Disease relevance of levonordefrin

• 2-Methoxyidazoxan, but not idazoxan, also reversed the hypotension when alpha-methylnoradrenaline was administered into the nucleus tractus solitarius [1].
• Centrally induced hypotension and bradycardia after administration of alpha-methylnoradrenaline into the area of the nucleus tractus solitarii of the rat [2].

Psychiatry related information on levonordefrin

• On the other hand, alpha-methylnoradrenaline much less intensively triggers the mechanisms underlying withdrawal symptoms than clonidine or guanfacine [3].

High impact information on levonordefrin

• Since alpha-methylnoradrenaline does not penetrate the central nervous system, any blockade of its action by a drug must be peripherally mediated [4].
• Idazoxan injected into the RVLM reversed the hypotension and completely restored the baroreflex curve at doses that did not affect the hypotension produced by the selective alpha2-adrenoceptor agonist alpha-methylnoradrenaline [5].
• During alpha-methylnoradrenaline infusion, elevation of total peripheral resistance was not increased relative to controls [6].
• Comparison of renal sympathetic baroreflex effects of rilmenidine and alpha-methylnoradrenaline in the ventrolateral medulla of the rabbit [7].
• Adrenoceptors mediating the cardiovascular and metabolic effects of alpha-methylnoradrenaline in humans [8].

Biological context of levonordefrin

• These results suggest that the fall in blood pressure observed after administration of alpha-methylnoradrenaline involves a beta-endorphin-like peptide, a probable site of this interaction being the n. tractus solitarii [9].
• Unilateral microinjection of alpha-methylnoradrenaline into the nucleus tractus solitarii (NTS) induced a dose-related fall in blood pressure and heart rate [9].
• Whereas alpha-methylnoradrenaline is selective for alpha2- over alpha1-adrenoceptors, beta-adrenoceptor blockade is required to unmask alpha-adrenoceptor-mediated vasoconstriction [8].
• By considering the fusion protein as an agonist-activated enzyme and measuring Vmax of GTP hydrolysis a range of agonist ligands displayed varying efficacy in their capacity to activate the receptor-associated G protein with adrenaline = noradrenaline = alpha-methylnoradrenaline > UK14304 > BHT933 > or = xylazine = clonidine [10].
• Alpha methylnoradrenaline infusion resulted in a dose and time dependent decrease in the pro-aggregatory response of platelet to adrenaline without any significant change in the response to ADP or in the number of [3H]yohimbine binding sites [11].

Anatomical context of levonordefrin

• Changes in protein secretion by rat submandibular glands in response to isoproterenol, alpha-methylnoradrenaline, and clonidine during post-natal development [12].
• Inhibition of the activity of sympathetic preganglionic neurones and neurones activated by visceral afferents, by alpha-methylnoradrenaline and endogenous catecholamines [13].
• In the neostriatum 7.7% of all boutons absorbed alpha-methylnoradrenaline, thus staining their synaptic vesicles profiles granular [14].
• Hypotensive response in spontaneously hypertensive rats following microinjection of alpha-methylnoradrenaline in the caudal brain-stem [15].
• Ablation of the rostral or caudal part of the NTS, or removal of the area postrema did not diminish the effect of alpha-methylnoradrenaline [16].

Associations of levonordefrin with other chemical compounds

• 3 Prior administration of the alpha-adrenoceptor blocking agent, phentolamine, reversed the fall in blood pressure and heart rate induced by alpha-methylnoradrenaline into an increase [2].
• 4 Systemic administration of atropine combined with vagotomy potentiated the inhibitory effects of alpha-methylnoradrenaline on the cardiovascular system [2].
• All antagonists caused parallel shifts to the right of the concentration-response curves of clonidine, noradrenaline, and alpha-methylnoradrenaline. pA2 values were calculated either from linear regression of log [agonist concentration ratio - 1] on log [antagonist concentration] or from sigmoid curve fitting [17].
• Phenylephrine (10 mumol/l), alpha-methylnoradrenaline (10 mumol/l) and adrenaline (1 mumol/l) enhanced the electrically evoked [3H]acetylcholine release from the rat phrenic nerve [18].
• Higher doses of noradrenaline and alpha-methylnoradrenaline caused an initial rise of blood pressure, while the blood pressure lowering effect of noradrenaline was diminished, and that of alpha-methylnoradrenaline and dopamine delayed [16].

Gene context of levonordefrin

• The sole stimulation of A2Rs within the NRL/RVLM region was not sufficient to decrease blood pressure as much as IMs did, as shown by the lack of significant blood pressure lowering effect of alpha-methylnoradrenaline (alpha-MNA) [19].

Analytical, diagnostic and therapeutic context of levonordefrin

• Intravenous infusions of the selective alpha 2-adrenoceptor agonist alpha-methylnoradrenaline (2 micrograms/kg per min) and the alpha 1-agonist phenylephrine (6 micrograms/kg per min) produced equipressor responses [20].
• An assay for the quantitative estimation of L-3,4-dihydroxyphenylalanine in human plasma has been developed, using alpha-methylnoradrenaline as internal standard and ion-pair reversed-phase (C8), isocratic high-performance liquid chromatography with amperometric detection [21].
• 2. By a combination of radioenzymatic assay and paper chromatography the concentrations of adrenaline, noradrenaline, dopamine, alpha-methylnoradrenaline and alpha-methyldopamine were determined concurrently in the same sample [22].
• The hypotensive responses evoked by electrical stimulation or alpha-methylnoradrenaline application were found to have a common distribution of the most effective site, comprising the middle-caudal part of the nucleus tractus solitarii at the obex level [23].

References