The Effect of Analgesic Drugs on the Release of Acetylcholine from Electrically Stimulated Guinea-Pig Ileum (original) (raw)
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Effect of morphine and acetylcholine on contractile activity and cyclic AMP in guinea-pig ileum
Bioscience Reports, 1990
Neither acute nor prolonged exposure to morphine altered cAMP content or spontaneous movements of longitudinal muscle-myenteric plexus strips of the guinea-pig ileum. By contrast, exogenous acetylcholine or electrical stimulation of the strips elicited both a decrease of cAMP concentration and a twitch response. Atropine blocked the effects of stimulation on these parameters. Addition of morphine to electrically stimulated strips inhibited the twitch response but did not affect cAMP levels. Incubation with morphine led to the development of tolerance to the inhibitory effect on twitch activity and prevented the fall in cAMP normally elicited by electrical stimulation. These results suggest that muscarinic activation is associated with a reduction of cAMP content, an effect which would be impaired in opiate-tolerant tissues.
Clinical and Experimental Pharmacology and Physiology, 1987
1. The effects of corticosteroid pretreatment on the contraction caused by acetylcholine or electrical stimulation of guinea-pig ileum and duodenum were studied. 2. The acetylcholine dose-response curves for steroid pretreated ileum but not duodenum were significantly shifted to the right; evidence that pretreated ileum required higher dose of acetylcholine than normal to cause 50% maximal contraction. 3. Naloxone enhanced the contraction of normal ileum caused by acetylcholine given at the dose of ED,,, but not that of normal duodenum. 4. The dose of morphine required to abolish electrically induced contraction was higher in steroid pretreated ileum than in normal ileum. 5. Hence, corticosteroid pretreatment may affect intestinal contractility via opioidergic mechanisms which are found in the ileum but not in the duodenum.
Sites of action of morphine on the ascending excitatory reflex in the guinea-pig small intestine
Neuroscience Letters, 1992
The effect of morphine on the ascending excitatory reflex of the circular muscle elicited by radial distension of the gut wall was studied in the isolated guinea-pig small intestine~ A three compartment bath, in which an intermediate compartment divided the site of intraluminal stimulation (caudal compartment) from the site of reflex contraction recording (oral compartment), was used. Morphine (0.01-10 gM) applied independently to each compartment, caused a concentration-dependent depression (up to 90%) of the amplitude of distension-evoked reflex contractions. Concentration-response curves to morphine were shifted to the right by naloxone (30 nM) with an apparent pA2 value of about 8.5, which suggests an interaction with opioid or-receptor subtypes. Our results indicate that morphine not only depressed transmission from excitatory motor neurons to the circular muscle but also neuro-neuronal transmission along the ascending excitatory reflex pathway.
Subcutaneous morphine reduces intestinal propulsion in rats partly by a central action
European Journal of Pharmacology, 1981
Rats were given intracerebroventricular or intravenous injections of the quarternary opioid receptor antagonist N,N-diallylnormorphinium (DANM, 100/~g). Ten min later morphine (7.5 mg/kg) or loperamide (10 mg/kg) was injected subcutaneously. Intestinal propulsion was assessed by measuring the progress of radioactive chromium (Na~ ~ CrO a, 0.5 ~Ci) along the small intestine. The radioactive chromium was instilled into the proximal duodenum 20 min after injection of morphine or loperamide, and the animals sacrificed 35 rain after, giving radioactive chromium. Morphine and loperamide both inhibit intestinal propulsion. DANM (100/tg i.c.v.) reduces the effect of morphine but not loperamide. Intravenous injection of DANM does not reduce anti-propulsive action of morphine. By itself DANM neither increases nor decreases intestinal propulsion. These experiments indicate that morphine, when administered by a peripheral route, reduces small intestinal propulsion in the rat partly through an action on brain opioid receptors.
Effect of preservation conditions on autonomic transmission in rat small bowel
Transplantation Proceedings, 2002
I N small bowel, acetylcholine (ACh) released from intramural cholinergic nerves acts at nicotinic cholinergic receptors to cause excitation of enteric nerves and at muscarinic cholinergic receptors to cause contractions of intestinal smooth muscle. 1 Thus, contractile function of small bowel regulated by ACh is highly dependent on structural and functional integrity of enteric nerves. 2 Histological studies performed on small bowel submitted to cold ischemic preservation prior to transplantation suggest that neurological lesions following prolonged ischemia severely compromises contractile functions of the intestine. 3-5 However, autonomic dysfunction has not been studied in small bowel grafts preserved for transplantation.
European Journal of Pharmacology, 1993
Some factors known to affect jejunal motility (recorded as volume changes of an intraluminal balloon) were investigated in anaesthetized cats (ether-chloralose) pretreated with guanethidine and atropine. Indomethacin, morphine (both compounds administered systemically) or vagal nerve stimulation elicited jejunal excitatory motor responses. The effect of indomethacin seemed to be independent of cyclooxygenase inhibition and probably did not involve opioid receptors. It is suggested that the spasmogenic stimuli caused jejunal hypermotility by inhibiting tonically active, inhibitory motor neurons that are intrinsic to the gut. Furthermore, when the jenunal tone had been raised by indomethacin or morphine spontaneous relaxations were observed, and these could be mimicked by vagal stimulation. Hexamethonium antagonized these relaxations but did not attenuate the drug-induced jejunal hypermotility.
British Journal of Pharmacology, 1990
Brief exposure for 2 min of guinea-pig isolated ileum to [Met5]enkephalin (MEnk) and noradrenaline has been shown previously to produce withdrawal contractures on washout of the agonist or addition of naloxone (MEnk) or phentolamine (noradrenaline). 2 The present study was undertaken to investigate firstly, whether other putative neurotransmitters and/or related drugs which inhibit transmitter release also produced withdrawal responses following 2 min contact with the ileum and secondly, whether they affected the opioid withdrawal response. 3 Adenosine (1-5 uM), but not U-50,488H (1-5 pM), somatostatin (0.01-5 pM), ocreotide (1-5 UM), baclofen (1-25uMm) or dopamine (5, 5O#M), produced a contracture on washout following 2min contact with the ileum. The adenosine (5,UM) washout contracture, in common with MEnk and noradrenaline washout contractures, was inhibited by the substance P antagonist, spantide (10pM). 4 Added 30s before washout at a concentration of 5pgM, noradrenaline, U-50,488H, adenosine, somatostatin and ocreotide significantly inhibited the washout withdrawal response following 2 min contact of the ileum with MEnk, 1 M. A higher concentration of baclofen, 250,UM, also inhibited this response. 5 The naloxone (1 pM)-precipitated withdrawal response following contact of the ileum with MEnk, 1 ,UM, for 2 min, was inhibited only by noradrenaline (5pM) and U-50,488H (5pM). 6 It is concluded that during naloxone-precipitated opioid withdrawal an additional population of enteric motor neurones is recruited which is not involved in the washout withdrawal response and these neurones have less diversity of presynaptic receptors mediating inhibition of transmitter release than cholinergic motor neurones.