Effects of morphine on non-adrenergic inhibitory responses of the guinea-pig taenia coli

Shimo, Yasuo; Ishii, Takeo

doi:10.1111/j.2042-7158.1978.tb13337.x

Cited by 29 publications

(14 citation statements)

References 6 publications

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“…However, although the action of opiates on transmitter release at adrenergic and cholinergic neuroeffector junctions has been extensively studied, less is known about their effects at other sites. However, morphine has been shown to depress the non-adrenergic inhibitory responses of guinea-pig taenia coli to transmural stimulation (Shimo & Ishii, 1978). In the present study, morphine may have blocked the release of inhibitory transmitter by a direct action on nerve terminals of inhibitory nerves but this seems unlikely, since morphine-induced contractions could be abolished by field stimulation.…”

Section: Discussionmentioning

confidence: 49%

Acute Effects of Morphine and Opioid Peptides on the Motility and Responses of Rat Colon to Electrical Stimulation

Gillan

Pollock

1980

British J Pharmacology

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1 Morphine and leucine-and methionine-enkephalins inhibited the contractile response of the pithed rat colon to electrical stimulation of the spinal motor outflows and inhibited motor responses of the isolated colon to field stimulation. 2 Morphine and the opioid peptides also had an excitatory action in the colon. In the pithed rat, opiates caused regular fluctuations in intracolonic pressure and in the isolated colon, caused regular waves of contraction. This excitatory response was produced by low concentrations of the enkephalins (2 x 10'8 M, 2 x 10o-M), was stereospecific and was antagonized by naloxone.3 Opiate-induced contractions in the isolated colon were inhibited by catecholamines, adenine nucleotides and by phosphodiesterase inhibitors. These contractions were unaffected by ergotamine and tolazoline, or by propranolol. 4 The excitatory action of opiates in the isolated colon was not antagonized and usually was potentiated by atropine, (+ -tubocurarine and hexamethonium. In the absence of opiates, these drugs also produced similar waves of contraction, which were unaffected by naloxone. 5 Opiate-induced contractions occurred in colon rendered unresponsive to 5-hydroxytryptamine (5-HT) and these contractions were potentiated by the 5-HT antagonist, lysergic acid diethylamide, which, when administered alone, caused similar contractions. The 5-HT antagonist, cyproheptadine, inhibited opiate-induced contractions but was non-specific, since it also inhibited responses of the colon to carbachol and KCI. 6 Opiate-induced contractions were unaffected by procaine and were potentiated by tetrodotoxin. Both of these drugs, when administered alone, produced waves of contractions, which were similar to those produced by opiates but were unaffected by naloxone. 7 Contractions produced in the isolated colon either by opiates, atropine or (+ )tubocurarine, or any combination of these drugs, were inhibited by field stimulation applied at the peak of a wave of contraction. This inhibitory response to field stimulation occurred at low frequencies of stimulation (< 10 Hz), and persisted in colon from rats pretreated with reserpine to deplete, or 6-hydroxydopamine to destroy, adrenergic nerve endings. It was unaffected by guanethidine but abolished by tetrodotoxin. 8 The implications of these results are considered and it is concluded that the excitatory action of opiates in the rat colon is probably not mediated by the release of acetylcholine or 5-HT but instead, may be due either to a direct action on smooth muscle or to a presynaptic inhibitory action at a ganglionic site in a non-adrenergic inhibitory mechanism, which normally suppresses myogenic activity.

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Section: Discussionmentioning

confidence: 49%

Acute Effects of Morphine and Opioid Peptides on the Motility and Responses of Rat Colon to Electrical Stimulation

Gillan

Pollock

1980

British J Pharmacology

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“…Moreover, morphine has been shown to depress the non-adrenergic inhibitory responses of guinea-pig taenia coli to transmural stimulation (Shino & Ishu, 1978).…”

Section: Discussionmentioning

confidence: 99%

Contractor responses of the isolated colon of the mouse to morphine and some opioid peptides

Fontaine¹,

Reuse²

1985

British J Pharmacology

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Morphine (1 times 10−8‐1 times 10−4M), fentanyl (1 times 10−9− 1 times 10−5M) and alfentanyl (1 times 10−10 − 1 times 10−5M) as well as methionine enkephalin [Met5]enkephalin (1 times 10−11 − 1 times 10−8M), [D‐Ala2, Met5]enkephalin (1 times 10−12 − 1 times 10−8M) and dynorphin A(1 − 13) (1 times 10−9 − 1 times 10−6M) caused a contractor response of the longitudinal musculature of the terminal colon of the mouse. These effects were competitively antagonized by naloxone. The pA2 values obtained for naloxone antagonism of morphine and opioid peptides and the high sensitivity of the preparation to enkephalins suggest the presence of δ‐opiate receptors in this preparation but μ‐and κ‐receptors may also be present. Opiate‐induced contractions in the mouse colon were abolished by tetrodotoxin and after incubation with indomethacin. It is concluded that the excitatory actions of the opiates in the mouse colon are mediated via opiate receptors located on nerves which do not release acetylcholine, noradrenaline or 5‐hydroxytryptamine. The opiates may produce their action by removing an inhibitory neural influence (the nature of which remains to be elucidated) allowing a prostaglandin‐mediated effect to predominate, thereby increasing muscle tone.

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“…Several enteric neurotransmitters have been claimed to modulate ATP release by acting on NANC neuronal cell bodies in the myenteric plexus. For example, morphine or enkephalin inhibition of NANCevoked relaxations was reversed by nalaxone [356,616]. Enkephalin is very effective in inhibiting NANC IJPs evoked in human colon [339].…”

Section: Enteric Gangliamentioning

confidence: 99%

Purinergic signalling in the gastrointestinal tract and related organs in health and disease

Burnstock

2013

Purinergic Signalling

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Purinergic signalling plays major roles in the physiology and pathophysiology of digestive organs. Adenosine 5′-triphosphate (ATP), together with nitric oxide and vasoactive intestinal peptide, is a cotransmitter in nonadrenergic, non-cholinergic inhibitory neuromuscular transmission. P2X and P2Y receptors are widely expressed in myenteric and submucous enteric plexuses and participate in sympathetic transmission and neuromodulation involved in enteric reflex activities, as well as influencing gastric and intestinal epithelial secretion and vascular activities. Involvement of purinergic signalling has been identified in a variety of diseases, including inflammatory bowel disease, ischaemia, diabetes and cancer. Purinergic mechanosensory transduction forms the basis of enteric nociception, where ATP released from mucosal epithelial cells by distension activates nociceptive subepithelial primary afferent sensory fibres expressing P2X3 receptors to send messages to the pain centres in the central nervous system via interneurons in the spinal cord. Purinergic signalling is also involved in salivary gland and bile duct secretion.

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Effects of morphine on non-adrenergic inhibitory responses of the guinea-pig taenia coli

Cited by 29 publications

References 6 publications

Acute Effects of Morphine and Opioid Peptides on the Motility and Responses of Rat Colon to Electrical Stimulation

Acute Effects of Morphine and Opioid Peptides on the Motility and Responses of Rat Colon to Electrical Stimulation

Contractor responses of the isolated colon of the mouse to morphine and some opioid peptides

Purinergic signalling in the gastrointestinal tract and related organs in health and disease

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