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  • 1
    Electronic Resource
    Electronic Resource
    Effects of flow-stop on the metabolism of noradrenaline released by nerve stimulation in the perfused spleen (1973)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 278 (1973), S. 179-194 
    Details
    ISSN: 1432-1912
    Keywords: Noradrenaline ; Noradrenaline Metabolites ; Perfused Spleen ; Nerve Stimulation ; Transmitter Overflow
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The metabolic pathway of 3H-noradrenaline released spontaneously and by nerve stimulation was studied in the isolated perfused spleen of the cat. The deaminated glycol, DOPEG, (3,4 dihydroxyphenylglycol) was the main metabolite in spontaneous outflow, accounting for 62.5±1.6% of the total radioactivity (n=13). Of the total increase in radioactive products elicited by nerve stimulation at 5 Hz or 10 Hz around 30% was accounted for by the noradrenaline metabolites, particularly DOPEG and the O-methylated fraction. In the presence of 2.9×10−6 M of cocaine the total overflow of radioactivity induced by stimulation was unchanged but DOPEG formation from released noradrenaline was abolished. These findings indicate that DOPEG formation results from the recapture of the released transmitter by adrenergic nerve endings and subsequent intraneuronal deamination. The total overflow of noradrenaline was reduced by flow-stop while the metabolism of the released transmitter was increased significantly. Cocaine, 2.9×10−6 M, prevented the increase in DOPEG when stimulation was applied under flow-stop conditions. The decrease in noradrenaline overflow induced by flow-stop is partly due to the increase in the metabolism of the released transmitter.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00500649
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  • 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
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  • 3
    Electronic Resource
    Electronic Resource
    Effects of the noradrenaline metabolites on tyrosine hydroxylase activity in guinea-pig atria (1973)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 280 (1973), S. 315-330 
    Details
    ISSN: 1432-1912
    Keywords: Tyrosine Hydroxylase ; Noradrenaline ; Noradrenaline Metabolites ; Dopa Decarboxylase ; Guinea-pig Atria ; Noradrenaline Synthesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of noradrenaline, its five metabolites and metanephrine, were studied on tyrosine hydroxylase activity in guinea-pig atria. The deaminated metabolite, (±)-3,4-dihydroxyphenylglycol (DOPEG), was equipotent with (±)-noradrenaline in its inhibitory action on tyrosine hydroxylase activity in the homogenates of guinea-pig atria. The inhibition by DOPEG was competitive with the cofactor, reduced pteridine. The deaminated acid, 3,4-dihydroxymandelic acid (DOMA) and the O-methylated deaminated acid, 3-methoxy, 4-hydroxymandelic acid (VMA) had 1/50th and 1/30th, respectively, the potency of noradrenaline in inhibiting tyrosine hydroxylase. The rest of the metabolites did not inhibit tyrosine hydroxylase in homogenates in concentrations up to 1.0 mM. In intact guinea-pig atria noradrenaline was considerably more potent than DOPEG in inhibiting tyrosine hydroxylase. Normetanephrine 1.4×10−4 M inhibited tyrosine hydroxylase in the intact tissue but failed to inhibited the enzyme in the homogenate even in higher concentrations. The effect of normetanephrine in the intact tissue is related to the ability of this compound to release endogenous noradrenaline. A reserpine-like agent, Ro 4-1284, did not inhibit tyrosine hydroxylase activity in the homogenate but in the intact tissue the inhibition was more than 50%. This effect of Ro 4-1284 in the intact tissue appears to be related to the releasing effects of this agent and to an increase in the axoplasmic levels of DOPEG. Since the formation of the deaminated glycol, DOPEG, represents the main metabolic pathway for the neurotransmitter in adrenergic nerve endings, the present results are compatible with the view that, in addition to the pool of extravesicular noradrenaline, the cytoplasmic concentration of DOPEG could also participate in the regulation of the activity of tyrosine hydroxylase.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501354
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  • 4
    Electronic Resource
    Electronic Resource
    Heterotopic heart transplant in the cat (1974)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 283 (1974), S. 389-407 
    Details
    ISSN: 1432-1912
    Keywords: Heterotopic heart transplant ; Cardiac denervation ; Noradrenaline ; Isoprenaline ; Supersensitivity of the allografted heart ; Cardiac Rate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A technique for the heterotopic heart transplant into the abdominal cavity of the cat has been developed as an experimental model for studies of the development of sympathetic denervation and of allograft rejection. Under our experimental conditions and in the absence of immunosuppressive treatment the survival rate of the transplant was higher than that reported for dogs. Immediately after the operation the cardiac rate of the transplanted heart was reduced from 153±9 (n=36) to 131±9 beats/min (n=36). After the third postoperative day the rate of the graft increased steadily, reaching 185±8 beats/min (n=15) on the seventh day. The endogenous noradrenaline (NA) content in the right atrium was completely depleted 3 days after the operation (controls 2.07±0.45 μg NA/g; transplants 0.09±0.04 μg NA/g). In the ventricles a similar degree of depletion was obtained on the seventh postoperative day (controls 1.69±0.25 μg NA/g; transplants 0.06±0.02 μg NA/g). “In vitro” studies of strips of left atria revealed supersensitivity to the inotropic effect of (−)-noradrenaline 7 days after the surgical procedures. On the 7th day maximal responses of the atria to (−)-noradrenaline were significantly lower than those of the corresponding controls. There was no increase in sensitivity to (−)-isoprenaline 7 days after the operation. The results obtained demonstrate that the transplanted heart undergoes sympathetic denervation and develops supersensitivity to noradrenaline. The latter appears to be the reason for the tachycardia which develops between the third and the seventh day after the operation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501112
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  • 5
    Electronic Resource
    Electronic Resource
    Evidence for the presynaptic location of the alpha-adrenoceptors which regulate noradrenaline release in the rat submaxillary gland (1978)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 304 (1978), S. 21-26 
    Details
    ISSN: 1432-1912
    Keywords: Submaxillary glands ; Presynaptic receptors ; Potassium ; Phentolamine ; Transmitter release ; Noradrenaline
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Fifteen days after duct ligation, the wet weight of the rat submaxillary gland was reduced to 40% of the contralateral control. Under these experimental conditions, the noradrenaline (NA) content expressed as μg/g was 1.2±0.1 in the control glands and 1.9±0.2 in the atrophied glands. The accumulation of 3H-NA in the tissue expressed as μCi/gland, did not differ when the atrophied glands were compared with the corresponding controls. Consequently, the uptake and retention of 3H-NA was not modified by the atrophy of the secretory cells of the gland. The spontaneous efflux of radioactivity from normal and atrophied submaxillary glands prelabelled with 3H-NA was similar. The analysis of the metabolic pattern in both experimental groups revealed that in the spontaneous outflow and also during potassium-induced depolarization, the formation of the O-methylated metabolite, 3H-normetanephrine (NMN) was reduced by more than 50% in the atrophied glands. During depolarization induced by K+, a 2-fold increase in the outflow of the deaminated glycol 3H-3,4-dihydroxyphenylglycol (DOPEG) was observed. The effect of phentolamine on the release of radioactivity induced by 60 mM K+ in normal and in atrophied submaxillary gland slices prelabelled with 3H-NA was also investigated. In both experimental groups, the fractional release of total radioactivity induced by K+ was similar. Phentolamine, 3.1 μM, produced a 3-fold increase in the fractional release of radioactivity both in the control and the atrophied glands. These results indicate that the increase of K+-induced release of 3H-NA induced by phentolamine was independent of the presence or absence of the postsynaptic structures. It is concluded that phentolamine increases transmitter release by blocking alpha-adrenoceptors located in the noradrenergic nerve endings of the rat submaxillary gland.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501373
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  • 6
    Electronic Resource
    Electronic Resource
    Possible physiological significance of the initial step in the catabolism of noradrenaline in the central nervous system of the rat (1977)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 297 (1977), S. 119-131 
    Details
    ISSN: 1432-1912
    Keywords: Noradrenaline ; Monoamine oxidase ; K+ induced release ; Hypothalamus ; Cerebral cortex ; Noradrenaline catabolism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The hypothalamus, the cerebral cortex and the cerebellar cortex of the rat were labelled in vitro with 3H-noradrenaline (3H-NA) and the metabolism of the tritiated transmitter was studied during spontaneous outflow and under conditions of release elicited by exposure to 20 mM K+. In the three areas of the central nervous system of the rat, 3H-NA accounted for approximately 40% of the total radioactivity in spontaneous outflow while the 3H-O-methylated deaminated fraction (3H-OMDA) and 3H-3,4-dihydroxyphenylglycol (3H-DOPEG) were the main metabolites. Exposure to the reserpine-like agent, Ro 4-1284 induced a selective increase in the spontaneous outflow of 3H-DOPEG, while the contribution of the 3H-OMDA metabolites to the release induced by Ro 4-1284 was very small. During 3H-transmitter release elicited by exposure to 20 mM K+, approximately 80% of the radioactivity was collected as unmetabolized 3H-NA, while 3H-DOPEG was the main metabolite formed under these experimental conditions. Exposure to cocaine prevented 3H-DOPEG formation from 3H-NA released by K+, indicating that 3H-DOPEG was formed after neuronal reuptake of the transmitter released by K+. After in vitro labelling with 3H-NA, the unmetabolized transmitter represented approximately 70% of the total radioactivity retained in the tissue. However, when 3H-NA was administered in vivo, by intraventricular injection, only 30% of the total radioactivity retained by the tissue was accounted for by 3H-NA, and 60% of the radioactivity corresponded to the 3H-OMDA fraction, most of which was retained as 3H-MOPEG sulfate. When the rats were pretreated with pyrogallol, free 3H-DOPEG accounted for nearly 50% of the radioactivity retained in the three areas of the central nervous system after in vivo labelling with 3H-NA. When monoamine oxidase was inhibited by pargyline and 3H-NA was administered by intraventricular injection, 3H-NMN accounted for approximately 50% of the total radioactivity retained in the three areas of the central nervous system of the rat. The results obtained are compatible with the view that formation of the deamined glycol is the first step in the metabolism of 3H-NA in the rat central nervous system. In addition, it is concluded that the determination of the levels of some NA metabolites retained in the central nervous system does not necessarily represent an accurate reflection of the degree of central noradrenergic activity or of selective metabolic pathways. Consequently, in studies on the metabolism of NA it is important to take into account not only the transmitter and its metabolites in the tissue but also in the outflow from the structures studied either under in vivo or in vitro conditions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00499921
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  • 7
    Electronic Resource
    Electronic Resource
    Prejunctional effects of a purified toxin from the scorpion Tityus serrulatus (1975)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 287 (1975), S. 243-259 
    Details
    ISSN: 1432-1912
    Keywords: Scorpion Toxin ; Noradrenaline ; Noradrenaline Metabolites ; Guinea-Pig Atria ; Nerve Stimulation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of a purified fraction of the venom of the Brazilian scorpion, Tityus serrulatus, were studied in isolated guinea-pig atria previously labelled with 3H-noradrenaline. Exposure to 0.3 and 1.0 μ/ml of the scorpion toxin resulted in a long lasting positive chronotropic effect which was concentration-dependent. The increase in atrial rate coincided with an enhancement in spontaneous outflow of radioactivity. The increase in outflow of radioactive products elicited by exposure to 1.0 μg/ml of the scorpion toxin was approximately 3-fold. 3H-noradrenaline accounted for 60% of the total increase in outflow of radioactivity elicited by the scorpion toxin and the 3H-deaminated glycol (3,4-dihydroxyphenylglycol) represented the main metabolite formed, accounting for approximately 35% of the total release. 20 min after exposure to 1.0 μg/ml of the scorpion toxin the overflow of the labelled transmitter elicited by accelerans nerve stimulation (4 Hz, during 60 sec, supramaximal voltage) was increased 8-fold. This effect of the scorpion toxin appears to be unrelated to inhibition of neuronal uptake, block of α-adrenoceptors or stimulation of β-adrenoceptors. Consequently, in addition to releasing noradrenaline, the scorpion toxin enhances transmitter overflow elicited by nerve stimulation through a prejunctional effect which appears to reflect a nove mechanism of action.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501471
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  • 8
    Electronic Resource
    Electronic Resource
    Facilitation by GABA of the potassium-evoked release of 3H-noradrenaline from the rat occipital cortex (1979)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 306 (1979), S. 161-168 
    Details
    ISSN: 1432-1912
    Keywords: Noradrenaline ; GABA ; Tyramine ; Rat occipital cortex ; Cat nictitating membrane
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of GABA were studied on the release of 3H-noradrenaline (3H-NA) evoked by potassium or by tyramine from slices of the rat occipital cortex and on the release of 3H-NA elicited by nerve stimulation from the cat nictitating membrane. GABA (30–1000μM) facilitated the potassium-evoked release of 3H-NA in a concentration dependent manner. This facilitatory effect was not antagonized by bicuculline (1–100 μM) or by picrotoxin (1–100 μM). Exposure to the GABA agonist muscimol (1–100 μM) did not affect either the spontaneous or the potassium-evoked release of 3H-NA. The facilitatory effect of GABA on the release of 3H-NA elicited by potassium was observed when the occipital cortex slices were exposed to 20 mM K+ during 1 min. When depolarization was induced by 35 mM K+ exposure to GABA failed to enhance the release of the neurotransmitter. GABA 300 μM did not affect the release of the labelled neurotransmitter evoked by exposure to tyramine 0.6 μM. In the cat nictitating membrane prelabelled with 3H-NA, the stimulation evoked release of the labelled neurotransmitter was not affected by GABA (10–300 μM). In conclusion, GABA has a facilitatory effect on the calcium-dependent, potassium evoked release of 3H-NA when the depolarization is of moderate degree. This effect of GABA appears to be selective for the central nervous system.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00498986
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