Reduction in the Cholinesterase Activity of the Rat Anococcygeus Muscle Produced by Corticosterone

Gibson, Alan; Pollock, David

doi:10.1111/j.1476-5381.1975.tb07612.x

Cited by 13 publications

(14 citation statements)

References 12 publications

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“…Although histochemical techniques have failed to demonstrate butyryl or acetylcholinesterase in the rat anococcygeus (Gillespie, 1972;Bumstock et al, 1978), cholinesterase activity has been demonstrated colorimetrically (Gibson & Pollock, 1975;Smith & Spriggs, 1979) and the ability of neostigmine to potentiate responses to acetylcholine (but not to carbachol) confirmed (Gillespie & McGrath, 1974). The present study demonstrates that the potentiating effects of neostigmine were limited to the contractile responses to cholinomimetics and appeared to be correlated with a susceptibility to cholinesterase, i.e.…”

Section: Discussionmentioning

confidence: 66%

“…Cholinesterase activity has also been detected in the tissue (Gibson & Pollock, 1975;Smith & Spriggs, 1979). However, although Gillespie's original paper (1972) demonstrated atropinesensitive, acetylcholine-induced contractions and a subsequent study (Gillespie & McGrath, 1974) illustrated the ability of neostigmine to potentiate responses to acetylcholine, no further detailed studies on the muscarinic antagonist/agonist interaction have been undertaken.…”

Section: Introductionmentioning

confidence: 99%

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Effect of Antimuscarinic Agents on the Contractile Responses to Cholinomimetics in the Rat Anococcygeus Muscle

Doggrell

1981

British J Pharmacology

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The effects of antimuscarinic agents alone and in the presence of neostigmine on the contractile responses to exogenously applied cholinomimetics or (‐)‐noradrenaline were studied in the rat anococcygeus muscle. Atropine (1 × 10_9‐1 × 10−6m) alone, in the presence of hexamethonium (1 × 10−4m), or phentolamine (1 × 10−6m), inhibited responses to acetylcholine but not to (—)‐noradrenaline. The inhibitory effect with the higher concentrations of atropine (1 × 10−8— × 10−6m), was seen as an increase in the slopes of the concentration‐response curves. Atropine (1 × 10−8m) alone inhibited the responses to methacholine and carbachol without altering the slopes of the concentration‐response curves. Homatropine (1 × 10−6m) alone had no effect on responses to (‐)‐noradrenaline and inhibited responses to acetylcholine and methacholine. The inhibitory effect on responses to acetylcholine but not to methacholine, included an increase in the slopes of the concentration‐response curves. Neostigmine (1 × 10−6m) alone had no effect on responses to (—)‐noradrenaline and potentiated responses to acetylcholine and methacholine. The potentiating effect included an increase in the slopes of the concentration‐response curves. In the presence of neostigmine (1 × 10−6m), atropine (1times10−9m‐1times 10−6m) caused a parallel concentration‐dependent shift of the concentration‐response curves to acetylcholine. The pA2 values, in the presence of neostigmine, were independent of the concentration of atropine and of the agonist (acetylcholine, methacholine, or carbachol) used. In the presence of neostigmine (1 × 10−6m), homatropine (1 × 10−6m) also failed to alter the slopes of the concentration‐response curves to acetylcholine and was approximately 100 times less potent than atropine as an antimuscarinic agent. These results illustrate that, in the rat anococcygeus muscle, it is necessary to inhibit acetylcholinesterase before determining the relative potencies of antagonists at muscarinic receptors.

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Section: Discussionmentioning

confidence: 66%

Section: Introductionmentioning

confidence: 99%

Effect of Antimuscarinic Agents on the Contractile Responses to Cholinomimetics in the Rat Anococcygeus Muscle

Doggrell

1981

British J Pharmacology

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“…Some authors reported a reduction in AChE activity after stress [22][23][24]44]. Similar effect was observed in striate muscles of animals treated with CORT [26,45] or dexamethasone, a syntetic glucocorticoid [27]. These observations suggest that an excess of glucocorticoids might downregulate, directly or indirectly, the ChE activity.…”

Section: Discussionmentioning

confidence: 54%

“…No changes were observed in adrenalectomized animals [18,20,25]. Treatment with CORT also results in changes in AChE activity [20,26,27], which suggests that the changes observed in stressed animals IJOMEH 2013;26(4) 638 before the CVP injection and was repeated during the following four days at approximately the same hour (between 8:00 and 9:00 a.m.). The CVP doses were selected on the basis of data from our earlier studies on the same compound [14].…”

Section: Animalsmentioning

confidence: 99%

Partial protection from organophosphate-induced cholinesterase inhibition by metyrapone treatment

Świercz

Lutz

Gralewicz

et al. 2013

International Journal of Occupational Medicine and Environmental Health

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Background: Organophosphates are cholinesterase (ChE) inhibitors with worldwide use as insecticides. Stress response, evidenced by a dramatic and relatively long-lasting (several hours) rise in the plasma glucocorticoid concentration is an integral element of the organophosphate (OP) poisoning symptomatology. In rodents, corticosterone (CORT) is the main glucocorticoid. There are several reports suggesting a relationship between the stressor-induced rise in CORT concentration (the CORT response) and the activity of the cerebral and peripheral ChE. Thus, it seems reasonable to presume that, in OP intoxication, the rise in plasma CORT concentration may somehow affect the magnitude of the OP-induced ChE inhibition. Metyrapone (MET) [2-methyl-1,2-di(pyridin-3-yl)propan-1-one] blocks CORT synthesis by inhibiting steroid 11β-hydroxylase, thereby preventing the CORT response. Chlorfenvinphos (CVP) [2-chloro-1-(2,4-dichlorophenyl) ethenyl diethyl phosphate] is an organophosphate insecticide still in use in some countries. Material and Methods: The purpose of the present work was to compare the CVP-induced effects -the rise of the plasma CORT concentration and the reduction in ChE activity -in MET-treated and MET-untreated rats. Chlorfenvinphos was administered once at 0.0, 0.5, 1.0 and 3.0 mg/kg i.p. Metyrapone, at 100 mg/kg i.p., was administered five times, at 24-h intervals. The first MET dose was given two hours before CVP. Conclusion: The following was observed in the MET-treated rats: i) no rise in plasma CORT concentration after the CVP administration, ii) a reduced inhibition and a faster restitution of blood and brain ChE activities. The results suggest that MET treatment may confer significant protection against at least some effects of OP poisoning. The likely mechanism of the protective MET action has been discussed.

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“…The former change appears to result from the steroid-induced reduction in muscle cholinesterase activity (Gibson & Pollock, 1975b), thus explaining the specific increase in sensitivity to ACh. However, the second effect, on muscle contractility is as yet unexplained, and in this paper a possible explanation is presented.…”

Section: Introductionmentioning

confidence: 99%

THE POSSIBLE INVOLVEMENT OF Na+ IONS IN CORTICOSTERONE‐INDUCED HYPERCONTRACTILITY IN THE RAT ANOCOCCYGEUS MUSCLE

Gibson

Pollock

1976

British J Pharmacology

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The possibility that corticosterone‐induced hypercontractility in the rat anococcygeus muscle might be due to an intramuscular redistribution of Na+ was investigated. The contractility of the isolated muscle to noradrenaline (NA) was directly dependent on the Na+ concentration of the Krebs solution. There was a linear relationship between the maximum contractile response of the muscle to NA and the Na+ concentration of the Krebs solution. Muscle contractility was also increased by the presence of ouabain (10−4m) in the bathing medium. Muscles from rats treated with corticosterone exhibited increases in both total and ouabain‐sensitive ATPase activity. The relationship between corticosterone, Na+ distribution, and muscle contractility is discussed.

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Reduction in the Cholinesterase Activity of the Rat Anococcygeus Muscle Produced by Corticosterone

Cited by 13 publications

References 12 publications

Effect of Antimuscarinic Agents on the Contractile Responses to Cholinomimetics in the Rat Anococcygeus Muscle

Effect of Antimuscarinic Agents on the Contractile Responses to Cholinomimetics in the Rat Anococcygeus Muscle

Partial protection from organophosphate-induced cholinesterase inhibition by metyrapone treatment

THE POSSIBLE INVOLVEMENT OF Na+ IONS IN CORTICOSTERONE‐INDUCED HYPERCONTRACTILITY IN THE RAT ANOCOCCYGEUS MUSCLE

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