Document Detail


Carbon monoxide-prostaglandin E2 interaction in the hypothalamic circulation.
MedLine Citation:
PMID:  18815586     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The heme oxygenase (HO)-carbon monoxide pathway was earlier shown to increase hypothalamic blood flow after inhibition of nitric oxide synthesis in rats. We hypothesized that this effect is mediated by prostaglandin E2 (PGE2). Inhibition of constitutive HO activity decreased cerebral PGE2 production and simultaneously increased hypothalamic nitric oxide synthase (NOS) activity without changing hypothalamic blood flow. Furthermore, HO blockade induced cyclooxygenase-dependent decrease and NOS-mediated increase of the hypothalamic blood flow after inhibition of NOS and cyclooxygenase, respectively. Therefore, constitutive carbon monoxide release seems to have two indirect effects on the hypothalamic circulation: vasodilation mediated by PGE2 and vasoconstriction as a result of NOS inhibition.
Authors:
Béla Horváth; László Hortobágyi; Gábor Lenzsér; Horst Schweer; András Hrabák; Péter Sándor; Zoltán Benyó
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Neuroreport     Volume:  19     ISSN:  1473-558X     ISO Abbreviation:  Neuroreport     Publication Date:  2008 Oct 
Date Detail:
Created Date:  2008-10-10     Completed Date:  2008-11-26     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9100935     Medline TA:  Neuroreport     Country:  England    
Other Details:
Languages:  eng     Pagination:  1601-4     Citation Subset:  IM    
Affiliation:
Institute of Human Physiology and Clinical Experimental Research, Molecular Biology and Pathobiochemistry, Semmelweis University, Budapest, Hungary.
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MeSH Terms
Descriptor/Qualifier:
6-Ketoprostaglandin F1 alpha / cerebrospinal fluid,  metabolism
Animals
Blood Gas Analysis / methods
Blood Pressure / drug effects,  physiology
Carbon Monoxide / metabolism*
Cyclooxygenase Inhibitors / administration & dosage,  pharmacology
Deuteroporphyrins / administration & dosage,  pharmacology
Diclofenac / administration & dosage,  pharmacology
Dinoprost / cerebrospinal fluid,  metabolism
Dinoprostone / cerebrospinal fluid,  metabolism*
Enzyme Inhibitors / administration & dosage,  pharmacology
Heart Rate / drug effects,  physiology
Heme Oxygenase (Decyclizing) / antagonists & inhibitors,  metabolism*
Hypothalamus / blood supply*,  drug effects,  metabolism
Injections, Intraperitoneal
Injections, Intravenous
Male
NG-Nitroarginine Methyl Ester / administration & dosage,  pharmacology
Prostaglandin D2 / cerebrospinal fluid,  metabolism
Prostaglandin-Endoperoxide Synthases / metabolism
Rats
Rats, Wistar
Chemical
Reg. No./Substance:
0/Cyclooxygenase Inhibitors; 0/Deuteroporphyrins; 0/Enzyme Inhibitors; 119700-81-1/zinc deuteroporphyrin IX 2,4-bis(glycol); 15307-86-5/Diclofenac; 363-24-6/Dinoprostone; 41598-07-6/Prostaglandin D2; 50903-99-6/NG-Nitroarginine Methyl Ester; 551-11-1/Dinoprost; 58962-34-8/6-Ketoprostaglandin F1 alpha; 630-08-0/Carbon Monoxide; EC 1.14.99.1/Prostaglandin-Endoperoxide Synthases; EC 1.14.99.3/Heme Oxygenase (Decyclizing)

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


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