Document Detail

Melatonin potentiates contractile responses to serotonin in isolated porcine coronary arteries.
MedLine Citation:
PMID:  11123220     Owner:  NLM     Status:  MEDLINE    
The present study was designed to determine the effects of melatonin on coronary vasomotor tone. Porcine coronary arteries were suspended in organ chambers for isometric tension recording. Melatonin (10(-10)-10(-5) M) itself caused neither contraction nor relaxation of the tissues. Serotonin (10(-9)-10(-5) M) caused concentration-dependent contractions of coronary arteries, and in the presence of melatonin (10(-7) M) the maximal response to serotonin was increased in rings with but not without endothelium. In contrast, melatonin had no effect on contractions produced by the thromboxane A(2) analog U-46619 (10(-10)-10(-7) M). The melatonin-receptor antagonist S-20928 (10(-6) M) abolished the potentiating effect of melatonin on serotonin-induced contractions in endothelium-intact coronary arteries, as did treatment with 1H-[1, 2,4]oxadiazolo[4,3-a]quinoxalin-1-one (10(-5) M), methylene blue (10(-5) M), or N(G)-nitro-L-arginine (3 x 10(-5) M). In tissues contracted with U-46619, serotonin caused endothelium-dependent relaxations that were inhibited by melatonin (10(-7) M). Melatonin also inhibited coronary artery relaxation induced by sodium nitroprusside (10(-9)-10(-5) M) but not by isoproterenol (10(-9)-10(-5) M). These results support the hypothesis that melatonin, by inhibiting the action of nitric oxide on coronary vascular smooth muscle, selectively potentiates the vasoconstrictor response to serotonin in coronary arteries with endothelium.
Q Yang; E Scalbert; P Delagrange; P M Vanhoutte; S T O'Rourke
Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  280     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2001 Jan 
Date Detail:
Created Date:  2001-02-02     Completed Date:  2001-02-02     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  H76-82     Citation Subset:  IM    
Department of Pharmaceutical Sciences, North Dakota State University, Fargo, North Dakota 58105, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid / pharmacology
Coronary Vessels / drug effects*,  physiology
Drug Synergism
Enzyme Inhibitors / pharmacology
Isoproterenol / pharmacology
Melatonin / antagonists & inhibitors,  pharmacology*
Muscle Contraction / drug effects
Muscle, Smooth, Vascular / drug effects*,  physiology
Naphthalenes / pharmacology
Nitric Oxide Donors / pharmacology
Nitric Oxide Synthase / antagonists & inhibitors
Nitric Oxide Synthase Type III
Nitroprusside / pharmacology
Receptors, Cell Surface / antagonists & inhibitors
Receptors, Cytoplasmic and Nuclear / antagonists & inhibitors
Receptors, Melatonin
Serotonin / pharmacology*
Vasoconstrictor Agents / pharmacology
Vasodilator Agents / pharmacology
omega-N-Methylarginine / pharmacology
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Naphthalenes; 0/Nitric Oxide Donors; 0/Receptors, Cell Surface; 0/Receptors, Cytoplasmic and Nuclear; 0/Receptors, Melatonin; 0/Vasoconstrictor Agents; 0/Vasodilator Agents; 15078-28-1/Nitroprusside; 152302-33-5/N-(2-(1-naphthalenyl)ethyl)cyclobutanecarboxamide; 17035-90-4/omega-N-Methylarginine; 50-67-9/Serotonin; 73-31-4/Melatonin; 7683-59-2/Isoproterenol; 76898-47-0/15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; EC Oxide Synthase; EC Oxide Synthase Type III

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

Previous Document:  Increased inactivation of nitric oxide is involved in coronary endothelial dysfunction in heart fail...
Next Document:  Adenosine A(2A) receptors mediate cardiovascular responses to hypoxia in fetal sheep.