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Gene Review

COMT  -  catechol-O-methyltransferase

Canis lupus familiaris

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Disease relevance of COMT


High impact information on COMT


Biological context of COMT


Anatomical context of COMT

  • It is concluded that COMT is related to smooth muscle cells in this tissue [8].
  • Our results strongly support the view that alpha-adrenoceptors are in close contract with the nerve endings and beta-adrenoceptors are in close proximity of COMT in a vessel with the nerve endings evenly distributed throughout the media [9].
  • Effect of catechol-O-methyl-transferase (COMT) inhibition on the vascular and metabolic responses to noradrenaline, isoprenaline and sympathetic nerve stimulation in canine subcutaneous adipose tissue [10].
  • Dog splenic artery strips were incubated with [3H]NA after inhibition of catechol-O-methyl-transferase (COMT) and of extraneuronal uptake [11].
  • Effect of cooling on COMT activity in canine saphenous vein homogenates determined by a micro radioenzymatic assay [12].

Associations of COMT with chemical compounds

  • Thus, the excretion of dopamine by the cat kidney is linked to an inactivation by the kidney enzymes MAO and COMT [13].
  • The activity of COMT was assayed with the method of Axelrod (1962, Methods in Enzymology, Vol. 5. Academic Press, New York) in the presence of epinephrine bitartrate as a substrate [14].
  • FS-32 tended to produce an increase in chatecholamine content in the brain without MAO or COMT inhibitory activity [15].
  • Cocaine was used to inhibit neuronal uptake and COMT was blocked with 3,4-dihydroxy-2-methyl propiophenone [16].
  • Using the oil immersion technique, the role of neuronal uptake, monoamine oxidase and COMT in the inactivation of 2 concentrations (0.23 and 2.3 mumol/l) of noradrenaline and adrenaline was determined by the prolongation of the inactivation time caused by cocaine (12 mumol/l), pargyline (1 mmol/l) and U-0521 (50 mumol/l), respectively [17].

Analytical, diagnostic and therapeutic context of COMT


  1. Effects of pharmacologic alterations of adrenergic mechanisms by cocaine, tropolone, aminophylline, and ketamine on epinephrine-induced arrhythmias during halothane-nitrous oxide anesthesia. Koehntop, D.E., Liao, J.C., Van Bergen, F.H. Anesthesiology (1977) [Pubmed]
  2. Effects of tolcapone, a catechol-O-methyltransferase inhibitor, and Sinemet on intestinal electrolyte and fluid transport in conscious dogs. Larsen, K.R., Dajani, E.Z., Dajani, N.E., Dayton, M.T., Moore, J.G. Dig. Dis. Sci. (1998) [Pubmed]
  3. Evidence for the beta-adrenergic receptor regulation of membrane-bound catechol-O-methyltransferase activity in myocardium. Wrenn, S., Homcy, C., Haber, E. J. Biol. Chem. (1979) [Pubmed]
  4. Inactivation of norepinephrine in an isolated vein. Brandao, F. J. Pharmacol. Exp. Ther. (1977) [Pubmed]
  5. Release and disposition of 3H-noradrenaline in the saphenous vein of neonate and adult dogs. Moura, D., Vaz-da-Silva, M.J., Azevedo, I., Brandão, F., Guimarães, S. Naunyn Schmiedebergs Arch. Pharmacol. (1993) [Pubmed]
  6. Identification of major metabolites of the catechol-O-methyltransferase inhibitor nitecapone in the rat and dog. Wikberg, T., Taskinen, J. Drug Metab. Dispos. (1993) [Pubmed]
  7. Breed differences in genotype and allele frequency of catechol O-methyltransferase gene polymorphic regions in dogs. Masuda, K., Hashizume, C., Kikusui, T., Takeuchi, Y., Mori, Y. J. Vet. Med. Sci. (2004) [Pubmed]
  8. Relation between the amount of smooth muscle of venous tissue and the degree of supersensitivity to isoprenaline caused by inhibition of catechol-O-methyl transferase. Guimarães, S., Azevedo, I., Cardoso, W., Oliveira, M.C. Naunyn Schmiedebergs Arch. Pharmacol. (1975) [Pubmed]
  9. Two different biophases for adrenaline released by electrical stimulation or tyramine from the sympathetic nerve endings of the dog saphenous vein. Guimarães, S., Paiva, M.Q. Naunyn Schmiedebergs Arch. Pharmacol. (1981) [Pubmed]
  10. Effect of catechol-O-methyl-transferase (COMT) inhibition on the vascular and metabolic responses to noradrenaline, isoprenaline and sympathetic nerve stimulation in canine subcutaneous adipose tissue. Belfrage, E., Fredholm, B.B., Rosell, S. Naunyn Schmiedebergs Arch. Pharmacol. (1977) [Pubmed]
  11. The influence of monoamine oxidase activity on the release of noradrenaline by tyramine. Brandão, F., Araújo, D., Monteriro, J.G. J. Pharm. Pharmacol. (1989) [Pubmed]
  12. Effect of cooling on COMT activity in canine saphenous vein homogenates determined by a micro radioenzymatic assay. Janssens, W.J., Vanhoutte, P.M. Archives internationales de pharmacodynamie et de thérapie. (1978) [Pubmed]
  13. Inactivation and excretion of dopamine by the cat kidney in vivo. Stöcker, W., Hempel, K. Naunyn Schmiedebergs Arch. Pharmacol. (1976) [Pubmed]
  14. The monoamine oxidase and catechol-O-methyltransferase activities in the dog liver. Ong, H., Yamaguchi, N. Can. J. Physiol. Pharmacol. (1982) [Pubmed]
  15. Pharmacological studies on a new thymoleptic antidepressant, 1-[3-(dimethylamino)propyl]-5-methyl-3-phenyl-1H-indazole (FS-32). Ikeda, Y., Takano, N., Matsushita, H., Shiraki, Y., Koide, T., Nagashima, R., Fujimura, Y., Shindo, M., Suzuki, S., Iwasaki, T. Arzneimittel-Forschung. (1979) [Pubmed]
  16. A comparative study of the role played by some inactivation pathways in the disposition of the transmitter in the rabbit aorta and the saphenous vein of the dog. Brandão, F. Blood vessels. (1976) [Pubmed]
  17. An unusually important role of O-methylation in the disposition of noradrenaline and adrenaline by the dog renal artery. Nunes, J.P., Vaz-Da-Silva, M.J., Brandão, F., Guimarães, S. Archives internationales de pharmacodynamie et de thérapie. (1987) [Pubmed]
  18. Myocardial ischemia stimulates catecholamine synthesis and catabolism in the dog adrenal medulla. Parvez, H., Ichihara, K., Parvez, S., Sakai, K., Abiko, Y., Nagatsu, T. Japanese heart journal. (1986) [Pubmed]
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