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
    Effects of the noradrenaline metabolites on the adrenergic receptors (1973)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 276 (1973), S. 71-88 
    Details
    ISSN: 1432-1912
    Keywords: Noradrenaline Metabolites ; Guinea-Pig Atria ; Nictitating Membrane ; Normetanephrine ; Metanephrine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of the five noradrenaline (NA) metabolites and of the O-methylated metabolite of adrenaline, metanephrine, were studied in a tissue with adrenergic beta-receptors (guinea-pig atria) and in a tissue with predominance of alpha-receptors (cat's nictitating membrane). In atria, normetanephrine and metanephrine elicited positive chronotrophic effects which were mediated through the beta-receptors. Both O-methylated metabolites had only 1/1000th of the potency of NA. In the normally innervated nictitating membrane normetanephrine and metanephrine elicited maximal responses of the same magnitude as NA. While normetanephrine had one half of the potency of NA, metanephrine was even more potent than NA. The effects of normetanephrine or metanephrine were mediated through the activation of the alpha-receptors and were not potentiated by either cocaine or denervation. Neither the deaminated nor the deaminated-O-methylated metabolites of NA had activity as agonists on alpha-or beta-receptors in concen-of up to 1×10−4M. These metabolites did not elicit alpha-or beta-receptor block in concentrations of up to 1×10−4M.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00500780
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Inhibition by dopamine of 3H-noradrenaline release elicited by nerve stimulation in the isolated cat's nictitating membrane (1975)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 289 (1975), S. 179-203 
    Details
    ISSN: 1432-1912
    Keywords: Nerve Stimulation ; Noradrenaline ; Dopamine ; Nictitating Membrane ; Neurotransmission ; α-Adrenoceptors ; Dopamine Receptors
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary After loading the isolated nerve-muscle preparation of the cat nictitating membrane with 3H-(±)-noradrenaline the effects of exogenous dopamine and (-)-noradrenaline were determined on 3H-transmitter overflow elicited by nerve stimulation in the presence of cocaine, 29 μM. Dopamine, 0.20 μM, and (-)-noradrenaline, 0.18 μM, inhibited 3H-noradrenaline release elicited by nerve stimulation at 4 or 10 Hz. Similar results were obtained with apomorphine 0.03 or 0.1 μM. Chlorpromazine, 1 μM, or pimozide, 1 μM, antagonized selectively the reduction in 3H-noradrenaline release obtained with dopamine or apomorphine, without affecting the inhibition obtained with (-)-noradrenaline. Phentolamine, 1 μM, antagonized more effectively the inhibitory effects of (-)-noradrenaline than those of dopamine. Phenoxybenzamine, 0.29 μM, prevented the inhibition of 3H-transmitter overflow obtained with (-)-noradrenaline, dopamine or apomorphine. In the absence of cocaine neither chlorpromazine nor pimozide were able to increase 3H-transmitter overflow during nerve stimulation. In contrast to these results, block of α-adrenoceptors by phentolamine or phenoxybenzamine resulted in an increase 3H-transmitter overflow during nerve stimulation. Inhibition by dopamine of 3H-transmitter overflow appears to be mediated through dopamine receptors probably located in the outer surface of adrenergic nerve endings. These dopamine receptors differ from the prejunctional α-adrenoceptors that mediate the negative feed-back regulatory mechanism for noradrenaline release by nerve stimulation. The prejunctional inhibitory dopamine receptors are not involved in an endogenously mediated regulatory mechanism for noradrenaline release by nerve stimulation under normal conditions. The possibility that these dopamine receptors are involved in the hypotension commonly observed in patients with chronic l-Dopa treatment is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501305
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Selective inhibition by hydrocortisone of 3H-normetanephrine formation during 3H-transmitter release elicited by nerve stimulation in the isolated nerve-muscle preparation of the cat nictitating membrane (1975)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 287 (1975), S. 261-275 
    Details
    ISSN: 1432-1912
    Keywords: Nerve Stimulation ; Noradrenaline Metabolites ; Hydrocortisone ; Extraneuronal Uptake ; Normetanephrine ; Nictitating Membrane
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The metabolism of 3H-noradrenaline released by nerve stimulation in the isolated nerve-muscle preparation of the cat nictitating membrane was determined under control conditions and in the presence of hydrocortisone, 28 μM, a concentration which inhibits the high affinity extraneuronal uptake of noradrenaline in this tissue. in the controls the main fraction in the overflow elicited by stimulation at 10 Hz during 2 min was the deaminated glycol, 3H-DOPEG (3,4-dihydroxyphenylglycol), which accounted for 45.2±2.96% of the total radioactivity. Under these conditions, 3H-noradrenaline represented 30.8±1.92%, while 3H-normetanephrine accounted for 14.5±0.94% of the total overflow of radioactivity. During exposure to hydrocortisone there was a selective inhibition in 3H-normetanephrine formation from 3H-noradrenaline released by stimulation while the other fractions were not affected significantly. In contrast to these results, there were no changes in the spontaneous outflow of 3H-normetanephrine during exposure to hydrocortisone. The results obtained support the view that 3H-normetanephrine in sponteneous release originates from the activity of prejunctional catechol-O-methyltransferase. On the other hand, 3H-normetanephrine formed during transmitter release elicited by nerve stimulation is due to the activity of extraneuronal catechol-O-methyltransferase. Access of 3H-noradrenaline released by nerve stimulation to extraneuronal catechol-O-methyltransferase is mediated through the high-affinity, hydrocortisone-sensitive extraneuronal uptake mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501472
    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...