The effect of catecholamines and sympathetic stimulation on the release of acetylcholine from the guinea‐pig colon

Beani, L.; Bianchi, Clementina; Crema, A.

doi:10.1111/j.1476-5381.1969.tb08298.x

Cited by 86 publications

(25 citation statements)

References 53 publications

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“…Other workers have reported that continued stimulation does not maintain the cholinergic response (Garry & Gillespie, 1955;Rand & Ridehalgh, 1965;Bianchi, Beani, Frigo & Crema, 1968, Hukovic & Somogyi, 1969Kottegoda, 1969). Beani, Bianchi & Crema (1969) have shown that the rate of release of acetylcholine declines during extended stimulation of the intramural nerves of the guinea-pig colon at moderate frequencies. These results make it seem unlikely that secondary contractions are due to the persistence of the action of acetylcholine.…”

Section: Discussionmentioning

confidence: 98%

Secondary excitation of intestinal smooth muscle

Furness

1971

British J Pharmacology

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Summary1. A period of stimulation of intrinsic or extrinsic nerves to intestinal muscle is often followed by a secondary contraction. In the present work, the basis for such secondary contractions in the longitudinal muscle of the large bowel of guinea-pigs and rabbits was examined. 2. In general, the action of cholinergic nerves did not contribute significantly to the secondary contractions. Concentrations of atropine or hyoscine, which completely blocked primary cholinergic contractions, potentiated or did not significantly reduce secondary contractions. 3. Atropine resistant, nerve mediated primary contractions of the guinea-pig ileum were inhibited by anticholinesterases, although these drugs potentiated secondary contractions in other segments of the gut. 4. The occurrence of a secondary contraction following inhibition of smooth muscle activity did not depend on the nature of the initial inhibition. Thus, secondary contractions were observed following the responses to both nonadrenergic and adrenergic inhibitory nerves, adenosine triphosphate, noradrenaline and brief periods of anoxia. The secondary contractions following hyperpolarizing drugs or anoxia were not prevented by tetrodotoxin in a concentration sufficient to paralyse all nerves. 5. It is concluded that cholinergic nerves do not contribute significantly to secondary contractions except at frequencies of stimulation higher than about 50 Hz or after the inhibition of cholinesterases. In the segments of gut examined, the secondary contractions were principally myogenic.

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Section: Discussionmentioning

confidence: 98%

Secondary excitation of intestinal smooth muscle

Furness

1971

British J Pharmacology

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“…Gershon (1967) did not find a reduction in acetylcholine output from the intestine when noradrenergic nerves were stimulated. Beani, Bianchi & Crema (1969) found that the mesenteric nerves reduced the output of acetylcholine only if parasympathetic nerves were stimulated at very low frequencies. suggested that splanchnic stimulation at <4 Hz acted via parasympathetic ganglia but at > 8.Hz it also appeared to have a direct effect on muscle.…”

Section: Introductionmentioning

confidence: 99%

Interactions between splanchnic and vagus nerves in the control of mean intragastric pressure in the ferret.

Andrews¹,

Lawes²

1984

The Journal of Physiology

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SUMMARY1. To determine whether splanchnic nerves relax the stomach by direct or indirect mechanisms, ramp inflations of the stomach, section and electrical stimulation of the vagus and greater splanchnic nerves, and step inflations of the duodenum were used.2. A high threshold, sustained inhibition of the gastric pressure response to ramp inflation was mediated by the vagus. Prior splanchnectomy increased vagal inhibition.3. The greater splanchnic nerves had no effect on gastric responses to inflation, although after vagotomy they were shown to be mediators of a low threshold, powerful but transient inhibition of the stomach. This was not dependent on intrinsic neurones with nicotinic receptors.4. Electrical stimulation of the greater splanchnic nerves produced a relaxation of the stomach, the magnitude of which was determined by resting pressure. Splanchnically mediated relaxation was not abolished by atropine, nor was it reduced by concurrent vagal stimulation. At submaximal levels of vagal stimulation the two nerves had a partially additive effective on relaxation.5. Duodenal inflation had an effect on intracorpus pressure similar to that of electrical stimulation of the greater splanchnic nerves on intragastric pressure. Reflex relaxation of the corpus evoked by duodenal distension was decreased by atropine but greatly increased by atropine coupled with vagotomy. These changes were caused by variations in resting pressure.6. It was concluded that the principal effect of splanchnic nerves on mean gastric pressure is direct and does not depend on inhibition of cholinergic neurones either centrally or peripherally. Evidence is presented for central interactions between the vagus and the greater splanchnic nerves in the anaesthetized ferret.

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“…When the preparation is given a train of stimuli there is an initial rapid fall in output per volley, followed by a relatively constant output (Paton, 1963 ;Paton & Vizi, 1969). Noradrenaline and adrenaline reduce the acetylcholine output per volley at low frequencies of stimulation (0-1-2 Hz) and this action is prevented by a-adrenoceptor blocking agents (Paton & Vizi, 1969;Kosterlitz, Lydon & Watt, 1970); sympathetic stimulation also inhibits acetylcholine release from guinea-pig colon (Beani, Bianchi & Crema, 1969) and from rabbit jejunum (Vizi, 1970).…”

Section: Introductionmentioning

confidence: 99%

Effect of frequency of stimulation on the inhibition by noradrenaline of the acetylcholine output from parasympathetic nerve terminals

Knoll

Vízi

1971

British J Pharmacology

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The relationship between the number of shocks delivered, the frequency of stimulation and the acetylcholine output per volley from nerve terminals of the longitudinal muscle strip of the guinea-pig ileum was studied.2. There was an inverse correlation between acetylcholine output per volley and the frequency of stimulation when the same number of shocks was applied in each train. 3. With sustained stimulation, the volley output declined more rapidly the higher the frequency of stimulation. There was no decrease in volley output (11-7 (ng/g)/volley) when the frequency applied was 0-1 Hz or less. 4. Noradrenaline (10-6 g/ml) reduced the acetylcholine output per volley to the level produced by sustained stimulation at 10 Hz (14-19 (ng/g)/volley). The acetylcholine output following application of the first shocks of a train at high frequency stimulation was much reduced by noradrenaline as the output was higher than 1-4-1-9 (ng/g)/volley. This action of noradrenaline was antagonized by phentolamine (2 ,ug/ml for 20 min). 5. Amphetamine and methylamphetamine, which release NA from sympathetic nerve terminals, were active in reducing the acetylcholine output to low frequency parasympathetic nerve stimulation. Reserpine and a-methyl-ptyrosine pretreatment prevented the effect of amphetamine and reduced that of methylamphetamine. 6. The fact that addition or release of noradrenaline, reduced acetylcholine output when the firing rate was high but short in duration, suggests that noradrenaline plays a general modulator role in controlling the output of acetylcholine from the parasympathetic nerve terminals.

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The effect of catecholamines and sympathetic stimulation on the release of acetylcholine from the guinea‐pig colon

Cited by 86 publications

References 53 publications

Secondary excitation of intestinal smooth muscle

Secondary excitation of intestinal smooth muscle

Interactions between splanchnic and vagus nerves in the control of mean intragastric pressure in the ferret.

Effect of frequency of stimulation on the inhibition by noradrenaline of the acetylcholine output from parasympathetic nerve terminals

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