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  • 1
    Electronic Resource
    Electronic Resource
    Antagonist discrimination between subtypes of tachykinin receptors in the guinea-pig ileum (1986)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 334 (1986), S. 181-187 
    Details
    ISSN: 1432-1912
    Keywords: Substance P ; Eledoisin ; Substance P antagonists ; Acetylcholine release ; Substance P receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The effects of substance P and eledoisin on spontaneous and electrically-evoked release of [3H]acetylcholine, and on smooth muscle were studied in the guineapig myenteric plexus-longitudinal muscle preparation preloaded with [3H]choline. Substance P and eledoisin caused transient increases in spontaneous release of [3H]acetylcholine and in longitudinal muscle tone. Both tachykinins were equipotent in contracting the muscle, but eledoisin was more potent than substance P in eliciting [3H]acetylcholine release. The release caused by substance P was enhanced in the presence of naloxone and scopolamine which suggests that the release is modulated through opioid and muscarinic receptors. 2. Substance P and eledoisin inhibited the release of [3H]acetylcholine evoked by electrical stimulation at 0.1 Hz. The inhibition was not due to an activation of α-adrenoceptors, histamine or opioid receptors. The substance P antagonists (d-Pro2, d-Trp7,9)SP (10 and 30 μM) and (Arg5, d-Trp7,9, Nle11)SP5–11 (1 and 10 μM) competitively antagonized both the contractile effects of substance P and eledoisin, and the inhibition by the tachykinins of the electrically-evoked release of [3H]acetylcholine. The increase in spontaneous [3H]acetylcholine release elicited by substance P and eledoisin was not prevented by the substance P antagonists. 3. The results suggest that the neuronal receptor whose activation causes inhibition of acetylcholine release and the smooth muscle receptor correspond to the SP-P type, whereas the neuronal receptor mediating an increase in spontaneous acetylcholine release is of the SP-E type. The two antagonists, (d-Pro2, d-Trp7,9)SP and (Arg5, d-Trp7,9, Nle11)SP5–11, selectively block only the SP-P receptor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00505819
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  • 2
    Electronic Resource
    Electronic Resource
    Release of [3H]acetylcholine from a modified rat phrenic nerve-hemidiaphragm preparation (1986)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 334 (1986), S. 357-364 
    Details
    ISSN: 1432-1912
    Keywords: Phrenic nerve ; Whole nerve-muscle preparation ; End-plate preparation ; Release of [3H]acetylcholine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Two different preparations of the rat phrenic nerve-hemidiaphragm (whole nerve-muscle preparation, end-plate preparation) were used for studying synthesis and release of radioactive acetylcholine in the absence and presence of cholinesterase inhibitors. When the whole nerve-muscle preparation (110–180 mg) was incubated with [3H]choline, only small amounts of radioactive acetylcholine were synthesized within the tissue. Electrical nerve stimulation of the whole nerve-muscle preparation produced no increase in tritium outflow. Incubation of the end-plate preparation (16–29 mg) which was obtained after removal of most of the muscle mass led to the formation of large amounts of [3H]acetylcholine. Synthesis depended on nerve activity and increased 13-fold during a high loading stimulation (50 Hz), as compared to the synthesis at rest. In a denervated end-plate preparation the formation of [3H]acetylcholine was reduced to 4% of the control preparation. Electrical nerve stimulation of the end-plate preparation produced a release of tritium that could be attributed entirely to the release of [3H]acetylcholine. The stimulated tritium efflux was completely suppressed in a calcium-free medium or in the presence of tetrodotoxin (300 nM). Release could even be detected during a short train of 50 pulses (5 Hz) with a fractional release of about 0.04% of the [3H]acetylcholine tissue content per pulse. It is concluded that the large muscle mass interferes with nerve labelling by a reduction of the [3H]choline supply to the nerve terminals when the whole nerve-muscle preparation is used. Removal of most of the muscle fibres reduces the possibility for [3H]choline to be captured by them and then more radioactive choline can enter the end-plate region. From this end-plate preparation a calcium-dependent release of radioactive transmitter can be measured in the absence of cholinesterase inhibitors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00569370
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  • 3
    Electronic Resource
    Electronic Resource
    Temperature-dependent effects of increased intraluminal pressure on serotonin release from the vascularly perfused guinea pig ileum (1987)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 336 (1987), S. 483-486 
    Details
    ISSN: 1432-1912
    Keywords: Serotonin release ; Enterochromaffin cells ; Peristaltic reflex ; Guinea pig ileum ; Naloxone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Isolated segments of the guinea pig ileum were vascularly perfused and the release of endogenous serotonin into the portal effluent was measured. Peristalsis was induced by raising the intraluminal hydrostatic pressure by 500 Pa for 5 min. Serotonin release increased during peristalsis induced by fluid of 37°C, but decreased when the temperature of the intraluminal fluid was between 13°C and 22°C. In the presence of naloxone (0.3 μmol/l) raising the intraluminal pressure with fluid of 37°C caused an inhibition of the serotonin release which was blocked by scopolamine (0.1 μmol/l). Naloxone did not affect the inhibition of Serotonin release during peristalsis caused by fluid of 19°C, neither did indometacin (1 μmol/l). In conclusion, liquid distension of the guinea pig isolated ileum elicits peristaltic activity, and affects the release of serotonin into the portal circulation. The changes in serotonin release depend on the temperature of the fluid passing through the intestinal lumen, whereas peristalsis is not affected by the temperature of the intraluminal fluid.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169303
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  • 4
    Electronic Resource
    Electronic Resource
    Inhibition by oxotremorine of acetylcholine resting release from guinea pig-ileum longitudinal muscle strips (1975)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 287 (1975), S. 47-60 
    Details
    ISSN: 1432-1912
    Keywords: Guinea-Pig Ileum Longitudinal Muscle Strips ; Acetylcholine Resting Release ; Acetylcholine Content ; Oxotremorine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. Longitudinal muscle strips of the guinea-pig ileum were incubated in Tyrode solution containing either DFP or physostigmine as cholinesterase inhibior. After a 90 min preincubation period the acetylcholine resting release into the medium was determined. Acetylcholine was estimated by gas chromatography. 2. The resting release was 0.39 nmol/g×min irrespective of the cholinesterase inhibitor used. In the presence of hexamethonium, or after omission of external calcium, the resting release fell by 50 and 55%, respectively. 3. Oxotremorine (10−5 and 10−4 M) significantly inhibited the resting release of acetylcholine by 25 and 33%, respectively. The inhibitory effect of oxotremorine was completely reversed by atropine (3×10−7M). Oxotremorine did not reduce the spontaneous release of acetylcholine that occurred either in the presence of hexamethonium or in the absence of external calcium. 4. The acetylcholine content of the muscle strips was approximately doubled during the preincubation with a cholinesterase inhibitor. The subsequent incubation with oxotremorine did not lead to a further increase in the endogenous acetylcholine content. However, incubation of the muscle strips with oxotremorine in the absence of a cholinesterase inhibitor led to a rise in the endogenous acetylcholine concentration. Inin vivo experiments, oxotremorine also caused an increase in the acetylcholine content of the muscle strips. The possibility is discussed that the rise in the acetylcholine concentration following the administration of oxotremorine is a consequence of the decreased release. 5. It is concluded that oxotremorine inhibits the resting release of acetylcholine by activation of neuronal muscarinic receptors. The inhibitory effect of oxotremorine is linked to that fraction of the acetylcholine resting release that is calcium-dependent and that arises from propagated activity in cholinergic neurones. The results are consistent with the hypothesis of a feed-back control of acetylcholine release mediated by inhibitory muscarinic receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00632637
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  • 5
    Electronic Resource
    Electronic Resource
    Modulation by oxotremorine and atropine of acetylcholine release evoked by electrical stimulation of the myenteric plexus of the guinea-pig ileum (1977)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 300 (1977), S. 145-151 
    Details
    ISSN: 1432-1912
    Keywords: Myenteric plexus ; Presynaptic muscarine receptors ; Acetylcholine release ; Oxotremorine ; Atropine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The effects of oxotremorine and atropine on the release of acetylcholine from longitudinal muscle strips of the guinea-pig ileum stimulated at frequencies between 0.1 and 3 Hz in the presence of eserine were investigated. In control experiments the acetylcholine output per stimulus declined with increasing frequencies of stimulation. 2. Oxotremorine inhibited the release of acetylcholine in a concentration-dependent fashion. At a concentration of 10−6 M oxotremorine, the release evoked by 0.1 Hz was reduced by 54%. With increasing frequencies of stimulation the inhibitory effect of oxotremorine became smaller. 3. Atropine enhanced the output of acetylcholine evoked by electrical stimulation. In the presence of 10−8 M atropine, the concentration-effect curve for the inhibitory action of oxotremorine was shifted to the right in a parallel manner. From the dose-ratio a pA2 value for atropine against oxotremorine of 8.8 was calculated. 4. Hexamethonium (2.8×10−4 M) did not affect the modulating effects of oxotremorine or atropine on acetylcholine output. 5. It is concluded that the guinea-pig ileum myenteric plexus contains inhibitory muscarine receptors whose stimulation by oxotremorine or by liberated endogenous acetylcholine leads to a diminished output of transmitter. Atropine, by blocking these receptors facilitates acetylcholine release. Further, the results suggest that the depression of acetylcholine release per stimulus with increasing frequencies of stimulation is due to the presence of the inhibitory muscarine receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00505045
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  • 6
    Electronic Resource
    Electronic Resource
    Increase by α-adrenolytic drugs of acetylcholine release evoked by field stimulation of the guinea-pig ileum (1979)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 309 (1979), S. 255-257 
    Details
    ISSN: 1432-1912
    Keywords: Myenteric plexus ; Acetylcholine release ; Yohimbine ; Tolazoline ; Phentolamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The release of acetylcholine evoked by field stimulation of the guinea-pig ileum (3 Hz) is increased by yohimbine and tolazoline but not affected by phentolamine. It is proposed that yohimbine and tolazoline by blocking α-adrenoceptors of the cholinergic nerves abolish the inhibition caused by endogenous noradrenaline, and thus facilitate the output of acetylcholine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00504758
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  • 7
    Electronic Resource
    Electronic Resource
    Cholinergic modulation of the release of 5-hydroxytryptamine from the guinea pig ileum (1987)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 336 (1987), S. 127-132 
    Details
    ISSN: 1432-1912
    Keywords: Enterochromaffin cells ; 5-Hydroxytryptamine ; Guinea pig ileum ; Muscarine receptor ; Nicotine receptor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Isolated segements of the guinea pig ileum were vascularly perfused and the release of 5-HT and its metabolite 5-HIAA into the portal venous effluent determined by HPLC with electrochemical detection. Test substances were applied via the arterial perfusion medium. Oxotremorine inhibited concentration-dependently the release of 5-HT and 5-HIAA (by 47% at 1 μmol/l). Scopolamine (0.1 μmol/1) did not affect the release of 5-HT and 5-HIAA, but antagonized the effect of oxotremorine. In the presence of TTX (1 μmol/1) oxotremorine (1 pmol/1) increased the release of 5-HT by 150% and that of 5-HIAA by 220%. This increase was completely blocked by scopolamine. Hexamethonium (100 pmol/1) and TTX (1 pmol/1) reduced the release of 5-HT by 32 and 40%, respectively. DMPP (10 pmol/1) increased the release of 5-HT by 57%, and this effect was prevented by hexamethonium. Neither DMPP nor hexamethonium significantly affected the release of 5-HIAA. The enhancing effect of DMPP on 5-HT release was increased and prolonged in the presence of TTX or scopolamine. Nicotine (1, 10 or 30 μmol/l) alone did not cause a consistent increase in the release of 5-HT. However, in the presence of scopolamine nicotine increased the release of 5-HT by 57%. In conclusion, the release of intestinal 5-HT is facilitated via muscarine and nicotine receptors located on the enterochromaffin cells. Indirect evidence suggests that the release of 5-HT is additionally modulated by an as yet unknown inhibitory neurotransmitter released by muscarine receptor activation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00165795
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  • 8
    Electronic Resource
    Electronic Resource
    Absence of muscarinic modulation of vasopressin release from the isolated rat neurohypophysis (1975)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 287 (1975), S. 391-397 
    Details
    ISSN: 1432-1912
    Keywords: Isolated Rat Neurohypophysis ; Vasopressin Release ; Acetylcholine ; Atropine ; Oxotremorine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. Isolated rat neurohypophyses were incubated in Locke solution at 37°C and the vasopressin output into the medium determined by bioassay. 2. Potassium chloride 60 mM caused a 9-fold increase in the rate of vasopressin release that was abolished when calcium chloride was omitted from the Locke solution. 3. Acetylcholine 5.5×10−4 M neither alone nor in the presence of atropine 2.9×10−6 M changed the “resting” release of vasopressin. 4. Neither acetylcholine 5.5×10−4 M nor oxotremorine 10−4 and 3×10−4 M altered the vasopressin release evoked by potassium chloride 60 mM. 5. In contrast to the peripheral adrenergic nerve fibres, the secretory terminal fibres of the neurohypophysis do not appear to contain muscarinic inhibitory or nicotinic excitatory receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00500040
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  • 9
    Electronic Resource
    Electronic Resource
    Some pharmacological properties of the false cholinergic transmitter acetylpyrrolidinecholine and its precursor pyrrolidinecholine (1976)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 295 (1976), S. 81-87 
    Details
    ISSN: 1432-1912
    Keywords: Acetylpyrrolidinecholine ; Pyrrolidinecholine ; Muscarine receptors ; Nicotine receptors ; Neuromuscular transmission
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The acetylcholine analogue acetylpyrrolidinecholine as well as the chline analogue pyrrolidinecholine were synthesized and the cholinergic properties of both substances were investigated on the guinea-pig ileum, rat blood pressure and frog rectus abdominis muscle. Acetylpyrrolidinecholine was 3–5 times less potent than acetylcholine on the three preparations tested. The dose-response curves to acetylpyrrolidinecholine were shifted to the right in a parallel manner by atropine and (+)-tubocurarine. The dissociation constants for atropine and (+)-tubocurarine obtained with acetylpyrrolidinecholine as agonist were not different from those obtained with acetylcholine. This indicates that acetylpyrrolidinecholine specifically stimulates muscarine and nicotine receptors. Eserine potentiated the effects of acetylcholine more than those of acetylpyrrolidinecholine. Pyrrolidinecholine was only a weak agonist on the guinea-pig ileum. It caused a rise of rat blood pressure in doses higher than 10 μmol per rat. Neuromuscular transmission of the phrenic nerve-diaphragm preparation of the rat was not impaired during a 150 min incubation period with 1 mM pyrrolidinecholine. It is suggested that the possible formation and release of acetylpyrrolidinecholine as a false cholinergic transmitter does not modify neuromuscular transmission in skeletal muscle.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00509777
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  • 10
    Electronic Resource
    Electronic Resource
    The effects of LSD in the guinea-pig ileum (1985)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 331 (1985), S. 311-315 
    Details
    ISSN: 1432-1912
    Keywords: Guinea-pig ilcum ; LSD ; 5-HT receptors ; Histamine receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The effects of lysergic acid diethylamide (LSD) on acetylcholine release and on smooth muscle tone were studied in the myenteric plexus-longitudinal muscle preparation of the guinea pig. 2. LSD (0.01–10 μM) depressed in a concentration-dependent manner the electrically-evoked [3H]-acetylcholine outflow from strips preincubated with [3H]-choline. The maximal effect was a 45% inhibition by 1 μM LSD. The spontaneous outflow was not affected. Metitepine competitively antagonized (pA2 8.0) the LSD-induced reduction of the evoked outflow. Tolazoline and mepyramine did not affect the inhibitory action of LSD. 3. The contractions in response to electrical stimulation were enhanced by 34% in the presence of 0.1 μM LSD. Other concentrations of LSD did not affect the twitches. 4. LSD caused an increase in muscle tone which was antagonized non-competitively by mepyramine, metitepine and ketanserin. Ketanserin was a competitive antagonist against the histamine-induced contractions of the longitudinal muscle (pA2 8.49). 5. The results suggest that LSD stimulates presynaptically located 5-HT receptors and thereby decreases the evoked acetylcholine release. In addition, LSD increases smooth muscle tone either directly through stimulation of H1 receptors or indirectly via histamine release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00500812
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