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  • Rat vas deferens  (8)
  • Efflux of noradrenaline metabolites  (2)
  • Rabbit heart  (2)
  • 11
    Electronic Resource
    Electronic Resource
    The inhibitory effect of some monovalent cations on the stimulation by Na+ of the neuronal uptake of noradrenaline (1979)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 309 (1979), S. 89-97 
    Details
    ISSN: 1432-1912
    Keywords: Neuronal noradrenaline uptake ; Na+-dependent noradrenaline transport ; Effect of monovalent cations ; Rat vas deferens
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. Vasa deferentia obtained from reserpine-pretreated rats were incubated (after inhibition of both monoamine oxidase and catechol O-methyltransferase) in media containing 1.1 μmol·l−1 3H-(−)noradrenaline and various concentrations of Na+ (0–140 mmol·l−1; isosmolality maintained by sucrose or by several monovalent cations). Initial rates of neuronal uptake were determined in each single vas from the difference between “total” and “cocaine-resistant” uptake of 3H-noradrenaline. 2. The “cocaine-resistant” uptake (i.e., the distribution of 3H-noradrenaline observed in the presence of 100 μmol·l−1 cocaine) was considered to be nonneuronal. It was entirely independent of both the external Na+ concentration and the substance used to replace Na+ (or NaCl) in the medium. 3. The neuronal uptake of 3H-noradrenaline was virtually absent in Na+-free medium and was progressively stimulated by increasing Na+ concentrations. The stimulation of uptake by low Na+ concentrations was most pronounced when Tris+ was used to replace Na+; i.e., all other substitutes tested here (including sucrose, Li+, choline+ and K+) inhibited neuronal uptake when compared with Tris+. 4. While the Na+-dependent stimulation of neuronal uptake followed Michaelis-Menten kinetics in Tris+- or Li+-containing media, the kinetics of uptake stimulation by Na+ were rather complex in media containing choline+ or K+ as the substitute cation. 5. Li+ and K+ acted as competitive inhibitors with respect to Na+, whereas the inhibition of neuronal uptake by choline+ was the more pronounced, the higher the concentration of external Na+. 6. At concentrations higher than 25 mmol·l−1, the impairment of neuronal uptake by K+ exceeded that predictable from competitive inhibition of the action of Na+. This was due to the fact that high external K+ concentrations decelerated net uptake very early in the time course of amine accumulation, so that initial rates of uptake are likely to be underestimated under these conditions. 7. Thus, apart from maintaining isosmolality, several substances used to replace Na+ in the medium have inhibitory effects which must be considered in experiments designed to examine the role of Na+ in membrane transport of noradrenaline.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501215
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    Paper (German National Licenses)
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  • 12
    Electronic Resource
    Electronic Resource
    The effect of (±)-dobutamine on adrenergic nerve endings (1989)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 339 (1989), S. 79-84 
    Details
    ISSN: 1432-1912
    Keywords: Chromaffin granule ghosts ; PC-12 cells ; Rat vas deferens ; Dobutamine ; Uptake1
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Possible effects of (±)-dobutamine on adrenergic nerve endings were determined in experiments with ghosts of bovine chromaffin granules, with rat phaeochromocytoma (PC-12) cells and with the rat vas deferens. Dobutamine inhibited the vesicular uptake of a mixture of 70% adrenaline + 30% 3H-noradrenaline into ghosts, with an IC50 of 1.7 μmol/l. Dobutamine inhibited uptake, of 3H-noradrenaline in PC-12 cells (with an IC50 of 0.38 μmol/l) without being a substrate. However, dobutamine easily entered PC-12 cells by diffusion. After inhibition of MAO, COMT and vesicular uptake dobutamine (15 and 45 μmol/l) released tritium from rat vasa deferentia preloaded with 3H-noradrenaline. Equi-inhibitory concentrations of dobutamine and desipramine (against uptake1) were equireleasing. On the other hand, when MAO and vesicular uptake were intact, dobutamine (15 μmol/l) increased the efflux of tritium from preloaded vasa deferentia much more than did an equi-inhibitory concentration of desipramine. Most of the released tritium was then 3H-DOPEG. Dobutamine is a potent inhibitor of uptake1 as well as of vesicular uptake; moreover, it easily diffuses into adrenergic nerve endings. Hence, it blocks the neuronal and the vesicular re-uptake of noradrenaline; consequently, when MAO and vesicular uptake are intact, dobutamine increases the net leakage of noradrenaline from the storage vesicles, thereby leading to an efflux of deaminated metabolites. However, dobutamine is virtually unable to release noradrenaline into the extracellular space.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00165130
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
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