The influence of temperature on the acetylcholine output from a sympathetic ganglion

Kostial, Krista; Vouk, Vale

doi:10.1113/jphysiol.1956.sp005518

Cited by 19 publications

(9 citation statements)

References 3 publications

(3 reference statements)

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“…Detailed studies in the present experiments on the relationship between the stimulus frequency and the nega tive chronotropic and inotropic effects showed that the optimal frequency was 20/sec in rabbit's preparation and 10 to 20/sec in guinea-pig's preparation . The stimulus fre quency giving a maximal response to the cat's heart in situ was 30/sec (14) and some what higher than the frequency required for the isolated rabbit's and guinea-pig's heart It was reported that the amount of acetylcholine released in the perfusate of the superior cervical ganglia by pregang lionic stimulation at a high frequency (10/sec) was reduced by cooling of the ganglia (19) but the acetylcholine release by a low frequency of stimulation (2/sec) was not af fected (20). Therefore, blockade of the cardiac ganglia and the postganglionic structures under cooling may possibly derive from the diminution of the release of acetylcholine from the pre and postganglionic terminals.…”

Section: Discussionmentioning

confidence: 99%

“…Guinea-pig's atria responded well to concentrations of 10_s to 3X10-' of acetylcholine, while rabbit's atria to a concentration of 10-6. In the physiological experiments the spontaneous contraction and the atrial responses to vagal stimulation were tested under variable experimental conditions. A number of investigators obtained the negative chronotropic and inotropic responses to vagal stimulation of the isolated atrial preparation but the frequency of stimuli used varied considerably (7,10,20,23 or 25/sec). Recently, Burn and Weetman (13) have reported that the responses of the vas deferens to hypogastric nerve stimulation of various fre quencies differ not only quantitatively but also qualitatively.…”

Section: Discussionmentioning

confidence: 99%

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Effects of Temperature Change, Oxygen Deprivation and Cations on the Atrial Responses to Vagal Stimulation

Toda

Fujiwara

Shimamoto

1964

Japanese Journal of Pharmacology

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It is generally believed that the cardiac fibers of the right vagus nerve terminate , in large part, near the sinoatrial node and some fibers distribute widely in the atria , and that most of the cardiac fibers of the left vagus supply the atrioventricular node and bundles.On the other hand, there are opposite conclusions regarding the existence of the vagus nerve endings in the ventricles. Electrical stimulation of the vagal fibers to the heart has usually been performed in the open chest animal or in the heart-lung preparation of the dog. Many investigators agree with the inhibitory nature of the vagal innervation on the heart, while there is some evidence for existence of the cardio-accele rator fibers in the vagus nerve (1-4). Middleton et al . (5) have concluded that some vagal fibers make connection with the chromaffin cells or the adrenergic neurons located in or near the heart by demonstrating an adrenaline-like substance in the perfusate of the cat's heart which is responding with the increase in rate and amplitude to vagal stimulation. McEwen (6) has observed an inhibitory effect of vagal stimulation in the rabbit's heart for many hours after the isolation.He , further, has demonstrated that the vagal stimulation restores the normal rhythmicity of contraction in the atria arrested by suspending in the bath for many hours , and that the same vagal stimula tion inihibits the regular rhythm restored by the addition of acetylcholine . Using the same type of preparations, Burn and Rand (7) have observed the restarting effect of vagal stimulation on the heart which ceased to beat by cooling.The marked acceleration of the repolarization phase in the atrial membrane poten tials of the dog's and rat's hearts in situ following vagal stimulation has been shown by Hoffman and Suckling (8) and Biersteker et al. (9). Similar observation was made on the turtle's heart in situ by Churney et al. (10). Although the vagal effect on the membrane potentials of the isolated frog's heart was demonstrated by Hutter and Trautwein (11), the vagal effect on the atrial or ventricular membrane potentials of the isolated mammalian heart has not hitherto been presented. During the study of the effect of va,al stimulation on the transmembrane potentials (12) , the authors have been confronted with many difficulties which should be previously removed in the iso-

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effects of Temperature Change, Oxygen Deprivation and Cations on the Atrial Responses to Vagal Stimulation

Toda

Fujiwara

Shimamoto

1964

Japanese Journal of Pharmacology

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“…3 shows that the amount of acetylcholine released by a period of tetanus in fact decreased with continued cooling to 200. This anomaly would be explained if, at and around room temperature, some further additive process were taking place, such as an increase in intermittent presynaptic failure at room temperature compared with 370 (as proposed by Krnjevic, 1958), or possibly a reduced rate of acetylcholine resynthesis with cooling as suggested by Kostial and Vouk (1956) for the cat perfused superior cervical ganglion.…”

Section: The Effects Of Temperature On Acetylcholinementioning

confidence: 99%

“…after corrections are made for the resting release. Intermittent presynaptic failure which is thought to be precipitated by anoxia in the intramuscular portions of the motor nerve is minimal at this rate of stimulation (Krnjevic andMiledi, 1958b, 1959); yet the postsynaptic changes observed in this preparation during stimulation at lower rates suggested that the deepest muscle fibres were anoxic (Creese, Hashish and Scholes, 1958). The use of neostigmine in the present experiments caused the rapid development of neuromuscular blockade, so by the end of the first minute of stimulation there was very little tension developed in the muscle.…”

Section: The Effects Of Temperature On Acetylcholinementioning

confidence: 99%

“…In contrast to motor nerve endings the acetylcholine release from the preganglionic nerve endings of the cat superior cervical ganglion perfused with saline is not decreased by cooling (Kostial and Vouk, 1956). Thus it would appear that the acetylcholine release mechanism in preganglionic sympathetic nerve endings is not temperature-sensitive like the acetylcholine release mechanism in motor nerve endings.…”

Section: The Effects Of Temperature On Acetylcholinementioning

confidence: 99%

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The Release of Acetylcholine From Mammalian Motor Nerve Endings

Straughan

1960

British Journal of Pharmacology and Chemotherapy

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The release of acetylcholine from rat and guinea-pig isolated diaphragm preparations stimulated through the phrenic nerve was optimal at 370 in Krebs solution with 5x 10-6 neostigmine methylsulphate. The amount of acetylcholine released by a 20 min. tetanus was reduced by cooling. At frequencies of stimulation above 6/sec. the release was less than that predicted. This " failure " was unaffected by the addition of 1 x 10-6 choline. The acetylcholine release declined with continued stimulation at 25/sec. In the absence of nerve stimulation, there was a small continuous resting release of acetylcholine which seemed to originate in the muscle fibres. These results are discussed in the light of current electrophysiological knowledge of the quantal release of acetylcholine.Nearly a quarter of a century has passed since Dale and his colleagues first showed that acetylcholine was released at the neuromuscular junction by motor nerve stimulation, and could be measured directly in the extracellular fluid if steps were taken to prevent its destruction by cholinesterase (Dale and Feldberg, 1934; Dale, Feldberg, and Vogt, 1936). Since that time it has been generally accepted that acetylcholine is the chemical mediator of nerve impulses at all neuromuscular junctions. Recently, Dale's observation has been confirmed and extended by others, in a perfused muscle preparation (Emmelin and MacIntosh, 1956) and in isolated diaphragm preparations (Burgen, Dickens and Zatman, 1949;Barnes and Duff, 1954;Brownlee, 1957; Brooks, 1954).The present experiments are concerned with the factors which modify the amounts of the transmitter released from motor nerve endings; and in particular with the effect of changes in the frequency and duration of stimulation, changes in temperature and the presence of choline on acetylcholine release.

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