Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Release of Endogenous 3,4-Dihydroxyphenylethylamine and Its Metabolites from the Isolated Neurointermediate Lobe of the Rat Pituitary Gland. Effects of Electrical Stimulation and of Inhibition of Monoamine Oxidase and Reuptake (1986)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 46 (1986), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Isolated rat neurointermediate lobes were incubated in vitro. The release of 3,4-dihydroxyphenylethylamine (dopamine, DA), dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), and methoxyphenylethanol (MOPET) was determined by HPLC with electrochemical detection. Under resting conditions, the outflow of metabolites was 35–50 times that of DA. HVA accounted for 50%, DOPAC for 45%, and MOPET for 5% of the metabolites. Although an equivalent of 40–50% of the tissue DA content was released per hour as metabolites, the tissue DA content was not reduced after 110 min of incubation. The spontaneous outflow of DA and its metabolites was not affected by the DA uptake inhibitor GBR 12921 (100 μM). Pargyline (10 μM) caused a time-dependent decrease of all metabolites (up to 90%). In the presence of GBR 12921 and pargyline, the spontaneous outflow of DA increased sevenfold. Removal of the intermediate lobe caused a 78% reduction in tissue DA content and a corresponding reduction of the outflow of metabolites. Electrical stimulation of the pituitary stalk (0.2 ms, 10 V, 15 Hz, three times for 1 min at intervals of 1 min) induced an increase in outflow of DA and all metabolites. DA accounted for 15%, HVA for 41%, DOPAC for 32%, and MOPET for 12% of the evoked release. The electrically evoked release of DA increased fourfold in the presence of GBR 12921 or pargyline and the effects of both drugs were additive. The evoked release of metabolites was not significantly affected by GBR 12921 but completely abolished by pargyline. In conclusion, oxidative deamination and O-methylation are important pathways for the catabolism of DA in the neurointermediate lobe. Most of the DA metabolites released spontaneously originate from DA that had been degraded intraneuronally without undergoing prior release. Reuptake and extraneuronal metabolism contribute to the inactivation of DA released during electrical stimulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1986.tb13035.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    In Vitro Synthesis of Dopamine and Noradrenaline in the Isolated Rat Pineal Gland: Day-Night Variations and Effects of Electrical Stimulation (1989)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 53 (1989), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Isolated rat pineal glands were incubated in vitro in a medium containing [I4C]dopamine or [14C]tyrosine, and the tissue contents of l4C-labelled and total dopamine and noradrenaline were determined by HPLC followed by electrochemical detection and scintillation spectrometry. During incubation with [l4C]dopamine, the labelled amine accumulated in pineal glands and was partially converted into [l4C]noradrenaline. Nomifensine, a neuronal amine uptake blocker, largely inhibited the accumulation of [l4C]dopamine and the formation of [14C]noradrenaline. These experiments demonstrated dopamine β-hydroxylase activity in the sympathetic nerves of the pineal gland. During incubation with [14C]tyrosine, formation of [l4C]dopamine and [14C]noradrenaline was observed in the pineal tissue, indicating that noradrenaline can also be synthesized from dopamine, endogenously formed in the gland. Electrical stimulation of the stalk region of the pineal gland during incubation with [l4C]dopamine enhanced the accumulation of [l4C]dopamine and synthesis of [14C]noradrenaline. Electrical stimulation also enhanced the formation of [l4C]dopamine during incubation with [l4C]tyrosine. Compared to that at midday, the tissue content of endogenous noradrenaline at midnight was enhanced by 50% and that of dopamine by 450%. The in vitro accumulation of [14C]dopamine, as well as the synthesis of [14C]dopamine and [14C]noradrenaline, was also increased at midnight. In conclusion, sympathetic nerves in the rat pineal gland contain tyrosine hydroxylase and dopamine β-hydroxylase, the two enzymes required for the synthesis of noradrenaline. The capacity of the pineal gland to synthesize dopamine and noradrenaline is enhanced during the night.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1989.tb07342.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Uptake of [3H]Dopamine into Dopaminergic and Noradrenergic Neurones of the Isolated Neurointermediate Lobe of the Rat Hypophysis. Effects of Desipramine and Nomifensine (1983)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 41 (1983), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The isolated neurointermediate lobe (NIL) of the rat hypophysis accumulates [3H]dopamine from the incubation medium. Column chromatographic analysis showed that 92% of the tissue radioactivity was contained in the catecholamine fraction. [3H]Dopamine represented 70% and [3H]noradrenaline 30% of the [3H]catecholamines. Desipramine (1 μM) prevented the formation of [3H]noradrenaline without affecting the storage of [3H]dopamine. Nomifensine (10 μM) blocked the storage of [3H] dopamine and [3H]noradrenaline. Thus, in the NIL, [3H]dopamine is taken up into dopaminergic and noradrenergic neurones. In the latter, [3H] dopamine is converted to [3H]noradrenaline, indicating a significant dopamine β-hydroxylase activity in the NIL tissue. A selective labeling of the dopamine stores with [3H]dopamine can be achieved in the presence of desipramine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1983.tb00850.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Modulation of noradrenaline release in rat isolated stomach by prostanoids, but not by histaminergic mechanisms (1995)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 352 (1995), S. 631-639 
    Details
    ISSN: 1432-1912
    Keywords: Stomach ; Sympathetic nerves ; Noradrenaline release ; Prostaglandins ; EP receptors ; Histamine receptors ; Muscarine receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Several gastric functions are modulated by the sympathetic nervous system, but local mechanisms involved in the control of noradrenaline release are largely unknown. Overflow of endogenous noradrenaline was studied from isolated rat stomach incubated in Ussing chambers allowing the separate determination of mucosal and serosal overflow. Spontaneous noradrenaline overflow was similar at the mucosal and serosal side, but electrical field stimulation caused a frequency-dependent increase in noradrenaline overflow selectively at the serosal side. Evoked noradrenaline overflow was blocked by tetrodotoxin, not affected by indometacin and markedly enhanced (by about 250%) by yohimbine. In the presence of indometacin and yohimbine, sulprostone (an agonist at EP1/EP3 receptors) and misoprostol (an agonist at EP2/EP3 receptors) reduced the noradrenaline overflow evoked by stimulation at 3 Hz maximally by about 80% (EC50: 6 nmol/l and 11 nmol/l, respectively). The EP1 receptor selective antagonist AH 6809 (6-isopropoxy-9-oxoxanthene-2-carboxylic acid) did not antagonize the inhibition by sulprostone. Noradrenaline overflow evoked by stimulation at 1 Hz and 3 Hz was increased by scopolamine by about 50% and almost completely inhibited by oxotremorine. Neither, histamine nor the H3 receptor selective agonist (R)-α-methyl-histamine, nor the H1, H2 and H3 selective receptor antagonists mepyramine, cimetidine and thioperamide significantly affected noradrenaline overflow evoked by stimulation at 1 Hz or 3 Hz. In conclusion, impulse-induced noradrenaline release in the rat stomach is controlled by multiple presynaptic mechanisms involving α2-adrenergic autoreceptors, EP3 prostanoid and muscarine heteroreceptors, whereas histaminergic mechanisms do not appear to be significant.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00171322
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Nitric oxide, via activation of guanylyl cyclase, suppresses α2-adrenoceptor-mediated 5-hydroxytryptamine release from neuroendocrine epithelial cells of rabbit tracheae (1997)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 356 (1997), S. 856-859 
    Details
    ISSN: 1432-1912
    Keywords: Key words Trachea ; Airway mucosa ; 5-HT secretion ; Nitric oxide ; Neuroendocrine epithelial cells ; α-Adrenoceptors ; Guanylyl cyclase ; ODQ
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Isolated tracheae of newborn rabbits were incubated in vitro and the outflow of 5-hydroxytryptamine (5-HT) was determined by HPLC with electrochemical detection. Evidence has previously been provided that this 5-HT outflow derives from neuroendocrine epithelial (NEE) cells of the airway mucosa. Phenylephrine, at a maximally effective concentration of 10 μM, caused a transient increase in 5-HT outflow by about 250%, an effect mediated by α2B-adrenoceptors, as previously shown. The phenylephrine-induced 5-HT release remained unchanged in calcium-free medium, but was reduced by 75% when the tracheae were incubated in calcium-free medium which contained 0.5 mM EDTA, a treatment known to lower also intracellular calcium. The NO donor SNAP (S-nitroso-N-acetyl-penicillinamine, 10 μM) almost completely inhibited phenylephrine-induced 5-HT release. The inhibitory effect of SNAP was prevented by ODQ, (1H-[1, 2, 4]oxadiazolo[4, 3-a]quinoxalin-1-one), an inhibitor of soluble guanylyl cyclase. In contrast, 5-HT release induced by depolarizing concentrations of potassium (45 mM), which was reduced by 96% in calcium-free medium, was not affected by SNAP. In conclusion, NO, via activation of soluble guanylyl cyclase, inhibits 5-HT release from NEE cells in a stimulus-dependent manner. α2-Adrenoceptor-mediated 5-HT release, which appears to be triggered by liberation of calcium from intracellular stores, is suppressed by NO, whereas high potassium-evoked 5-HT release which is triggered by calcium influx through voltage regulated channels, is not affected.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00005129
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Characterization of 5-hydroxytryptamine release from isolated rabbit and rat trachea: the role of neuroendocrine epithelial cells and mast cells (1995)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 353 (1995), S. 55-63 
    Details
    ISSN: 1432-1912
    Keywords: Trachea ; Airway mucosa ; 5-HT secretion APUD cells ; Neuroendocrine epithelial cells ; 5-Hydroxytryptophan ; α-Adrenoceptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Rabbit or rat isolated tracheae were incubated in vitro, and the release of 5-hydroxytryptamine (5-HT) and its metabolite 5-hydroxyindoleacetic acid (5-HIAA) was determined by HPLC with electrochemical detection. Release of 5-HT from rabbit tracheae could be evoked by the calcium ionophore A 23187 and, in a calcium-dependent manner, by depolarizing concentrations of potassium (45 mmol/1), but not by the mast cell degranulating drug compound 48/80. High potassium-and A 23187-evoked release of 5-HT was markedly higher from tracheae of newborn compared to adult rabbits. In rabbit tracheae, mechanical removal of the mucosa resulted in 80–90% reduction in tissue 5-HT and in a similar reduction in high potassium-evoked 5-HT release. 5-Hydroxytryptophan, but not tryptophan, caused a marked increase in the spontaneous outflow of 5-HT and 5-HIAA from tracheae of newborn rabbits, and the effect on 5-HT, but not that on 5-HIAA, required an intact mucosa. Furthermore, treatment with 5-hydroxytryptophan caused an increase in tissue 5-HT and 5-HIAA, and these effects required an intact mucosa. In tracheae of adult rabbits 5-hydroxytryptophan caused similar, although less profound, effects. Adrenaline (I μmol/l) enhanced the release of 5-HT from newborn rabbit tracheae, and this effect was inhibited by 1 μmol/l phentolamine or 1 μmol/l prazosin, but not affected by 100 nmol/1 propranolol. In rat tracheae, compound 48/80 evoked a large release of 5-HT, whereas depolarizing concentrations of potassium (45 mmol/1) had only a very minor effect. In rat tracheae, 5-hydroxytryptophan had small effects on the outflow and tissue contents of 5-HT and 5-HIAA in comparison to the effects on rabbit tracheae; and removal of the mucosa resulted in only a minor reduction in tissue 5-HT. In conclusion, neuroendocrine epithelial (NEE) cells and mast cells are the major source of 5-HT in tracheae of the rabbit and rat, respectively. Isolated tracheae of newborn rabbits appear to be a useful model to study 5-HT secretion from NEE cells. 5-HT secretion from NEE cells is activated by a rise in intracellular calcium, and calcium influx through voltage-regulated channels appears to be one activating pathway. 5-HT secretion from NEE cells can be stimulated via α-adrenoceptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00168916
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Non-neuronal acetylcholine, a signalling molecule synthezised by surface cells of rat and man (1997)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 355 (1997), S. 515-523 
    Details
    ISSN: 1432-1912
    Keywords: Key words Non-neuronal acetylcholine ; Surface cells of rat and man ; Choline acetyltransferase ; Cell proliferation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Acetylcholine acts as a prominent transmitter in the central and peripheral nervous system. The aim of the present study was to investigate whether mammalian non-neuronal cells can synthesize and store acetylcholine. A cotton tipped applicator (Q-tip) was used to collect surface cells from airways and alimentary tract. Histological inspection indicated that rubbing of the luminal surface of human bronchi did not penetrate the basal membrane. Acetylcholine was measured by an HPLC-method using substrate-specific enzyme reactor-columns. Non-neuronal acetylcholine was found in cells covering inner and outer surfaces of rat and man. For example, acetylcholine was detected in the surface epithelium of human bronchi (33 pmol/g), mouth (female 0.7 and male 8 pmol/sample), small and large intestine (800 and 16 pmol/g, respectively), gall bladder (12 pmol/g), vagina (6 pmol/sample), skin 1000 (pmol/g) and in pulmonary pleura (5 pmol/sample). Somewhat higher amounts of acetylcholine were found in rat tracheal and intestinal epithelium and in rat skin. The synthesizing enzyme choline acetyltransferase (ChAT) was demonstrated in human surface epithelium by immunohistochemistry and by Western blot analysis. Enzymatic ChAT activity was demonstrated in isolated epithelial cells of human bronchi and small intestine (3.5 and 28 nmol/mg protein/h, respectively). Applied acetylcholine (in nM concentrations) increased, whereas inhibition of ChAT activity by bromoacetylcholine (10 μM) reduced the growth of cultured human bronchial epithelial cells. Inhibition of cell growth occurred also in the presence of atropine (1 μM) together with (±)-tubocurarine (30 μM). In conclusion, the present experiments demonstrate a widespread existence of non-neuronal acetylcholine in surface cells of man. Non-neuronal acetylcholine may act as a local signalling molecule.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00004977
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    Acetylcholine and nicotine stimulate the release of granulocyte-macrophage colony stimulating factor from cultured human bronchial epithelial cells (1998)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 357 (1998), S. 472-475 
    Details
    ISSN: 1432-1912
    Keywords: Key words Primary cultures of human bronchial ; epithelial cells ; GM-CSF release ; Non-neuronal epithelial acetylcholine ; Nicotinic receptor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Primary cultures of human bronchial epithelial cells (HBE-cells) were established to measure granulocyte-macrophage colony stimulating factor (GM-CSF) release. HBE-cells showed a basal GM-CSF release (82±20 ng/well/24 h; 30 donors), which was increased by interleukin-1 β (IL-1β, 1 ng/ml) by 270%. This effect was blocked by 1 μM dactinomycin or 10 μM cycloheximide, i.e. the stimulatory effect of IL-1β depended on de-novo synthesis. Histamine (100 μM) and acetylcholine (100 nM) stimulated GM-CSF release more than two-fold above the baseline. Nicotine (1 μM) increased GM-CSF release to a similar extent, and this effect was prevented by 30 μM (+)-tubocurarine. The stimulatory effect was attenuated or even lost with high agonist concentrations (10 μM acetylcholine; 100 μM nicotine) suggesting receptor desensitization. The muscarinic receptor agonist oxotremorine did not affect GM-CSF release. Serotonin, substance P and calcitonin-gene related peptide had no effect on GM-CSF release. In conclusion, acetylcholine can trigger GM-CSF release from human airway epithelial cells via stimulation of nicotinic receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00005195
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 9
    Electronic Resource
    Electronic Resource
    Nitric oxide synthase activity is inducible in rat, but not rabbit alveolar macrophages, with a concomitant reduction in arginase activity (1995)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 351 (1995), S. 651-659 
    Details
    ISSN: 1432-1912
    Keywords: Alveolar macrophages ; Airway inflammation ; Nitric oxide ; NO synthase ; Arginase ; Ornithine transport ; Citrulline transport ; Arginine metabolism ; Bacterial lipopolysaccharides ; Dexamethasone ; NG-monomethyl-l-arginine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Alveolar macrophages were obtained by broncho-alveolar lavage of isolated rat and rabbit lungs and cultured (2.5 × 106 cells/dish) for 18 h in the absence or presence of bacterial lipopolysaccharides (LPS) alone or in combination with cytokines. Thereafter, accumulation of 3H-citrulline (NO synthase activity) and 3H-ornithine (arginase activity) were determined. During incubation of rat alveolar macrophages with 3H-arginine clear amounts of 3H-citrulline and 3H-ornithine (3.8 and 4.6% of the added 3H-arginine, respectively) were formed and most of these metabolites appeared in the incubation medium (ratios extra-/intracellular of 17 and 70 for 3H-citrulline and 3H-ornithine, respectively). When rat alveolar macrophages had been cultured with LPS the formation of 3H-citrulline was increased about 30-fold and this was accompanied by a reduction in 3H-ornithine formation of about 60%. The effects of LPS were largely attenuated by dexamethasone (10 μmol/1). Inhibition of NO synthase by NG-monomethyl-l,-arginine (l-NMMA, 100 μmol/1) in LPS treated alveolar macrophages reduced the formation 3H-citrulline by more than 90% and restored the 3H-ornithine formation. After culturing in the presence of LPS the ratios extra/intracellular of 3H-citrulline and 3H-ornithine were markedly enhanced and this effect was not dexamethasone sensitive. During incubation of rabbit alveolar macrophages a marked formation of 3H-ornithine (about 5.3% of the added 3H-arginine), but no significant formation of 3H-citrulline could be detected. Pretreatment with LPS tended to enhance the formation of 3H-ornithine (by 50%) without effects on 3H-citrulline. Rabbit-interferon and/or tumor necrosis factor-α present together with LPS during the culture period did not result in a significant 3H-citrulline formation. Under all conditions tested, culture media of rabbit alveolar macrophages did not contain significant amounts of nitrite (less than 0.5 nmol) whereas in culture media of untreated rat alveolar macrophages 22 nmol nitrite (per 18 h) were detected, and LPS induced a 3-fold nitrite accumulation, an effect prevented by dexamethasone. In conclusion, in rabbit alveolar macrophages NO synthase activity was not detectable and could also not be induced by LPS and different cytokines, whereas in rat alveolar macrophages NO synthase was readily inducible. Alveolar macrophages of both species showed marked arginase activity. After induction of marked NO synthase activity, ornithine formation was largely reduced possibly by concomitant inhibition of arginase and/or “withdrawn” of arginine from arginase.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00170166
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 10
    Electronic Resource
    Electronic Resource
    Stimulation-induced 3H-l-citrulline accumulation in isolated longitudinal muscle myenteric plexus preparations of rat small intestine: a measure to characterize nitrergic neurons (1995)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 352 (1995), S. 506-511 
    Details
    ISSN: 1432-1912
    Keywords: Myenteric plexus ; Nitric oxide synthase ; L-Arginine ; L-Citrulline ; Muscarine receptor ; Small intestine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Abstract Nitric oxide (NO) synthase activity in rat isolated longitudinal muscle myenteric plexus preparations of the small intestine was determined by measuring the accumulation of 3H-L-citrulline during 30 min incubation with 3H-L-arginine. In untreated preparations a significant amount of 3H-L-citrulline accumulated in the tissue, about 2000 dpm/30 mg per 30 min, accounting for about 1.7% of the tissue radioactivity. Intermittent electrical field stimulation (15 Hz, 10 s trains with 10 s intervals for total of 20 min) caused a threefold increase in 3H-L-citrulline accumulation. The NO synthase inhibitor Nω-nitro-L-arginine methyl ester (L-NAME) reduced the spontaneous accumulation of 3H-L-citrulline by 65% and prevented the electrically evoked increase. Removal of extracellular calcium or addition of tetrodotoxin blocked the electrically evoked increase in 3H-L-citrulline accumulation without affecting spontaneous accumulation. Application of the calcium ionophore A 23187 (10 μmol/1) or 45 mmol/1 potassium caused a twofold increase in the accumulation of 3H-L-citrulline. The muscarine receptor agonist oxotremorine (1 μmol/l) had no effect on spontaneous accumulation of 3H-L-citrulline, but inhibited the electrically evoked increase by about 50%, and this effect was blocked by scopolamine. A substantial amount of 3H-L-citrulline (15 000 dpm) accumulated also in the incubation media, and this was increased 1.7-fold by the presence of A 23187 and 2.7-fold by electrical stimulation. However, electrically evoked increase in 3H-L-citrulline was not prevented by tetrodotoxin, in contrast to observation on tissue levels. In conclusion, during incubation with 3H-L-arginine tissue levels of 3H-L-citrulline in rat isolated longitudinal muscle myenteric plexus preparations, but not accumulation in incubation media may be used as a biochemical marker of the activity of nitrergic intestinal neurons which appear to be inhibited via muscarine receptors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169384
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...