall recovery of acetylcholine was 45%. The blood acetylcholine levels of healthy subjects varied over a wide range with a geometric mean of 0.49 mumole/liter, 90% of the levels falling into the range of 0.20 to 1.31 mumole/liter. There was no correlation between the blood acetylcholine level and age or sex.
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PMID:Determination of acetylcholine in human blood. 380 Dec 13

Escape from acetylcholine-induced dilatation of gastric submucosal arterioles was studied using in vivo microscopy in rats. Acetylcholine, physostigmine and atropine were applied topically to the submucosa. Experiments were videotaped and diameter changes of the submucosal arterioles were measured with an image splitting technique on playback of the videotapes. Acetylcholine, 10(-6) M and 10(-5) M, caused prompt dilatation of arterioles in a dose-dependent manner, and the dilatation was rapidly followed by escape (return of vessel diameter toward basal diameter in spite of the continued presence of acetylcholine). The escape from acetylcholine-induced dilatation was prevented by physostigmine in a dose-dependent manner, 10(-2) M completely inhibiting the escape. Physostigmine, by itself, 10(-4) M to 10(-2) M, dilated arterioles dose-dependently, and this dilatation was inhibited by atropine. These results indicate that escape of gastric submucosal arterioles from acetylcholine-induced dilatation is mediated by endogenous cholinesterase (catabolism of acetylcholine by endogenous cholinesterase), and basal arteriolar diameter may be determined, in part, by endogenous acetylcholine, this effect being modulated by endogenous cholinesterase.
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PMID:Escape of gastric submucosal arterioles from acetylcholine-induced dilatation. 382 94

Inhibition of four acetylcholinesterases (AChE) and a butyrylcholinesterase (BuChE) by 3-(2,3-dihydro-2,2-dimethyl-benzofuran-'7-yl)-5-methoxy-1,3,4-oxadiaz ol-2(3H)-one (DBOX) and 3-(2-methoxyphenyl)-5-methoxy-1,3,4-oxadiazol-2(3H)-one (MPOX) was measured by the Ellman spectrophotometric method. Both oxadiazolidinones inhibited AChE and BuChE irreversibly and with quasi first order kinetics. DBOX was 2-3 orders of magnitude more potent than MPOX. Housefly brain AChE and horse serum BuChE were more sensitive than AChEs of red blood cells or eel and Torpedo electric organs. Aldicarb, a carbamate anticholinesterase, which protected Torpedo AChE against irreversible phosphorylation by DFP, also protected it against irreversible inhibition by DBOX and MPOX. It is suggested that the nonesteratic oxadiazolidinones are converted to carbanillates on the surface of the enzyme, then acylate the active site of ChEs, producing carbanillated enzymes. At higher concentrations, the two oxadiazolidinones also affected the specific binding of (125I) alpha-bungarotoxin (alpha-BGT) and [3H]perhydrohistrionicotoxin (H12-HTX) to Torpedo nicotinic ACh-receptors, but did not affect the specific binding of [3H]quinuclidinyl benzilate (QNB) to rat brain muscarinic ACh-receptors.
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PMID:Oxadiazolidinones: irreversible inhibition of cholinesterases and effects on acetylcholine receptors. 382 52

At certain doses metoclopramide (MT), sulpiride and bromopride produce anti-cholinesterase effects as shown by studies on the serum and erythrocyte cholinesterases of the rabbit and the dog, and by those on the hypotensive effect of ACh incubated with rabbit serum in the presence or absence of MT. The anti-cholinesterase effect of MT was more intensive than that of sulpiride, bromopride, procainamide or procaine, but less pronounced than that of prostigmine.
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PMID:Benzamides and cholinesterases. 382 8

The in vivo regulation of [3H]acetylcholine [( 3H]ACh) recognition sites on nicotinic receptors in rat brain was examined by administering drugs that increase stimulation of nicotinic cholinergic receptors, either directly or indirectly. After 10 days of treatment with the cholinesterase inhibitor diisopropyl fluorophosphate, [3H]ACh binding in the cortex, thalamus, striatum, and hypothalamus was decreased. Scatchard analyses indicated that the decrease in binding in the cortex was due to a reduction in the apparent density of [3H]ACh recognition sites. In contrast, after repeated administration of nicotine (5-21 days), the number of [3H]ACh recognition sites was increased in the cortex, thalamus, striatum, and hypothalamus. Similar effects were observed in the cortex and thalamus following repeated administration of the nicotinic agonist cytisin. The nicotinic antagonists mecamylamine and dihydro-beta-erythroidine did not alter [3H]ACh binding following 10-14 days of administration. Further, concurrent treatment with these antagonists and nicotine did not prevent the nicotine-induced increase in these binding sites. The data indicate that [3H]ACh recognition sites on nicotinic receptors are subject to up- and down-regulation, and that repeated administration of nicotine results in a signal for up-regulation, probably through protracted desensitization at the recognition site.
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PMID:In vivo regulation of [3H]acetylcholine recognition sites in brain by nicotinic cholinergic drugs. 400 68

Effects of nine choline ethers, (CH3)3 NCH2CH(R)-O-R', on the muscarinic and nicotinic receptors of longitudinal smooth muscle of guinea-pig ileum were studied to understand the role of electronic/steric factors at the ether-oxygen in stimulating the cholinergic receptors. Their ED50S to cause contraction of the ileum in presence of hexamethonium (37 X 10(-6) M) were 2 to 307 times higher than that of acetylcholine (ACh; 2.9 X 10(-7) M). The relative maximal effects of 5 ethers (1.20 to 1.34) were higher than that of ACh (1.0), while 4 exhibited lower maximal effects (less than 0.71). These ethers exhibited no significant inhibition of choline acetyltransferase and cholinesterase activities from the longitudinal muscle at their ED50S. Hexamethonium significantly increased the ED50S of 5 choline ethers. The ED50S of some of the ethers also were significantly increased by treating the muscle with physostigmine (38.5 X 10(-8) M) or physostigmine and hexamethonium. Atropine (greater than 1 X 10(-6) M) blocked the contractions induced by these ethers. The steric hinderance caused by the beta-methyl and/or O-alkyl groups and the electron density around the ether-oxygen are limiting the muscarinic, as well as nicotinic, potencies of these choline ethers. Choline ethers possessing the beta-methyl and O-n-propyl, iso-propyl or ter-butyl groups presumably release ACh at a site causing inhibitory potential through a secondary pathway.
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PMID:Cholinergic properties of choline ethers. 406 29

1. The carotid body and the carotid nerve were removed from anaesthetized cats and placed in a small Perspex channel through which Locke solution (at various pH values and usually equilibrated with 50% O(2) in N(2)) was allowed to flow. The glomus was immersed in the flowing solution while the nerve was lifted into oil covering the saline. Sensory discharges were recorded from the nerve and their frequency was used as an index of receptor activity. At times, a small segment of carotid artery, containing pressoreceptor endings, was removed together with the glomus. In this case, pressoreceptor discharges were recorded from the nerve.2. The amplitude of either chemo- or pressoreceptor discharges was not changed by strong acid solutions. Acid decreased the frequency of the baroreceptor discharges only when pH fell to less than 4.0. Solutions at low pH increased the chemosensory discharge, but acid depressed the increased chemoreceptor discharge elicited by KCl. These experiments indicated that H(+) ions probably acted as membrane ;stabilizers' without depolarizing either the nerve fibres or endings.3. Acid solutions increased the action of acetylcholine chloride (AChCl) (100-200 mug) on chemoreceptors. This effect probably was due either to inactivation of tissue cholinesterase or to enhanced sensitivity of the sensory endings to ACh.4. Choline chloride (10(-3)M), which favours ACh synthesis, protected the preparation against decay during prolonged experimentation. Hemicholinium-3 (HC-3), which blocks ACh synthesis in low concentrations (10(-5)M), depressed the chemosensory response to acid and to hypoxia when such stimuli were applied repeatedly. This concentration of HC-3 did not change effects of applied ACh.5. Substances which affect ACh release markedly changed the chemoreceptor discharge increase induced by acidity and other forms of stimulation. In the absence of Ca(2+), acid, anoxia, and interruption of flow provoked receptor depression while receptor excitation induced by ACh and KCl persisted. All stimuli excited and showed increased effectiveness as the Ca(2+) concentration was raised, but their effects declined as Ca(2+) was increased above normal values. Mg(2+) ions depressed the chemoreceptor effects induced by all these stimuli. The action of Mg(2+) was not due entirely to nerve ending block. Morphine sulphate (which decreases ACh release in other structures) also depressed the receptor response to acid and flow interruption.6. Cholinergic blocking agents such as mecamylamine, hexamethonium, atropine, dihydro-beta-erithroidine (DHE), HC-3 (10(-4)M), choline and acetylcholine (in combination with choline) depressed the effects of acid and ACh on the chemoreceptors. The effect induced by interruption of flow was depressed only by mecamylamine and DHE.7. Agents which affect the fate of released ACh, such as acetylcholinesterase and eserine salicylate, did not affect clearly the response of chemoreceptors to acid.8. The results suggest that acid stimulates chemoreceptor fibres through an indirect mechanism, viz. through increased release and/or decreased destruction of a presynaptic transmitter from the glomus cell. This transmitter is probably ACh (see following paper, Eyzaguirre & Zapata, 1968).
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PMID:Pharmacology of pH effects on carotid body chemoreceptors in vitro. 429 75


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