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Neurotransmission adrenergic

Unlike aniracetam, pramiracetam does not appear to interact with dopaminergic, serotonergic, or adrenergic neurotransmission (72). The agent inhibits prolylendopeptidase in certain brain areas, but its inhibition constant, iC, is only 11 ]lM (69). The absence or weak activity of this compound with various neuronal systems appears to make it less likely to be of significant therapeutic value than other members of this class of agents. [Pg.95]

Westfall TC (1977) Local regulation of adrenergic neurotransmission. Physiol Rev 57,659-728... [Pg.185]

Fig. 2. Schematic drawing of the adrenergic neurotransmission. Dependent on the target organ, the postsynaptic, G-protein-coupled receptors are of the a -, 2- or /Sj-adrenoceptor subtype. A presynaptic 2-adrenoceptor acts as an inhibitory autoreceptor. The predominant elimination pathway of the transmitter noradrenaline (NA) is the neuronal re-uptake... Fig. 2. Schematic drawing of the adrenergic neurotransmission. Dependent on the target organ, the postsynaptic, G-protein-coupled receptors are of the a -, 2- or /Sj-adrenoceptor subtype. A presynaptic 2-adrenoceptor acts as an inhibitory autoreceptor. The predominant elimination pathway of the transmitter noradrenaline (NA) is the neuronal re-uptake...
FIGURE 7—38. Shown here are various drug combinations for use in treatment resistant unipolar depression to boost adrenergic neurotransmission, which include either norepinephrine, dopamine, or both. [Pg.286]

Tubocurine In isolated rabbit ear artery, antagonized dopamine-induced inhibition of adrenergic neurotransmission 649... [Pg.201]

Hedqvist P, Fredholm BB (1976) Effects of adenosine on adrenergic neurotransmission prejunctional inhibition and postjunctional enhancement. Naunyn Schmiedeberg s Arch Pharmacol 293 217-23... [Pg.366]

The action of tyramine on nerve receptors is mainly indirect by release of norepinephrine and dopamine from neuronal storage sites (363, 384). Tyramine and its /3-oxidized counterpart octopamine have been referred to as false neurotransmitters because these compounds can be taken up, stored, and released from nerve endings in a way similar to those of the principal neurotransmitters norepinephrine and dopamine (385). Octopamine was first discovered in salivary glands of octopods (386). The compound is widely distributed in the animal kingdom and is present in high amounts in the nervous system of several species of invertebrates such as molluscs and arthropods, where it acts as a specific transmitter substance (387). Octopamine may also play a role in the regulation of adrenergic neurotransmission in mammals (387). Administration of octopamine to intact animals produces a transient rise in blood pressure (388). [Pg.143]

Haas, D.A. George, S.R. (1989) Neuropeptide Y-induced effects on hypothalamic corticotropin-releasing factor content and release are dependent on noradrenergic/adrenergic neurotransmission. Brain Res. 498, 333 338. [Pg.32]

Adrenergic neurotransmission can be blocked either by decreasing sympathetic outflow from the brain (Table 2.3), suppressing norepinephrine release from presynaptic neurons (Table 2.3) or blocking postsynap-tic adrenergic receptors (Table 2.4). [Pg.20]

Adrenergic Receptors and Drugs Affecting Adrenergic Neurotransmission... [Pg.571]

Prostaglandins have also been suggested to have a modulating function on neuronal activity. Administration of exogenous PGE compounds has been shown to have an inhibitory effect on adrenergic neurotransmission in the peripheral nervous system [229]. This could be shown to be due to an inhibitory effect on norepineph-... [Pg.18]

Rusch NJ, Shepherd JT, Vanhoutte PM. The effect of profound cooling on adrenergic neurotransmission in canine cutaneous veins. J Physiol 311,57-65, 1981. [Pg.210]

Many drugs are known to deplete tissue stores of catecholamines. The most thoroughly studied example of this type is reserpine. This drug produces an almost complete depletion of catecholamines from all sites in the body. This depletion is long lasting, with recovery taking up to a week or more. The depletion is associated with a severe impairment of adrenergic neurotransmission and medullary function. [Pg.265]

Although the concept of false transmitters as substances with weaker agonist activity diluting the normal stores of adrenergic transmitter is attractively simple and elegant, the true pharmacological situation is in fact quite complex. The overall effect of the introduction of a false transmitter on adrenergic neurotransmission depends on a number of different factors. [Pg.295]

Adrenergic Neurotransmission. CIBA Foundation Study Group, Churdiill, London, 1968. [Pg.305]

Malmfors, Tq Histocheinical Studies of Adrenergic Neurotransmission, in Adrenergic Neurotransmission. CIBA Foundation Study Group, Churchill, London, 1968, pp. 26-36. [Pg.305]

Griffith, R., Drugs affecting adrenergic neurotransmission, in Foy s Principles of Medicinal Chemistry,D.A. andLemke, T.L., Eds., Lippincott Williams WiMns, 2002, 292. [Pg.303]


See other pages where Neurotransmission adrenergic is mentioned: [Pg.299]    [Pg.524]    [Pg.528]    [Pg.778]    [Pg.431]    [Pg.967]    [Pg.395]    [Pg.516]    [Pg.549]    [Pg.571]    [Pg.130]    [Pg.303]   
See also in sourсe #XX -- [ Pg.289 ]




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Affecting Adrenergic Neurotransmission

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