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
Filter
  • Articles: DFG German National Licenses  (14)
  • Noradrenaline Release  (10)
  • Rabbit pulmonary artery  (4)
  • 1
    Electronic Resource
    Electronic Resource
    Wirkung von Angiotensin auf Funktion und Noradrenalinabgabe isolierter Kaninchenherzen in Ruhe und bei Sympathicusreizung (1969)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 265 (1969), S. 170-186 
    Details
    ISSN: 1432-1912
    Keywords: Angiotensin ; Noradrenaline Release ; Isolated Rabbit Heart ; Sympathetic Nerves ; Angiotensin ; Noradrenalinabgabe ; Isoliertes Kaninchen herz ; Sympathische Nerven
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. The influence of angiotensin on the isolated rabbit heart perfused at constant pressure or constant flow was investigated at rest and during electrical stimulation of the postganglionic sympathetic nerves. 2. In low concentrations (32–100ng/min or 1.4–5.3 ng/ml) angiotensin had considerable positive inotropic effects, while its chronotropic effects were weak and variable. High concentrations decreased the rate of beat, and an increase in the height of contraction was preceded by a transient phase of inhibition. In hearts perfused at constant pressure, angiotensin diminished coronary flow. The positive inotropic effect of angiotensin was not accompanied by the appearance of increased amounts of noradrenaline in the venous effluent. 3. Angiotensin caused a dose-dependent increase in the output of noradrenaline induced by sympathetic nerve stimulation. The peptide was most potent in hearts perfused at constant flow; the threshhold dose of angiotensin for this procedure was 3.2 ng/min (128 pg/ml), and maximal effects (i.e., an increase by 81%) were observed with 32 ng/min (1.28 ng/ml). Doses about three times higher were required to obtain similar effects in hearts perfused at constant pressure. The reduction of coronary flow as seen under these conditions may be responsible for the weaker effect of angiotensin. Continuous infusion increased the output of noradrenaline during several successive stimulation periods. 4. In most cases, the increase in output of noradrenaline induced by angiotensin did not lead to an increase in the response of the pacemaker or of the myocardium to sympathetic stimulation. Only in hearts perfused at constant flow during infusion of 32 ng/min of angiotensin the positive inotropic effect of sympathetic stimulation was significantly augmented. 5. The results indicate that angiotensin may modulate the activity of the autonomic nervous system by influencing peripheral sympathetic nerves.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00997149
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    An analysis of the effects of amezinium on postganglionic sympathetic neurones (1980)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 314 (1980), S. 1-11 
    Details
    ISSN: 1432-1912
    Keywords: Amezinium ; Rabbit heart ; Rabbit pulmonary artery ; Intraneuronal monoamine oxidase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Effects of amezinium on postganglionic sympathetic neurones were studied in the heart and pulmonary artery of the rabbit. 1. In isolated perfused hearts, amezinium increased the rate of beat. The effect was antagonized by propranolol or cocaine and by pretreatment with reserpine or 6-hydroxydopamine. 2. In hearts pre-perfused with 3H-noradrenaline, amezinium 0.003 μM reduced the outflow of 3H-DOPEG by 50%. 0.1 μM and higher concentrations in addition reduced the outflow of 3H-MOPEG and increased the outflow of 3H-noradrenaline and 3H-NMN. The outflow of 3H-DOMA and 3H-VMA was not changed. Cocaine prevented the effects of amezinium. When hearts were first perfused with amezinium and then with 3H-noradrenaline, the subsequent outflow of 3H-DOMA was abolished. 3. Hearts were perfused with 3H-noradrenaline 50 nM, and the arterio-venous difference of the 3H-amine was determined. Amezinium 0.29 μM reduced the arterio-venous difference by 50%. 4. Rabbits received intravenous injections of amezinium and were killed 30 min later. The hearts were perfused with 3H-noradrenaline. Pretreatment with amezinium 10 μg/kg diminished the outflow of 3H-DOPEG during the perfusion with 3H-noradrenaline, whereas pretreatment with 1 mg/kg was necessary to decrease the arterio-venous difference of 3H-noradrenaline. 5. Amezinium 4 μM caused 50% inhibition of MAO in crude homogenates and mitochondrial preparations from rabbit hearts, with 3H-noradrenaline as substrate. 6. In pulmonary artery strips preincubated with 3H-noradrenaline, the effects of amezinium on the outflow of 3H-compounds were similar to its effects in the heart. In addition, amezinium reduced the overflow of 3H-DOPEG and enhanced contractions elicited by electrical stimulation. 7. Amezinium is a relatively weak inhibitor of MAO in cell-free preparations. However, in the intact tissue it is a very potent inhibitor of the MAO inside noradrenergic neurones because it is concentrated in these neurones by the noradrenaline uptake mechanism. Being a substrate of uptake, amezinium also inhibits the uptake of noradrenaline. In contrast to bretylium which also inhibits intraneuronal MAO, amezinium is not an adrenergic neurone blocking agent. Concentrations higher than those needed to block intraneuronal MAO in addition release noradrenaline and thereby increase the rate of cardiac contraction.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00498425
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Interactions of angiotensin and cocaine on the output of noradrenaline from isolated rabbit hearts (1970)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 265 (1970), S. 383-386 
    Details
    ISSN: 1432-1912
    Keywords: Angiotensin ; Cocaine ; Isolated Rabbit Heart ; Sympathetic Nerves ; Noradrenaline Release
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The output of noradrenaline from isolated rabbit hearts during sympathetic nerve stimulation is increased by angiotensin (1.3 ng/ml) to 176% of the preceding control stimulation period. During inhibition of noradrenaline re-uptake by cocaine (5 or 15 μg/ml), the augmentation caused by the peptide is unchanged (181 and 171%, respectively). The result favours the assumption that angiotensin enhances the output of noradrenaline by an increase of the amount of transmitter liberated from the nerve terminals rather than by interfering with transmitter inactivation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00997196
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Morphine tolerance and dependence in noradrenaline neurones of the rat cerebral cortex (1975)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 288 (1975), S. 415-426 
    Details
    ISSN: 1432-1912
    Keywords: Brain Cortex Slices ; Noradrenaline Release ; Morphine ; Drug Tolerance ; Drug Dependence
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary By subcutaneous implantation of 2 or 13 morphine pellets (75 mg morphine/pellet), rats were made tolerant to, and dependent on narcotic analgesics. Occipital cortex slices from dependent animals and placebo-implanted controls were incubated with (-)-3H-noradrenaline and subsequently superfused with physiological salt solution. The accumulation of 3H-noradrenaline was not changed by pretreatment with 2, but was slightly decreased by pretreatment with 13 morphine pellets. The overflow of tritium evoked by electrical field stimulation was higher in slices from morphine-implanted rats than in those from placebo controls. Morphine and levorphanol, added in vitro, inhibited the stimulation-induced overflow of tritium at, similar concentrations and to a similar degree in slices from morphine-and placebo-pretreated animals. —It is concluded that, during chronic treatment with morphine, an adaptation takes place in the brain to compensate for the acute effect of narcotic analgesics, i.e. inhibition of the release of noradrenaline by nerve impulses. The chain of events from the drug-receptor interaction to the depression of the release process can be excluded as substrate of this adaptation. During with-drawal, the compensatory changes provoke an enhanced increase of extracellular noradrenaline during nerve impulses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501286
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Sympathomimetic inhibition of noradrenaline release: Mediated by prostaglandins? (1973)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 278 (1973), S. 111-116 
    Details
    ISSN: 1432-1912
    Keywords: Rabbit Heart ; Noradrenaline Release ; α-Receptors ; Prostaglandins ; Feed-Back Inhibition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In isolated perfused rabbit hearts, the effec of oxymetazoline and phentolamine on the stimulation-induced overflow of noradrenaline was tested after the synthesis of prostaglandins had been blocked by indomethacin. Indomethacin changed neither the decrease of overflow caused by oxymetazoline nor the increase caused by phentolamine. It is concluded that prostaglandins are not involved to any major degree in the modulation of noradrenaline release by drugs with affinity to α-receptors, or in the feed-back inhibition of transmitter release mediated by the effect of liberated noradrenaline on α-receptive sites.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501869
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Alpha-receptor-mediated modulation of transmitter release from central noradrenergic neurones (1973)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 279 (1973), S. 53-60 
    Details
    ISSN: 1432-1912
    Keywords: Brain Slices ; Central Noradrenergic Neurones ; Noradrenaline Release ; α-Receptors ; Feed-Back Inhibition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Slices of rat cerebral cortex were preincubated with 10−7 M (-)-3H-noradrenaline, and the outflow of tritium was determined. Oxymetazoline, phentolamine and cocaine did not change the spontaneous efflux. The overflow of tritium evoked by electrical field stimulation was decreased by oxymetazoline, and enhanced by phentolamine, phenoxybenzamine, and cocaine. Oxymetazoline did not counteract the increase of the stimulation-induced overflow caused by cocaine, but strongly antagonized the increase caused by phentolamine and phenoxybenzamine. When the stimulation-induced overflow was large under control conditions (high frequency of stimulation, addition of cocaine), the inhibitory effect of oxymetazoline was diminished. The results indicate that an α-receptor-mediated feed-back control of noradrenaline release, previously demonstrated in postganglionic sympathetic nerves, also operates in central noradrenergic neurones.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00502067
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Influence of morphine and naloxone on the release of noradrenaline from rat brain cortex slices (1974)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 283 (1974), S. 357-369 
    Details
    ISSN: 1432-1912
    Keywords: Brain Cortex Slices ; Noradrenaline Release ; Morphine ; Naloxone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In slices of rat brain cortex preincubated with (−)-3H-noradrenaline, the influence of morphine and naloxone on the efflux of tritium was investigated. The spontaneous outflow of tritium was not changed by 10−7–10−5 M morphine and by 10−6–10−4 M naloxone, but was accelerated by 10−4 M morphine. Electrical field stimulation augmented tritium outflow. The overflow evoked per ppulse decreased as the frequency of stimulation was increased from 0.3 to 3 Hz, but remained approximately constant when it was further increased to 10 Hz. At frequencies of 0.3, 1, and 3 Hz, but not at 10 Hz, morphine in concentrations of 10−7–10−5 M depressed the stimulation-induced overflow of tritium. 10−4 M morphine did not influence the overflow induced by stimulation at 0.3 and 1 Hz and increased that evoked by stimulation at 10 Hz. Naloxone (10−6–10−4 M) did not change the response to stimulation. In the presence of 10−4 M naloxone, 10−6 M morphine did not diminish, and 10−5 M morphine even enhanced the stimulation-induced overflow of tritium. The inhibitory effect of 10−6 M morphine was not reduced, after tyrosine hydroxylase had been blocked by α-methyltyrosine-methylester. It is concluded that morphine through an action on specific opiate receptors inhibits the release of transmitter from cerebrocortical noradrenergic neurones evoked by nerve impulses. By an action unrelated to opiate receptors, morphine at high concentrations increases the stimulation-induced overflow of noradrenaline, presumably by inhibiting its re-uptake into nerve endings.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501109
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    Bradykinin and postganglionic sympathetic transmission (1977)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 299 (1977), S. 23-32 
    Details
    ISSN: 1432-1912
    Keywords: Bradykinin ; Prostaglandins ; Noradrenaline release ; Rabbit pulmonary artery ; Rabbit heart
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of bradykinin on postganglionic sympathetic neuroeffector transmission was studied in superfused strips of rabbit pulmonary artery and in perfused rabbit hearts. 1. In pulmonary artery strips preincubated with 3H-noradrenaline, bradykinin (1–100 nM) diminished the overflow of total tritiated compounds evoked by transmural stimulation at 2 Hz and simultaneously reduced stimulation-evoked contractions. The inhibition was stronger, the less time was allowed to elapse between addition of bradykinin and stimulation. The effect of bradykinin was not changed by atropine, but was abolished by indometacin and 5,8,11,14-eicosatetraynoic acid. 2. Separation of individual 3H-compounds showed that bradykinin and prostaglandin E2 (PGE2) caused proportionate reduction of the stimulation-evoked overflow of total radioactive material, 3H-noradrenaline, 3H-3,4-dihydroxyphenylglycol, and 3H-normetanephrine. 3. Bradykinin (1–100 nM) greatly increased the outflow of PGE from the tissue. The outflow peaked in the 3-min period after addition of bradykinin and then declined rapidly. PGF2α and the metabolites 15-keto-PGF2α, 13,14-dihydro-15-keto-PGF2α and 13,14-dihydro-15-keto-PGE2 were not detected. 4. In the heart, bradykinin (100 nM) diminished the overflow of endogenous noradrenaline evoked by sympathetic nerve stimulation at 3 Hz. Similar results were obtained in hearts perfused with atropine-containing medium. Indometacin, on the other hand, abolished the effect of bradykinin. 5. Bradykinin (100 mM) greatly increased the venous outflow of PGE. PGE2α and the metabolites 15-keto-PGF2α, 13,14-dihydro-15-keto-PGF2α and 13,14-dihydro-15-keto-PGE2 were not detected. 6. It is concluded that bradykinin inhibits the nerve impulse-evoked release of noradrenaline, and consequently postganglionic sympathetic neuroeffector transmission, by enhancing the biosynthesis of prostaglandins of the E series; however, a contribution to the inhibition by other products of the fatty acid cyclooxygenase pathway cannot be ruled out. No prostaglandin-independent presynaptic effect of bradykinin was found.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00508633
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 9
    Electronic Resource
    Electronic Resource
    Influence of extracellular noradrenaline on the stimulation-evoked secretion of noradrenaline from sympathetic nerves: Evidence for an α-receptor-mediated feed-back inhibition of noradrenaline release (1972)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 275 (1972), S. 11-23 
    Details
    ISSN: 1432-1912
    Keywords: Rabbit Heart ; Adrenergic Transmission ; Noradrenaline Release ; α-Receptors ; Feed-Back Inhibition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The influence of infusions of unlabelled (−)-noradrenaline on the release of previously stored (±)-14C-noradrenaline was investigated in the isolated perfused rabbit heart. 1. The spontaneous outflow of 14C-noradrenaline and total radioactivity was accelerated by unlabelled noradrenaline in concentrations of 10 and 100 ng/ml. The acceleration was prevented by cocaine (25 μg/ml) and was diminished by phenoxybenzamine (1 μg/ml). 2. In the presence of cocaine, unlabelled noradrenaline caused a concentrationdependent decrease of the stimulation-induced outflow of 14C-noradrenaline and total radioactivity, 10 ng/ml being significantly effective. In contrast, the unlabelled amine did not influence the response to stimulation in the presence of phenoxybenzamine. 3. It is concluded that extracellular noradrenaline lowers the liberation of intraneuronal noradrenaline evoked by nerve impulses. The inhibition is mediated by α-receptors which may be localized in the neuronal membrane. An analogous action of endogenous, previously liberated noradrenaline will result in a feed-back inhibition of the secretory response to stimulation.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00505064
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 10
    Electronic Resource
    Electronic Resource
    Influence of fentanyl, levorphanol and pethidine on the release of noradrenaline from rat brain cortex slices (1974)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 283 (1974), S. 371-377 
    Details
    ISSN: 1432-1912
    Keywords: Brain Cortes Slices ; Noradrenaline Release ; Fentanyl ; Levorphanol ; Pethidine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In slices of rat brain cortex preincubated with (−)-3H-noradrenaline, the influence of fentanyl, levorphanol and pethidine on the efflux of tritium was investigated. The spontaneous outflow of tritium was not changed by low, and was accelerated by high concentrations of the drugs. The overflow of tritium evoked by electrical stimulation at 3 Hz was diminished by 10−8–10−7 M fentanyl and by 10−7–10−6 M levorphanol, but was augmented by 10−5 M levorphanol. Naloxone prevented the inhibitory effect of fentanyl and levorphanol. In contrast to fentanyl and levorphanol, pethidine did not decrease, but at concentrations of 10−6–10−5 M greatly increased the stimulation-induced overflow of tritium. However, the increase was abolished, and the stimulation-evoked overflow slightly reduced, after the re-uptake of noradrenaline had been blocked by cocaine. It is concluded that fentanyl, levorphanol and pethidine share with morphine the ability to inhibit the release of transmitter from cerebrocortical noradrenaline neurones evoked by nerve impulses.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00501110
    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...