Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Noradrenaline enhancement

Modulation of second-messenger pathways is also an attractive target upon which to base novel antidepressants. Rolipram [61413-54-5] an antidepressant in the preregistration phase, enhances the effects of noradrenaline though selective inhibition of central phosphodiesterase, an enzyme which degrades cycHc adenosiae monophosphate (cAMP). Modulation of the phosphatidyl iaositol second-messenger system coupled to, for example, 5-HT,, 5-HT,3, or 5-HT2( receptors might also lead to novel antidepressants, as well as to alternatives to lithium for treatment of mania. Novel compounds such as inhibitors of A-adenosyl-methionine or central catechol-0-methyltransferase also warrant attention. [Pg.234]

Antidepressants are used in the treatment of neuropathic pain and headache. They include the classic tricyclic compounds and are divided into nonselective nor-adrenaline/5-HT reuptake inhibitors (e.g., amitriptyline, imipramine, clomipramine, venlafaxine), preferential noradrenaline reuptake inhibitors (e.g., desipramine, nortriptyline) and selective 5-HT reuptake inhibitors (e.g., citalopram, paroxetine, fluoxetine). The reuptake block leads to a stimulation of endogenous monoaminer-gic pain inhibition in the spinal cord and brain. In addition, tricyclics have NMDA receptor antagonist, endogenous opioid enhancing, Na+ channel blocking, and K+ channel opening effects which can suppress peripheral and central sensitization. Block of cardiac ion channels by tricyclics can lead to life-threatening arrhythmias. The selective 5-HT transporter inhibitors have a different side effect profile and are safer in cases of overdose [3]. [Pg.77]

Ephedrine enhances the release of the hormone norepinephrine in the body, and also binds to the same receptors as that hormone, causing excess calories to be converted to heat instead of being stored as fat. It also raises blood pressure. Epinephrine and norepinephrine are also known as adrenaline and noradrenaline. Ephedrine thus acts to stimulate an adrenaline rush. [Pg.160]

With respect to in vivo noradrenaline release, several studies report increases in response to nicotine challenge after chronic administration, consistent with a sensitised response. Sharp and co-workers demonstrated that rats self-administering nicotine in an unlimited access paradigm exhibited markedly increased levels of endogenous noradrenaline in the hypothalamic paraventricular nucleus (Fu et al. 2001) and amygdala (Fu et al. 2003). Also, in rats that received a daily nicotine injection (0.4mgkg ) for 5 days, noradrenaline release in the ventral hippocampus was enhanced in response to a subsequent nicotine challenge (Benwell and Balfour 1997). [Pg.190]

Experimental studies have shown that the release of a transmitter from a nerve terminal can be decreased or increased by a variety of other neurotransmitters. For example, stimulation of 5-HT receptors on noradrenergic terminals can lead to an enhanced release of noradrenaline. While the physiological importance of such a mechanism is unclear, this could be a means whereby drugs could produce some of their effects. Such receptors have been termed heteroceptors (Figure 2.3). [Pg.23]

GABA-B receptors. There is evidence that GABA-B receptors play a role in enhancing noradrenaline release in the cortex and in this respect differ fundamentally from the inhibitory GABA-A receptors which facilitate central GABAergic transmission. A decrease in the activity of GABA-B receptors may therefore contribute to the reduced central noradrenergic tone reported to occur in depression. [Pg.162]

Figure 7.4. Summary of the site of action of mirtazepine (NaSSA). The inhibitory 2 adrenoceptors facilitate the release of both noradrenaline and serotonin (via the heteroceptor on the 5-HT neuron). This is further enhanced by the receptor on the serotonin cell body. Thus mirtazepine (and to a lesser extent mianserin) enhance both noradrenergic and serotonergic... Figure 7.4. Summary of the site of action of mirtazepine (NaSSA). The inhibitory 2 adrenoceptors facilitate the release of both noradrenaline and serotonin (via the heteroceptor on the 5-HT neuron). This is further enhanced by the receptor on the serotonin cell body. Thus mirtazepine (and to a lesser extent mianserin) enhance both noradrenergic and serotonergic...
Noradrenaline is the neurotransmitter most closely associated with the peripheral and central stress response (Figure 9.5). There is experimental evidence to show that drugs such as yohimbine that block the noradrenergic autoreceptors (e.g. on cell bodies and nerve terminals) and thereby enhance noradrenaline release cause fear and anxiety in both man and animals. Conversely, drugs that stimulate these autoreceptors (as exemplified by clonidine) diminish the anxiety state because they reduce the release of noradrenaline. Benzodiazepines have been shown to inhibit the fear-motivated increase in the functional activity of noradrenaline in experimental animals, but it is now widely believed that the action of the benzodiazepines on the central noradrenergic system is only short term and may contribute to the sedative effects which most conventional benzodiazepines produce, at least initially. Nevertheless, altered noradrenergic... [Pg.214]

In contrast to the highly specific structural requirement for ligands at the various adrenoceptor subtypes the re-uptake mechanism (into the axon and into the vesicle) are less discriminative. Compounds without hydroxyl moieties at the phenyl ring have no affinity towards the adrenoceptors but serve as a substrate for the re-uptake mechanisms, thereby competing with noradrenaline and as a consequence increasing its concentration in the synaptic cleft. Drugs enhancing the sympathetic tone by this mechanism are called indirect sympathomimetics, for example tyramine, ephedrine, amphetamine. [Pg.302]

The hydroxyl groups of the phenyl ring are a prerequisite for the activation of all adrenoceptors, if both are absent the molecule has only an indirect sympathomimetic effect (see Fig. 5). Indirect sympathomimetics only have a -, a2 and -adrenoceptor activity since they act via an increase of the noradrenaline concentration in the synaptic cleft. If the methyl-group at the N-position of adrenaline is substituted by a longer or more bulky moiety the molecule gains affinity for the and loses affinity for O -adrenoceptors. An isopropyl moiety is already the optimum for the affinity towards 0-adrenoceptors (isoprenaline), larger substituents enhance only the binding to the 2-subtype (for example fenoterol). [Pg.304]


See other pages where Noradrenaline enhancement is mentioned: [Pg.59]    [Pg.59]    [Pg.93]    [Pg.237]    [Pg.492]    [Pg.246]    [Pg.112]    [Pg.1067]    [Pg.29]    [Pg.255]    [Pg.497]    [Pg.227]    [Pg.33]    [Pg.34]    [Pg.37]    [Pg.42]    [Pg.46]    [Pg.132]    [Pg.339]    [Pg.77]    [Pg.93]    [Pg.130]    [Pg.524]    [Pg.191]    [Pg.162]    [Pg.183]    [Pg.186]    [Pg.22]    [Pg.42]    [Pg.176]    [Pg.177]    [Pg.183]    [Pg.183]    [Pg.202]    [Pg.142]    [Pg.195]    [Pg.201]    [Pg.202]    [Pg.237]    [Pg.175]    [Pg.317]    [Pg.323]   


SEARCH



© 2024 chempedia.info