Disease relevance of Bisnorephedrine

• Output of mandelic acid, a major but unexplained metabolite in phenylketonuria, was increased after the administration of phenylethanolamine or phenylpyruvic acid, whereas phenylethylamine or phenylalanine increased its excretion only marginally [1].
• Changes in tyrosine hydroxylase and phenylethanolamine N-methyl transferase activity in individual brain nuclei during the development of renovascular hypertension in the rat [proceedings] [2].
• Plasma phenylethanolamine in hepatic encephalopathy [3].
• Phenylethanolamine plasma levels correlated statistically with the presence of liver cirrhosis and severe coma [3].
• Elevated plasma catecholamines and adrenal phenylethanolamine N-methyl transferase in experimental renal hypertension [4].

Psychiatry related information on Bisnorephedrine

• (+/-)-Amphetamine and PEA increased spontaneous locomotor activity but phenylethanolamine had no effects on this measure [5].

High impact information on Bisnorephedrine

• The expression of phenylethanolamine N-methyl transferase and chromogranin B mRNA was similar in TH-null and wild-type mice [6].
• The majority of the phenylethanolamine N-methyltransferase-immunoreactive nerve cells of the adrenergic cell groups C1-C3 and of the dorsal subnuclei of the nucleus tractus solitarius in the medulla oblongata were also strongly immunoreactive for glucocorticoid receptor [7].
• Growth in glucocorticoid maintains the expression of the SA antigens in the sorted cells and induces the chromaffin cell marker enzyme phenylethanolamine N-methyl transferase [8].
• Importance of the aromatic ring in adrenergic amines. Nonaromatic analoques of phenylethanolamine as substrates for phenylethanolamine N-methyltransferase [9].
• Differential effects of increasing gestational age and placental restriction on tyrosine hydroxylase, phenylethanolamine N-methyltransferase, and proenkephalin A mRNA levels in the fetal sheep adrenal [10].

Chemical compound and disease context of Bisnorephedrine

• Influence of phenylethanolamine on octopamine plasma determination in hepatic encephalopathy [11].

Biological context of Bisnorephedrine

• The folded phenylethanolamine derivative 4-hydroxy-1,2,3,4-tetrahydroisoquinoline (8) is not a substrate and does not interact with the enzyme active site as an inhibitor as well as 1,2,3,4-tetrahydroisoquinoline (6) [12].
• Synthesis and structure-activity relationships among alpha-adrenergic receptor agonists of the phenylethanolamine type [13].
• Physiologic effects and plasma kinetics of phenylethanolamine and its N-methyl homolog in the dog [14].
• In several species of obese animals, a group of phenethanolamine beta-agonists stimulates lipolysis and thermogenesis, resulting in the loss of body fat and weight [15].
• Ontogenesis and sex differences in rabbit fetal adrenal phenylethanolamine N-methyltransferase [16].

Anatomical context of Bisnorephedrine

• To determine whether adrenergic axons synapse on preganglionic neurons which project to the adrenal medulla, adrenal preganglionic neurons were retrogradely labeled with horseradish peroxidase and adrenergic axons were stained for phenylethanolamine N-methyltransferase-immunoreactivity [17].
• Five ganglia from three other dogs were stained for dopamine beta-hydroxylase and phenylethanolamine N-methyltransferase [18].
• Simultaneous demonstration of phenylethanolamine N-methyltransferase immunofluorescent and catecholamine fluorescent nerve cell bodies in the rat medulla oblongata [19].
• Phenylethanolamine N-methyltransferase-immunoreactive terminals synapse on adrenal preganglionic neurons in the rat spinal cord [17].
• Phenylethanolamine N-methyltransferase-immunoreactivity was observed in the cytoplasm of unmyelinated axonal varicosities and intervaricose segments in the neuropil of intermediolateral nucleus [17].

Associations of Bisnorephedrine with other chemical compounds

• These results, in conjunction with others from these laboratories, indicate that the PNMT active site beyond the zone that interacts with the central aromatic ring portion of phenylethanolamine substrates and alpha-methylbenzylamine inhibitors is essentially a flat, hydrophobic pocket [20].
• Finally, carbachol failed to stimulate luciferase expression in cells transfected with a mutant construct, in which the Egr-1 binding element in the phenylethanolamine N-methyl-transferase promoter was mutated [21].
• Octopamine and phenylethanolamine (PeOH) were not SSAO substrates and inhibited BZ metabolism in the fluorimetric assay [22].
• The relative potencies of these compounds in maintaining self-administration behavior during the 4-hr session were d-amphetamine greater than cocaine greater than phenylethanolamine greater than or equal to N-methyl phenylethylamine greater than or equal to beta-phenylethylamine [23].
• In order to resolve this question, we have examined the distribution of chromaffin-like cells in dog paravertebral ganglia (T7-S2) using formaldehyde-induced fluorescence of catecholamines and immunohistochemical localization of dopa decarboxylase, dopamine beta-hydroxylase and phenylethanolamine N-methyltransferase [18].

Gene context of Bisnorephedrine

• Phenylethanolamine N-methyltransferase (PNMT) was identified as the primary, high affinity N-methylating enzyme for phenylethanolamine (PEA) in rat, dog and Rhesus monkey lung [24].
• In parkinsonian brain, TH and the BP cofactor, as well as DBH and PNMT with phenylethanolamine as substrate, are decreased [25].
• We have previously described regions of steric bulk tolerance in the aromatic-ring binding site of phenylethanolamine N-methyltransferase (PNMT, EC 2.1.1.28) for phenylethanolamine substrates and alpha-methylbenzylamine inhibitors [20].
• Interleukin-1 receptor antagonist immunoreactivity was seen in the adrenal medulla, and the immunofluorescence intensity was stronger in the adrenergic, phenylethanolamine N-methyltransferase-positive cells than in the noradrenergic chromaffin cells [26].
• The distribution of interleukin-1 receptor antagonist protein is complementary to that of interleukin-1 alpha-like immunoreactivity found in phenylethanolamine N-methyltransferase-negative cells and overlaps with and resembles the distribution of interleukin-1 beta-immunoreactive material [26].

Analytical, diagnostic and therapeutic context of Bisnorephedrine

• Cellular expression of TH and phenylethanolamine N-methyl transferase was evaluated by protein immunohistochemistry and in situ hybridization of the corresponding mRNA species [27].
• In PR fetuses, distribution of staining for dopamine-beta-hydroxylase, phenylethanolamine N-methyltransferase, and ENK-containing peptides in the adrenal medulla was similar when compared with the control group; however, staining was less intense and not all adrenomedullary cells were stained [28].
• Electron microscopy of the medial central nucleus showed phenylethanolamine N-methyltransferase-immunoreaction product in the cytoplasm of intervaricose axons and boutons [29].
• Using hot plate method, analgesia induced by noncatecholic phenylethylamines, phenethylamine, phenylethanolamine and amphetamine, was inhibited by naloxone, reserpine, apomorphine and p-chlorophenylalanine, while potentiated by haloperidol [30].

References