Nor adrenalin

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]. 

Dopamine hydroxylase synthesizes norepinephrine (Nor-adrenalin) from dopamine. 

Fig. 2.20 Efferent pathways into bulb showing (a) cholinergic (ACh) fibres projecting to MOB from basal forebrain nuclei. AON = ant. olfactory nucleus, OT = olfactory tract, DB = diagonal band nuc. (from Davis et al., 1978). (b) Nor-Adrenalin input to AOB, via MFB pathway from brain stem centres (nuclei A1-2, A6) (from Keveme, 1971).

The organ also contains neuroactive compounds as constituents of the vasomotor and neuro-glandular tissues (Zancanaro et al., 1997). These include the amine transmitters Nor-adrenalin and Serotonin (5-HT), whose presence is presumably related to the non-olfactory innervations. Local stimulation effects [Figs. 5.2 and 5.5(a)] can alter the biogenic amine levels in the VNO of female mice, as a result of exposure to male conspecific urine, and consequent arousal of the suction-pump [c.f. Fig. 5.7(a)]. 

Figure 1-1 shows an example of the detection limits that can be reached with EC detection. The chromatogram shows the separation and detection of the catecholamines noradrenaline (nor), adrenaline (adr), dihydroxybenzylamine (dhba), and dopamine (dopa), using a glassy carbon electrode at a working potential of +0.6 V. The minimum detectable quantity is less than 3 Pg-... 

Tyramine is an amino acid which is present in large quantities in protein rich, fermented and stored products like some cheeses, sausages, red wines, beers etcetera. Tyramine is metabolized into nor-adrenaline by the enzyme mono-amino-oxidase (MAO). If MAO is inhibited by drags nor-adrenaline is accumulated and can give hypertensive crises. 

Holtje, H.-D. and Vogelgesang, L. (1979). Theoretische Untersuchung zur Hemmung der Nor-adrenalin-Riickresorption durch Phenylethylaminanaloge Verbindungen. Arch.Pharm.(Wein-heim Ger), 312,578-586. 

Lundberg, J.M. Stjarne, L. (1984) Neuropeptide Y (NPY) depresses the secretion of 3H-nor-adrenaline and the contractile response evoked by field stimulation, in rat vas deferens. Acta Physiol. Scand. 120, 477-479. 

The biogenic amines (ref.2) are partly derivatives of brenzcatechin, partly indolalkylamines. The most important compounds are adrenaline, and nor-adrenaline (as catecholamines), well known from the animal kingdom as suprarenal hormones, as well as indolalkylamines of the bufotenin type. All indolalkylamines possess vasoconstrictive and hypotensive activity, and all of them are strong antibiotics. 

Biogenic amines, biological amines biologically and pharmacologically important naturally occurring amines, occurring widely in plants and animals. They can be divided into 1. derivatives of ethanolamine, e.g. choline, acetylcholine, muscarine 2. polymethylene diamines, e.g. putrescine, cadaverine 3.polyamines, e.g. spermine 4. imidazolylalkylamines, e.g. histamine 5.phenylalkylamines, e.g. mescaline, tyra-mine, hordenine 6. catecholamines, e. g. adrenalin, nor-adrenalin and dopamine 7. indolylalkylamines, e.g. tryptamine, serotonin and 8. betaines, e.g. carnitine. 

Stern, P., Hukovi6, S. and Misirlija, A., Cber die Ausscheidung des Adrenalin und Nor-Adrenalin bei Dystrophia musculorum progressiva. Arch. exp. Path. Pharmak. 228, 209 (1956). 

Lochner, W., Mercker, H. and Schurmeyer, E., Die Wirkung von Adrenalin, Nor-Adrenalin, Acethylcholin und Vagusreizung auf die Sauerstoffsattigung des Blutes im Sinus coronarius untersucht mit fortlaufender photometrischer Methode, Arch. exp. Path. Pharmak. Ill, 360 (1956). 

Golenhofen, K., Hensel, H. and Ruef, J., Ober die Wirkung von Adrenalin und Nor-adrenalin und die Muskeldurchblutung des Menschen und ihre Beeinflussung durch Regitin, Arch. exp. Path. Pharmak. 225, 269 (1955). 

Nashold, Bl. S. Jr. and Kirshner, N., The metabolism of adrenalin and nor-adrenalin in patients with basal ganglia disease, Neurol. 13, 753 (1963). 

Epinephrine, as it is known, exhibits a diphasic effect on the blood pressure. In hypertensive patients, if small amounts of epinephrine are used, the hypotension is more evident than hypertension (Greppi 1932, Goldenberger et al. 1948). The effect of nor-adrenaline is simply monophasic. The first phase by epinephrine, namely slight hypertension, is due to the alpha-receptor stimulation second phase, namely hypotension, is due to a beta-receptor stimulation (Alhquist 1948). 

In identical conditions the contact of pain receg, tors with nor-adrenaline, does not induce this sensitization to bradykinin. 

Fig. 6. Dose-response curves of the lipomobilizing effects of noradrenaline (NOR), adrenaline (ADR), and isoprenaline (ISO) tn vitro. Mean values SE. Identical maximal effects (activity) and only minimal differences in afSnity are to be noted, as also the afiinity sequence ISO > NOR > ADR.

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