Document Detail


Endogenous prostaglandins limit angiotensin-II induced regional vasoconstriction in conscious rats.
MedLine Citation:
PMID:  12827020     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In conscious rats, we tested the hypothesis that prostaglandins attenuate regional vasoconstriction caused by acute infusion of angiotensin II. Mean arterial pressure, regional blood flow, and vascular conductance in response to 2-minute infusions of 0.05 or 1 microg/kg/min Ang II were assessed before and during indomethacin treatment (5 mg/kg). Effects of the lower dose of Ang II (n=8) on regional blood flow were not altered by indomethacin, but conductance in the kidney (2.98+/-0.35 vs. 2.19+/-0.32), stomach (1.15+/-0.13 vs. 0.83+/-0.13), and white gastrocnemius muscle (0.11+/-0.02 vs. 0.07+/-0.01 mL/min/100g/mm Hg) were reduced. Changes in conductance were not seen in the pancreas or spleen. In response to the higher dose of Ang II (n=7), indomethacin reduced blood flow in the kidney, red and white gastrocnemius, and soleus muscles. Reductions in conductance were found in the kidney, stomach and small intestine, and in the red and white gastrocnemius, and soleus muscles (2.27+/-0.9 vs. 1.79+/-0.14, 0.44+/-0.07 vs. 0.27+/-0.03, 0.68+/-0.11 vs. 0.60+/-0.07, 0.43+/-0.08 vs. 0.16+/-0.03, 0.10+/-0.02 vs. 0.05+/-0.01, and 0.26+/-0.03 vs. 0.15+/-0.02 mL/min/100g, respectively). No changes occurred in the pancreas and spleen. Indomethacin had no effect on baseline blood flow or conductance in any of these organs. These results suggest that prostaglandins attenuate vasoconstriction caused by Ang II in a manner that is organ-specific and dependent on the dose of Ang II. Consequently, prostaglandins may limit vasoconstriction and potential ischemia caused by elevated levels of this hormone.
Authors:
Charles L Stebbins; J David Symons; K Sue Hageman; Timothy I Musch
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of cardiovascular pharmacology     Volume:  42     ISSN:  0160-2446     ISO Abbreviation:  J. Cardiovasc. Pharmacol.     Publication Date:  2003 Jul 
Date Detail:
Created Date:  2003-06-26     Completed Date:  2003-11-21     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  7902492     Medline TA:  J Cardiovasc Pharmacol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  10-6     Citation Subset:  IM    
Affiliation:
University of California, Department of Internal Medicine, Division of Cardiovascular Medicine, Davis, California 95616, USA. clstebbins@ucdavis.edu
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MeSH Terms
Descriptor/Qualifier:
Angiotensin II / pharmacology*
Animals
Blood Pressure / drug effects,  physiology
Cyclooxygenase Inhibitors / pharmacology
Dose-Response Relationship, Drug
Indomethacin / pharmacology
Organ Specificity
Prostaglandins / physiology*
Rats
Rats, Wistar
Regional Blood Flow / drug effects,  physiology
Vasoconstriction / drug effects*,  physiology
Vasoconstrictor Agents / pharmacology*
Grant Support
ID/Acronym/Agency:
AG-19228/AG/NIA NIH HHS
Chemical
Reg. No./Substance:
0/Cyclooxygenase Inhibitors; 0/Prostaglandins; 0/Vasoconstrictor Agents; 11128-99-7/Angiotensin II; 53-86-1/Indomethacin

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


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