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  • 1
    Online Resource
    Online Resource
    Verarbeitung und Anwendung der Fette : Ƶweiter Band. (1937)
    Vienna :Springer Wien,
    Details
    Keywords: Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (905 pages)
    Edition: 1st ed.
    ISBN: 9783709154120
    URL: https://ebookcentral.proquest.com/lib/geomar/detail.action?docID=6671406
    Language: German
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    GEOMAR EBL
  • 2
    Electronic Resource
    Electronic Resource
    Effects of Monovalent Ions on the Transport of Noradrenaline Across the Plasma Membrane of Neuronal Cells (PC-12 Cells) (1985)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 45 (1985), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The dependence on Na+, K+, and C1− of uptake and accumulation of [3H]noradrenaline was studied in plasma membrane vesicles isolated from PC-12 pheochromocytoma cells. Plasma membrane vesicles accumulated [3H]noradrenaline when an inward-directed gradient for Na+ and an outward-directed gradient for K+ were imposed across the vesicle membrane. Under these conditions, initial rates of uptake of [3H]noradrenaline were saturable (Km= 0.14 μM) and inhibited by a series of substrates and inhibitors of “uptake1.’ The IC50 values were positively correlated with those for inhibition of uptake into intact PC-12 cells. Uptake and accumulation [3H]noradrenaline in plasma membrane vesicles were absolutely dependent on external Na+ and C1−; they were dependent on an inwardly directed gradient for Na+ but less dependent on an inwardly directed gradient for C1−. Internal K+ strongly enhanced uptake and accumulation of [3H]noradrenaline. Rb+, but not Li+, had the capacity to replace internal K+. Two explanations are proposed for this effect of internal K+: (a) creation of a K+ diffusion potential (inside negative) provides a driving force for inward transport, and/or (b) K+ increases the turnover rate by formation of a highly mobile potassium–carrier complex. A hypothetical scheme for the transport of noradrenaline is presented.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1985.tb05536.x
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  • 3
    Electronic Resource
    Electronic Resource
    11th Meeting on Adrenergic Mechanisms: Porto, Portugal 25–27 September 2003.
Noradrenaline transporter knockout-mediated regulation of serotonin receptors in mice brain (2003)
    Oxford, UK : Blackwell Science Ltd
    Autonomic & autacoid pharmacology 23 (2003), S. 0 
    Details
    ISSN: 1474-8673
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Chemistry and Pharmacology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1474-8673.2004.00307.x
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    No Relationship of I1 and I2 Imidazoline Binding Sites to Inhibitory Effects of Imidazolines on Ligand-Gated Ion Channels (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 763 (1995), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1995.tb32431.x
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  • 5
    Electronic Resource
    Electronic Resource
    Inhibition of 5-HT3 receptor function by imidazolines in mouse neuroblastoma cells: potential involvement of σ2 binding sites (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 354 (1996), S. 245-252 
    Details
    ISSN: 1432-1912
    Keywords: N1E-115 cells ; Imidazoline receptor ; σ-Binding site ; 5-HT3 receptor ; Ligand-gated ion channels ; [3H]DTG binding sites ; [3H]GR65630 binding sites
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The influence of several imidazolines and σ-site ligands on cation influx through the 5-HT3 receptor channel in NIE-115 mouse neuroblastoma cells was studied by measuring the 2-min influx of the organic cation [14C] guanidinium induced by 1 μM 5-HT (in the presence of 10 μM substance P in all experiments). In addition, we determined specific binding of [3H]DTG (1,3-di(2-tolyl)-guanidine), a selective σ-site radioligand, and [3H] GR65630 (3-(5-methyl-1H-imidazol-4-yl)-1-(1-methyl-1H-indol-3-yl)-1-propanone), a selective 5-HT3 receptor antagonist, to membranes prepared from NIE-115 cells. The 5-HT-induced [14C]guanidinium influx was inhibited by the imidazolines, ondansetron, antazoline, idazoxan, BDF 6143 (4-chloro-2-(2-imidazolin-2-ylamino)-isoindoline), cirazoline, naphazoline, clonidine and by the guanidine agmatine, but not by the catecholamine adrenaline. The inhibitory effect of the imidazolines on cation influx through the 5-HT3 receptor channel was mimicked by the σ-site ligands, (±)-ifenprodil, (+)-3-PPP ((R)-3-(3-hydroxyphenyl)-N-propylpiperidine), DTG (1,3-di-tolyl-guanidine), haloperidol, dizocilpine, and ketamine as well as by the polyamines, arcane and spermidine. — Ondansetron inhibited [3H]GR65630 binding with high affinity, whereas inhibition of binding of this radioligand to the 5-HT3 receptor by antazoline, BDF 6143, idazoxan, cirazoline, (±)-ifenprodil, (+)-3-PPP, DTG and haloperidol occurred in the high micromolar range. In the competition experiments with [3H]DTG, (±)-ifenprodil, haloperidol, unlabelled DTG, BDF 6143 and (+)-3-PPP inhibited binding of the radioligand at moderate affinity (Ki values in the range of 1 μM or lower), whereas ondansetron, amazoline, idazoxan, cirazoline, naphazoline, clonidine, tolazoline, efaroxan, RX821002 (2-[2-(2-methoxy-1,4-benzodioxanyl)]imidazoline), ketamine and spermidine exhibited affinity in the high micromolar or millimolar range only. Comparison of the potencies of the ligands (pIC50% values) in inhibiting 5-HT-induced [14C]guanidinium influx with their affinities (pKi values) at the 5-HT recognition sites of the 5-HT3 receptor and at the σ2-sites of the N1E-115 cells by means of multiple regression analysis revealed a significant correlation with the affinities at both sites. In conclusion, our data suggest that imidazolines and σ-ligands, which as a rule possess low affinity for the 5-HT recognition site of the 5-HT3 receptor, may be assumed to exert their inhibitory effect on cation influx through the 5-HT3 receptor channels, at least in part, by interacting with σ2-binding sites.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00171054
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  • 6
    Electronic Resource
    Electronic Resource
    Saturation kinetics of the adrenergic neurone uptake system in the perfused rabbit heart. A new method for determination of initial rates of amine uptake (1978)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 302 (1978), S. 263-273 
    Details
    ISSN: 1432-1912
    Keywords: Neuronal uptake ; Initial rates of amine uptake ; Lag period for amine uptake ; Cocaine ; Rabbit heart
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. Hearts were obtained from normal or reserpine-pretreated rabbits and perfused at a constant rate (3.6 ml·g−1·min−1) with Tyrode's solution containing 14C- or 3H-sorbitol and various concentrations of 3H-(−)noradrenaline (NA), 14C-(+)NA or 3H-(±)metaraminol; when NA was used, monoamine oxidase and catechol-O-methyl transferase were inhibited. During perfusion for 2 min the arterio-venous difference for 3H and 14C activity (and in this way the removal of amine and sorbitol from the perfusion fluid) was determined at intervals of 5 s. The uptake of amine into intracellular spaces of the heart was obtained by subtraction of the removal of sorbitol from that of amine; it was cumulatively added and plotted against time (uptake curve). Uptake was overwhelmingly neuronal. 2. The uptake curves were sigmoidal: after a brief initial lag period, uptake curves became linear; there-after, the slope of the curves decreased. The last phase of divergence from linearity occurred the earlier and was the more pronounced, the higher the amine concentration. It was interpreted to indicate that neuronal efflux of amine then began to reduce net uptake. 3. From the slope of the linear phase of the uptake curves initial rates of amine transport were obtained. They were saturable with increasing amine concentrations and obeyed Michaelis-Menten kinetics. The apparent K m values of the three amines were similar in magnitude and ranged from 2.9 to 5.9 μM. Uptake was stereoselective in that the V max of (+)NA was significantly lower than that of (−)NA. Pretreatment with reserpine affected neither the K m nor the V max for uptake. Cocaine was a potent competitive inhibitor of amine transport (K i=0.5–1.0 μM). 4. The intercept of the linear phase of the uptake curves on the time axis (t lag) (corrected for the time necessary for transit through the dead space) was taken as a measure of the lag period. It declined when uptake was progressively saturated (or inhibited) by increasing substrate (or cocaine) concentrations. Moreover, t lag was always linearly correlated with the fraction of amine removed from the perfusion fluid. These findings indicate that the equilibration of the uptake sites with the substrate concentration in the perfusion fluid is delayed by the uptake process itself, especially under low saturation conditions (i.e., when S〈K m).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00508295
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  • 7
    Electronic Resource
    Electronic Resource
    Tetrodotoxin-sensitive and-resistant effects of veratridine on the noradrenergic neurone of the rat vas deferens (1983)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 324 (1983), S. 264-270 
    Details
    ISSN: 1432-1912
    Keywords: Veratridine ; Exocytotic release ; Neuronal efflux ; “Reserpine-like” effects ; Rat vas deferens
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1) The veratridine-induced release of 3H-noradrenaline from noradrenergic neurones was examined in the isolated vas deferens of either untreated or reserpine plus pargyline-pretreated rats. The rat vas deferens, whose catechol O-methyltransferase was inhibited, was first incubated with 0.4 μmol/l 3H-(−)noradrenaline (30 min) and then washed repeatedly with amine-free solution. After 120 min (i.e., well after the efflux of tritium from the tissue had reached a steady level and was predominantly of neuronal origin), washout was continued in the presence of veratridine for further 10–15 min. 2) In vasa deferentia of untreated rats, variatridine (1–100 μmol/l) caused a concentration-dependent increase in the efflux of tritium. At high concentrations of the drug (30 or 100 μmol/l), this increase in efflux was peak-like during the first 3 min (“peak response”) and then fell to a plateau (“plateau response”). In the presence of veratridine, unchanged 3H-noradrenaline accounted for about 75% of the tritium efflux (the rest being represented by deaminated 3H-catechol metabolites). 3) The “peak response” to veratridine (100 μmol/l) was abolished by tetrodotoxin (TTX; 1 μmol/l) or the absence of external Ca2+. Cocaine (10 μmol/l) affected neither the “peak response” as such nor the contribution by 3H-noradrenaline to the efflux of tritium during that response. Hence, the “peak response” was due to exocytotic release of 3H-noradrenaline from the neurone. 4) The “plateau response” to veratridine (100 μmol/l) was unaffected by the absence of external Ca2+, largely resistant to TTX (1 μmol/l) and moderately reduced by cocaine. However, both TTX and cocaine drastically changed the composition of the radioactivity during the “plateau response”: they greatly reduced or even abolished the efflux of unchanged 3H-noradrenaline and markedly increased the efflux of deaminated 3H-metabolites. Hence, the “plateau response” represented a “reserpine-like” vesicular effect of varatridine; the ensuing 3H-noradrenaline efflux out of the neurone was mediated by the neuronal amine carrier. 5) After pretreatment with reserpine (to inhibit vesicular uptake) and pargyline (to inhibit monoamine oxidase), veratridine (100 μmol/l) elicited a phasic, peak-like increase in the efflux of tritium (about 90% of which was unchanged 3H-noradrenaline). This response to veratridine was abolished by TTX (1 μmol/l) and unaffected by the absence of external Ca2+; moreover, it was greatly reduced by either cocaine (10 μmol/l) or desipramine (1 μmol/l) and, hence brought about by carrier-mediated outward transport across the axonal membrane. 6) It is concluded that, in addition to its well-known action on the fast sodium channel, veratridine somehow increases the leakage of noradrenaline from storage vesicles; this “reserpine-like” effect of veratridine is resistant to TTX and therefore not a consequence of the drug-induced changes in the sodium permeability of the axolemma.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00502621
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  • 8
    Electronic Resource
    Electronic Resource
    The effect of various ions on uptake2 of catecholamines (1985)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 328 (1985), S. 407-416 
    Details
    ISSN: 1432-1912
    Keywords: Extraneuronal catecholamine uptake ; Extraneuronal efflux of catecholamines ; Potassium gradient ; Membrane potential
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The effects of a decrease of the K+ gradient on the extraneuronal inward transport and outward movement of catecholamines were studied in rat heart, rabbit aortic rings and guinea-pig trachealis smooth muscle. Elevation of the extracellular K+ concentration caused a) inhibition of the corticosteroid-sensitive extraneuronal uptake (uptake2) of3H-isoprenaline in rat heart and of3H-noradrenaline in rabbit aorta, and b) acceleration of efflux of3H-isoprenaline from rat heart,3H-noradrenaline from rabbit aorta and adrenaline (measured by microphotometry) from guinea-pig trachealis muscle. 2. In rat heart and rabbit aorta, the acute omission of one or the other of the ions Na+, Cl−, K+ or Ca2+ from the perfusion or incubation medium had no effect on initial rates of uptake2 of catecholamines, except that the absence of K+ had a small inhibitory effect in the rat heart. 3. The prolonged absence of Na+, Ca2+ or K+ from the perfusion or incubation medium caused a marked inhibition of uptake2 of catecholamines. These inhibitory effects developed more quickly in rat heart than in rabbit aorta. 4. These results are compatible with the possibility that either the K+ gradient across the cell membrane or the resting membrane potential is the force driving uptake2.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00692909
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  • 9
    Electronic Resource
    Electronic Resource
    The extraneuronal compartments for the distribution of isoprenaline in the rat heart (1983)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 324 (1983), S. 169-179 
    Details
    ISSN: 1432-1912
    Keywords: Extraneuronal uptake ; 3H-Isoprenaline ; Rat heart ; Corticosterone ; Compartment analysis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The distribution of 3H-isoprenaline in the perfused rat heart was re-examined. After initial loading with 3H-isoprenaline hearts were washed out with amine-free solution; the efflux curves were subjected to the peeling technique, and half times for efflux and compartment sizes were determined. In contrast to earlier reports from this department (Bönisch et al. 1974; Bönisch 1978), 3H-isoprenaline was found to distribute mainly into one extraneuronal compartment, irrespective of whether COMT was intact or inhibited (by the presence of U-0521). It was also not influenced by pretreatment of the animals with reserpine. This type of distribution was influenced neither by the concentration of isoprenaline nor by the duration of the loading of the tissue with the amine. The one major extraneuronal distribution compartment of 3H-isoprenaline has the characteristics of the “old” compartment III: it has a relatively short half time for the efflux of 3H-isoprenaline and it has a high activity of COMT. Moreover, corticosterone inhibits the inward and outward flux of 3H-isoprenaline into and from compartment III. The K i for the inhibition by corticosterone of the efflux of 3H-isoprenaline (2 μmol/l) is very similar to the K i for impairment of uptake2 (determined by Bönisch 1978). Apart from the major distribution compartment III, two minor distribution compartments were detected: On the one hand, experiments with hearts which had an intact COMT revealed that a minor distribution compartment IV (Characterized by a long half time for efflux and by an absence of COMT activity) may exist, although its magnitude does not exceed one tenth of the former compartment IV. In addition, part of the quickly equilibrating (and rather small) compartment II was corticosterone-sensitive. When the results of Azevedo et al. (1983) are considered together with the present results, compartment III appears to represent the uptake of 3H-isoprenaline into myocardial cells, while it is likely that radioactivity accumulated in the smooth muscle of blood vessels may constitute the corticosterone-sensitive part of compartment II.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00503890
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  • 10
    Electronic Resource
    Electronic Resource
    The mechanism of the 3H-noradrenaline releasing effect of various substrates of uptake1: multifactorial induction of outward transport (1987)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 336 (1987), S. 602-610 
    Details
    ISSN: 1432-1912
    Keywords: Adrenergic nerve endings ; Outward transport of noradrenaline ; Uptake1 ; Indirectly acting sympathomimetic amines ; Release of noradrenaline
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The mechanism of action of indirectly acting sympathomimetic amines was studied in the rat vas deferens, after inhibition of vesicular uptake (by reserpine), of MAO (by pargyline) and of COMT (by U-0521). 1. K m-values for the neuronal uptake of 12 substrates were determined as the IC50 of the unlabelled substrate inhibiting the initial rate of neuronal uptake of 0.2 μmol/l 3H-(−)-noradrenaline. The IC50 ranged from 0.35 μmol/l (for (+)-amphetamine) to 44.3 μmol/l (for 5-HT). The V max (determined for 8 substrates) was substrate-dependent. 2. Tissues were loaded with 0.2 μmol/l 3H-(−)-noradrenaline and then washed out with amine-free solution. All 12 substrates of uptake1, induced an outward transport of 3H-noradrenaline, and equieffective concentrations were positively correlated with K m. Moreover, the EC50 for release greatly exceeded K m. It is proposed that this discrepancy between EC50 and K m is indicative of the fact that at least four factors (each one in strict dependence on K m) contribute to the initiation of outward transport of 3H-noradrenaline: a) the appearance of the carrier on the inside of the axonal membrane (facilitated exchange diffusion), b) the co-transport of Na+, c) the co-transport of Cl− (both lowering the K m for 3H-noradrenaline at the inside carrier), and d) inhibition of the re-uptake of released 3H-noradrenaline (through competition for the outside carrier). 3. At least for amezinium, V max. appears to limit the maximum rate of outward transport. 4. For some substrates (especially for the highly lipophilic ones) bell-shaped concentration-release curves were obtained. Apparently, inward diffusion of the substrates can lead to partial saturation of the inside carrier. Moreover, if release is expressed as a FRL (fractional rate of loss), loading with 37 μmol/l 3H-(−)-noradrenaline decreased the releasing effect of various substrates. In this case the inside carrier appears to be partially saturated by the high axoplasmic concentration of 3H-noradrenaline. 5. Very high concentrations (especially of highly lipophilic substrates) were able to induce an additional intraneuronal release mechanism, presumably by increasing the pH inside storage vesicles.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00165750
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