Document Detail


Statins decrease serotonin-induced contractions in coronary arteries of swine in vitro.
MedLine Citation:
PMID:  16428899     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Recent evidence suggests that statins improve the status of patients with coronary artery disease not only by reducing cholesterol levels, but also by acting at the level of the endothelium-smooth muscle unit. Previous results from our laboratory showed that these drugs interact with the vascular wall by partially inhibiting calcium-dependent, agonist-induced contractions in rat aortas. To evaluate whether this effect is also extended to the coronary vasculature, we assessed the effect of statins on serotonin (5-HT) induced contractions of left and right coronary arteries of swine. Concentration-response curves for the 5-HT-induced contractions (from 0.1 nmol/l to 100 micromol/l) were calculated on rings from both coronaries in the presence and absence of either (5 micromol/l) pravastatin, mevastatin, simvastatin, lovastatin, or atorvastatin. After a 45-min incubation period, all statins significantly reduced the Emax for the 5-HT-induced contractions, ranging from 51.9 +/- 1.9% (simvastatin) to 15.9 +/- 2.0% (pravastatin) in the left coronary artery and from 48.8 +/- 2.0% (simvastatin) to 17.8 +/- 2.5% (pravastatin) in the right coronary artery. The EC50 values for the 5-HT-induced contractions were 0.150 +/- 0.005 micromol/l for the left coronary artery and 0.171 +/- 0.010 micromol/l for the right coronary artery. These values significantly changed after incubation with statins, ranging from 1.240 +/- 0.101 micromol/l (for simvastatin) to 0.081+/- 0.008 micromol/l (for pravastatin) in the left coronary artery and from 1.410 +/- 0.075 micromol/l (for simvastatin) to 0.084 +/- 0.008 micromol/l (for pravastatin) in the right coronary artery. This evidence supports the possibility that, beyond their lipid-lowering properties, statins may provide a beneficial effect in atherosclerotic patients by reducing the tone in the coronary vasculature, facilitating blood flow to the myocardium.
Authors:
Maria J Crespo; José A Quidgley
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Publication Detail:
Type:  Comparative Study; In Vitro; Journal Article; Research Support, N.I.H., Extramural     Date:  2006-01-20
Journal Detail:
Title:  Pharmacology     Volume:  76     ISSN:  0031-7012     ISO Abbreviation:  Pharmacology     Publication Date:  2006  
Date Detail:
Created Date:  2006-02-21     Completed Date:  2006-04-19     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0152016     Medline TA:  Pharmacology     Country:  Switzerland    
Other Details:
Languages:  eng     Pagination:  141-7     Citation Subset:  IM    
Copyright Information:
Copyright 2006 S. Karger AG, Basel.
Affiliation:
Department of Physiology, University of Puerto Rico School of Medicine, San Juan, Puerto Rico. mcrespo@rcm.upr.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Coronary Vessels / drug effects*,  physiology
Dose-Response Relationship, Drug
Heptanoic Acids / pharmacology
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacology*
Lovastatin / analogs & derivatives,  pharmacology
Male
Pravastatin / pharmacology
Pyrroles / pharmacology
Serotonin / pharmacology*
Simvastatin / pharmacology
Swine
Time Factors
Vasoconstriction / drug effects*
Grant Support
ID/Acronym/Agency:
2 SO6 GM08224/GM/NIGMS NIH HHS; RR-03051/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Heptanoic Acids; 0/Hydroxymethylglutaryl-CoA Reductase Inhibitors; 0/Pyrroles; 110862-48-1/atorvastatin; 50-67-9/Serotonin; 73573-88-3/compactin; 75330-75-5/Lovastatin; 79902-63-9/Simvastatin; 81093-37-0/Pravastatin

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


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