The Response of the Cat Anococcygeus Muscle to Nerve or Drug Stimulation and a Comparison With the Rat Anococcygeus

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1 The effects of adrenoceptor agonists and other agonists on the contractile responses of the prostatic and epididymal portions of the rat isolated vas deferens to single pulse field stimulation were investigated. 2 a-Adrenoceptor agonists produced prejunctional c2-mediated inhibition and post-junctional cxl-mediated potentiation of the nerve-induced responses. Guanabenz and xylazine produced mainly inhibitory effects, xylazine being 10 times less potent. Clonidine and oxymetazoline produced inhibition with similar potency to guanabenz but at higher concentrations excitatory effects were present, particularly in the epididymal portion. Phenylephrine produced only potentiation of the nerveinduced response in both portions. Potentiation of nerve-induced responses was a more sensitive and quantitative index of excitation than was direct contraction of the tissue. 3 Isoprenaline and salbutamol both gave fl2-mediated inhibition of the nerve-induced responses in both portions of tissue. At least part of the effect was post-junctional since phenylephrine contractions were inhibited. Isoprenaline also produced a post-junctional ocx-mediated excitation. 4 Noradrenaline produced effects qualitatively similar to those of the other ax-adrenoceptor agonists, inhibition and excitation predominating in the prostatic and epididymal ends respectively. 5 Morphine produced inhibition in the mouse but not in the rat vas deferens. In rat vas, however, enkephalin analogues produced pre-junctional inhibition of responses in both portions which could be partly reversed by naloxone; restoration of the adrenergic component was more complete. Rat anococcygeus showed no equivalent effect. 6 Adenosine 5'-triphosphate (ATP) inhibited nerve-induced responses in each portion with a greater effect on the prostatic portion.

Section: Discussionmentioning

confidence: 74%

The Distribution of Adrenoceptors and Other Drug Receptors Between the Two Ends of the Rat Vas Deferens as Revealed by Selective Agonists and Antagonists

Macdonald

McGrath

1980

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“…The specificity of the effect on the pD2 value for ACh suggested that corticosterone might interfere with the metabolism of ACh, and in particular, that it might reduce the activity of cholinesterase (ChE), the enzyme of ACh degradation. Although neostigmine potentiated the response of the rat anococcygeus muscle to ACh (Gillespie & McGrath, 1974), Gillespie (1972) was unable to demonstrate the presence of the enzyme histologically. In this study, therefore, the ChE activity of the muscle was determined colorimetrically, and the effects of corticosterone, morphine withdrawal, or a single dose of reserpine on enzyme activity were investigated.…”

Section: Introductionmentioning

confidence: 99%

“…Plasma corticosteroids were not elevated in blood from rats treated chronically with reserpine (Table 3). (Gillespie & McGrath, 1974). The rat anococcygeus muscle, therefore, provides an example of a tissue which responds to ACh and contains the enzyme of ACh degradation, but which does not appear to receive a cholinergic innervation (Gillespie, 1972).…”

Section: Comparison Of Plasma Corticosteroid Levels With Concentratiomentioning

confidence: 99%

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

Gibson¹,

Pollock²

1975

1 Administration of corticosterone caused a 47% reduction in the cholinesterase (ChE) activity of homogenates of the rat anococcygeus muscle. 2 ChE activity was also reduced by morphine withdrawal and this effect was abolished by the corticosteroid synthesis inhibitor, metyrapone. 3 A single dose of reserpine reduced ChE activity in normal but not in adrenalectomized rats. 4 ChE activity was increased by adrenalectomy or by metyrapone treatment. 5 The mechanism of the corticosteroid-induced reduction in ChE activity is discussed. 6 The reduction in ChE activity produced by corticosterone, morphine withdrawal, or a single dose of reserpine might explain the leftward shift of the dose-% response curve to acetylcholine produced by these procedures in the isolated anococcygeus muscle of the rat.

“…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. The present paper describes ) Macmillan Publishers Ltd 1981 such a study and shows the effects of atropine and homatropine, alone and in the presence of neostigmine, on the contractile responses produced by exogenously applied cholinomimetics or noradrenaline.…”

Section: Introductionmentioning

confidence: 99%

“…Thus the excitatory and inhibitory responses to field stimulation were insensitive to both hexamethonium and atropine. In consequence, investigations which have used the rat anococcygeus muscle subsequently have been concerned either with aspects of noradrenergic transmission (e.g., Gibson & Gillespie, 1973;Gibson & Pollock, 1973;Gillespie & McGrath, 1974;Doggrell & Woodruff, 1977) or the nature of the inhibitory process (Gillespie & McGrath, 1973;Burnstock, Cocks & Crowe, 1978). 0007-1188/81/080829-07 $01.00…”

Section: Introductionmentioning

confidence: 99%

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

Doggrell

1981

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.