Document Detail


Modulation of the renin-aldosterone system by iodotyrosines as tyrosine hydroxylase inhibitors.
MedLine Citation:
PMID:  1981135     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
This study shows that MIT and DIT stimulate aldosterone secretion. This may be due to their tyrosine hydroxylase inhibitory property. Dopamine abolishes the stimulation. Prolonged MIT administration enhances the stimulation of aldosterone secretion and can cause hypokalemia. Volume expansion reverses the hyperaldosteronism. PRA and blood pressure do not change, even after prolonged MIT intake.
Authors:
S A Tan; L S Berk; L G Tan
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Biochemical medicine and metabolic biology     Volume:  44     ISSN:  0885-4505     ISO Abbreviation:  Biochem. Med. Metab. Biol.     Publication Date:  1990 Dec 
Date Detail:
Created Date:  1991-04-01     Completed Date:  1991-04-01     Revised Date:  2004-11-17    
Medline Journal Info:
Nlm Unique ID:  8605718     Medline TA:  Biochem Med Metab Biol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  252-8     Citation Subset:  IM    
Affiliation:
Department of Medicine, Loma Linda University, California 92350.
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MeSH Terms
Descriptor/Qualifier:
Adult
Aldosterone / secretion*
Diiodotyrosine / pharmacology
Dopamine / pharmacology
Humans
Hyperaldosteronism / chemically induced
Hypokalemia / chemically induced
Male
Monoiodotyrosine / pharmacology*
Renin-Angiotensin System / drug effects*,  physiology
Tyrosine 3-Monooxygenase / antagonists & inhibitors*
Chemical
Reg. No./Substance:
29592-76-5/Monoiodotyrosine; 52-39-1/Aldosterone; 66-02-4/Diiodotyrosine; EC 1.14.16.2/Tyrosine 3-Monooxygenase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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