eISSN: 1896-9151
ISSN: 1734-1922
Archives of Medical Science
Current issue Archive Special issues Abstracting and indexing Subscription
Editorial System
Submit your Manuscript
SCImago Journal & Country Rank
Search
Editorial Policies
Sarajevo Declaration on Integrity and Visibility of Scholarly Publications
3/2010
vol. 6
 
Share:
Send email
Share:
abstract:

Review paper
Catechol-O-methyltransferase: potential relationship to idiopathic hypertension

Kirk J. Mantione
,
Richard M. Kream
,
George B. Stefano

Arch Med Sci 2010; 6, 3: 291-295
DOI: https://doi.org/10.5114/aoms.2010.14246
Online publish date: 2010/06/30
View full text Get citation
 
Catecholamine signaling pathways in the peripheral and central nervous systems (PNS, CNS, respectively) utilize catechol-O-methyltransferase (COMT) as a major regulatory enzyme responsible for deactivation of dopamine (DA), norepinephrine (NE) and epinephrine (E). Accordingly, homeostasis of COMT gene expression is hypothesized to be functionally linked to regulation of autonomic control of normotensive vascular events. Recently, we demonstrated that morphine administration in vitro resulted in decreased cellular concentrations of COMT-encoding mRNA levels, as compared to control values. In contrast, cells treated with E up regulated their COMT gene expression. In sum, these observations indicate a potential reciprocal linkage between end product inhibition of COMT gene expression by E and morphine. Interestingly, the observed effects of administered E on COMT gene expression suggest an enhancement of its own catabolism or, reciprocally, a stimulation morphine biosynthesis.
keywords:

endogenous morphine, catecholamines, epinephrine, catechol-O-methyltransferase
Termedia
About us Contact
Copyright notice Privacy policy Advertising policy Contact us
Quick links
Journals Books eBooks Events
© 2024 Termedia Sp. z o.o.
Developed by Bentus.