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  • 1
    Electronic Resource
    Electronic Resource
    Benzimidazolones and renzapride facilitate acetylcholine release from guinea-pig myenteric plexus via 5-HT4 receptors (1995)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 351 (1995), S. 229-236 
    Details
    ISSN: 1432-1912
    Keywords: Key words BIMU 8 ; BIMU 1 ; Renzapride ; 5-HT4 receptors ; Acetylcholine release ; Myenteric plexus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The effects of the 5-HT4 receptor agonists BIMU 8, BIMU 1, renzapride and of the 5-HT1p receptor agonist 5-hydroxyindalpine on basal and electrically evoked outflow of tritium were studied in guinea-pig longitudinal muscle myenteric plexus preparations preincubated with [3H]choline. Muscle contractions were recorded simultaneously. BIMU 8 caused a calcium dependent and tetrodotoxin sensitive increase in basal [3H]outflow that was assumed to represent release of [3H]acetylcholine. In addition, BIMU 8 enhanced the release of [3H]acetylcholine and twitch contractions evoked by submaximal electrical stimulation. Ondansetron (1 μmol/l) did not change the effects of BIMU 8, but DAU 6285 and tropisetron (each 1 μmol/l) competitively antagonized the various facilitatory effects of BIMU 8 with pA2 values of 7.0–7.2 (DAU 6285) and 7.0–7.3 (tropisetron). The phosphodiesterase inhibitors IBMX and rolipram did not increase the effects of BIMU 8. BIMU 1 and renzapride also concentration-dependently increased basal release of acetylcholine, and release and contractions caused by submaximal stimulation. The effects of BIMU 1 and renzapride were competitively antagonized by 1 μmol/l tropisetron (pA2 6.6–7.1). The EC50 values for the increase in the evoked [3H]acetylcholine release and contractions were closely similar. 5-Hydroxyindalpine did not change basal release and slightly inhibited the evoked release of [3H]acetylcholine. Release of acetylcholine and contractions elicited by submaximal stimulation were strongly inhibited by (+)-tubocurarine which indicates that nicotinic ganglionic transmission is involved in this kind of release. The results suggest that BIMU 8, BIMU 1 and renzapride stimulate 5-HT4 receptors at cholinergic interneurones and thereby facilitate nicotinic ganglionic transmission in the myenteric plexus. Cyclic AMP is probably not involved in the 5-HT4 receptor mediated facilitation of acetylcholine release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00233241
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  • 2
    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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  • 3
    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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  • 4
    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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  • 5
    Electronic Resource
    Electronic Resource
    GABAergic inhibition of nitric oxide-mediated relaxation of guinea-pig ileum (1999)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 359 (1999), S. 500-504 
    Details
    ISSN: 1432-1912
    Keywords: Key words Guinea-pig ileum ; Nitric oxide ; GABA ; Baclofen ; Muscimol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of GABA receptor agonists were investigated on guinea-pig isolated ileum longitudinal muscle with intact myenteric plexus. Electrical field stimulation (1 Hz, 10 s) of the histamine (1 μM)-precontracted preparation caused a contraction followed by a relaxation. Relaxations were inhibited by l-N G-nitro-arginine (l-NA; EC50 3 μM) in a concentration-dependent manner. The inhibitory action of 10 μM l-NA was blocked by 10 μM l-arginine but not by d-arginine, which indicates that the relaxation was largely mediated by endogenous nitric oxide (NO). Tetrodotoxin (1 μM) reduced the relaxation only by about 50%. GABA and the GABAB agonist, baclofen, inhibited the field stimulation-induced longitudinal muscle relaxation in a concentration-dependent manner. The GABAB receptor antagonist, saclofen (10 μM), antagonised the effect of baclofen (apparent pA 2 of saclofen: 5.6). Muscimol (10 μM) similarly inhibited the relaxation, and this inhibition was prevented by bicuculline (1 μM). It is concluded that nitrergic nerves of the guinea-pig myenteric plexus are endowed with GABAA and GABAB receptors which mediate inhibition of NO release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00005382
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  • 6
    Electronic Resource
    Electronic Resource
    PACAP induces bradycardia in guinea-pig heart by stimulation of atrial cholinergic neurones (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 354 (1996), S. 424-430 
    Details
    ISSN: 1432-1912
    Keywords: Key words PACAP ; Acetylcholine release ; Guinea-pig heart ; ω-conotoxin ; Patch-clamp technique ; cAMP ; Phosphorylation ; Chronotropy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Based on previous studies which indicated that pituitary adenylate cyclase activating peptide (PACAP) acts as a positive inotropic and chronotropic substance in different species via the cAMP signal transduction pathway, the objective of the present work was to investigate cAMP-regulated myocardial key proteins in response to PACAP in isolated ventricular cells of the guinea pig. Surprisingly, the two molecular forms of PACAP, PACAP(1–27) and PACAP(1–38), showed no effect on intracellular cAMP-levels, L-type Ca2+channel current or phosphorylation of troponin inhibitor (TnI) and phospholamban (PLB). Additionally, inotropy of isolated guinea-pig ventricular strips was not affected by the neuropeptide. However, in isolated spontaneously beating guinea-pig atria, PACAP(1–27) and PACAP(1–38), but not VIP induced severe bradycardia in a dose-dependent manner. This effect could be prevented by preincubation with the PACAP receptor antagonist PACAP(6–38), by atropine and by ω-conotoxin, a blocker of neuronal N-type Ca2+channels. PACAP stimulates release of [3H]-labelled acetylcholine. Only preparations showing an increase in [3H]acetylcholine release developed bradycardia, indicating a causal relationship between both phenomena. It was concluded that PACAP exerts no influence on guinea-pig ventricular tissue, but induces negative chronotropic effects in isolated guinea-pig atria by stimulation of acetylcholine release from parasympathetic neurons via PACAP type 1 receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168432
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  • 7
    Electronic Resource
    Electronic Resource
    PACAP induces bradycardia in guinea-pig heart by stimulation of atrial cholinergic neurones (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 354 (1996), S. 424-430 
    Details
    ISSN: 1432-1912
    Keywords: PACAP ; Acetylcholine release ; Guinea-pig heart ; ω-conotoxin ; Patch-clamp technique ; cAMP ; Phosphorylation ; Chronotropy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Based on previous studies which indicated that pituitary adenylate cyclase activating peptide (PACAP) acts as a positive inotropic and chronotropic substance in different species via the cAMP signal transduction pathway, the objective of the present work was to investigate cAMP-regulated myocardial key proteins in response to PACAP in isolated ventricular cells of the guinea pig. Surprisingly, the two molecular forms of PACAP, PACAP(1–27) and PACAP(1–38), showed no effect on intracellular cAMP-levels, L-type Ca2+ channel current or phosphorylation of troponin inhibitor (TnI) and phospholamban (PLB). Additionally, inotropy of isolated guinea-pig ventricular strips was not affected by the neuropeptide. However, in isolated spontaneously beating guinea-pig atria, PACAP(1–27) and PACAP(1–38), but not VIP induced severe bradycardia in a dose-dependent manner. This effect could be prevented by preincubation with the PACAP receptor antagonist PACAP(6–38), by atropine and by ω-conotoxin, a blocker of neuronal N-type Ca2+channels. PACAP stimulates release of [3H]-labelled acetylcholine. Only preparations showing an increase in [3H]acetylcholine release developed bradycardia, indicating a causal relationship between both phenomena. It was concluded that PACAP exerts no influence on guinea-pig ventricular tissue, but induces negative chronotropic effects in isolated guinea-pig atria by stimulation of acetylcholine release from parasympathetic neurons via PACAP type 1 receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168432
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  • 8
    Electronic Resource
    Electronic Resource
    NK1- and NK3-receptor mediated inhibition of 5-hydroxytryptamine release from the vascularly perfused small intestine of the guinea-pig (1997)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 356 (1997), S. 689-693 
    Details
    ISSN: 1432-1912
    Keywords: Key words Guinea-pig ileum ; Enterochromaffin cells ; 5-HT release ; Tachykinins ; NK1 receptors ; NK3 receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of tachykinins on the spontaneous release of 5-hydroxytryptamine (5-HT) from the enterochromaffin cells into the portal circulation was investigated in vitro using the vascularly perfused isolated guinea-pig small intestine. 5-HT was determined by HPLC with electrochemical detection. Test substances were applied intraarterially. Substance P (SP) caused a concentration-dependent decrease in 5-HT outflow with an EC50 of 50pmol/l. Similarly, the selective NK1 receptor agonist SP methyl ester (1nmol/l) significantly inhibited 5-HT outflow (to 51±3%). When tetrodotoxin (1μmol/l) was added to the arterial perfusion medium, the inhibition by SP of 5-HT outflow was not affected. The selective NK1 receptor antagonist CP 99994 [(+)-(2S,3S)-3-(2-methoxyben-zylamino)-2-phenylpiperidine] (0.1μmol/l) prevented the inhibitory effect of SP (0.1μmol/l). Neither GR 94800 (PhCO-Ala-Ala-DTrp-Phe-DPro-Pro-NleNH2) (0.1μmol/l) nor SR 142801 [(S)-(N)-(1-(3-(1-benzoyl-3-(3, 4-dichlorophenyl)piperidin-3-yl)propyl)-4-phenyl-piperidin-4-yl)-N-methylacetamide] (10nmol/l), which are selective NK2 and NK3 receptor antagonists, changed the SP-mediated inhibition. The selektive NK3 receptor agonist senktide (10nmol/l) also decreased the 5-HT outflow (to 57±5%). This inhibition was prevented by SR 142801 (10nmol/l) and by tetrodotoxin. CP 99994 (0.1μmol/l) significantly antagonized the senktide-mediated inhibition of 5-HT outflow. The outflow of 5-HT was unaffected when CP 99994, GR 94800 or SR 142801 alone were added to the perfusion medium. It is concluded that the release of 5-HT from enterochromaffin cells is directly inhibited by NK1 receptors, and indirectly by neuronal NK3 receptors whose stimulation leads to the release of SP.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00005106
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  • 9
    Electronic Resource
    Electronic Resource
    Benzimidazolones and renzapride facilitate acetylcholine release from guinea-pig myenteric plexus via 5-HT4 receptors (1995)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 351 (1995), S. 229-236 
    Details
    ISSN: 1432-1912
    Keywords: BIMU 8 ; BIMU 1 ; Renzapride ; 5-HT4 receptors ; Acetylcholine release ; Myenteric plexus
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of the 5-HT4 receptor agonists BIMU 8, BIMU 1, renzapride and of the 5-HT1p receptor agonist 5-hydroxyindalpine on basal and electrically evoked outflow of tritium were studied in guinea-pig longitudinal muscle myenteric plexus preparations preincubated with [3H]choline. Muscle contractions were recorded simultaneously. BIMU 8 caused a calcium dependent and tetrodotoxin sensitive increase in basal [3H]outflow that was assumed to represent release of [3H]acetylcholine. In addition, BIMU 8 enhanced the release of [3H]acetylcholine and twitch contractions evoked by submaximal electrical stimulation. Ondansetron (1 μmol/l) did not change the effects of BIMU 8, but DAU 6285 and tropisetron (each 1 μmol/l) competitively antagonized the various facilitatory effects of BIMU 8 with pA2 values of 7.0–7.2 (DAU 6285) and 7.0–7.3 (tropisetron). The phosphodiesterase inhibitors IBMX and rolipram did not increase the effects of BIMU 8. BIMU 1 and renzapride also concentration-dependently increased basal release of acetylcholine, and release and contractions caused by submaximal stimulation. The effects of BIMU 1 and renzapride were competitively antagonized by 1 μmol/l tropisetron (pA2 6.6–7.1). The EC50 values for the increase in the evoked [3H]acetylcholine release and contractions were closely similar. 5-Hydroxyindalpine did not change basal release and slightly inhibited the evoked release of [3H]acetylcholine. Release of acetylcholine and contractions elicited by submaximal stimulation were strongly inhibited by ( + )-tubocurarine which indicates that nicotinic ganglionic transmission is involved in this kind of release. The results suggest that BIMU 8, BIMU 1 and renzapride stimulate 5-HT4 receptors at cholinergic interneurones and thereby facilitate nicotinic ganglionic transmission in the myenteric plexus. Cyclic AMP is probably not involved in the 5-HT4 receptor mediated facilitation of acetylcholine release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00233241
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  • 10
    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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