Document Detail


Renal effects of prostaglandin inhibition during increases in renal venous pressure.
MedLine Citation:
PMID:  2012205     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The role of prostaglandins (PGs) in mediating the hemodynamic and natriuretic responses to increases in renal interstitial pressure (RIP) induced by altering renal venous pressure (RVP) from control (3.6 +/- 0.6) to 15 and 30 mmHg was examined before and after PG inhibition in pentobarbital sodium-anesthetized dogs. These elevations of RVP resulted in RIP increasing from control (6 +/- 1) to 11 +/- 1 and 23 +/- 2 mmHg, respectively, without altering mean arterial pressure (MAP), renal blood flow (RBF), and glomerular filtration rate (GFR). Sodium excretion increased only when RVP reached 30 mmHg. During the inhibition of PG synthesis, 15 mmHg RVP induced a 10% decrease in RBF, and 30 mmHg RVP induced a further 20% decrease in RBF and a 50% decrease in GFR. PG synthesis inhibition did not alter either the RIP or the sodium excretory response. In conclusion, the natriuresis associated with the RIP increases induced by increasing RVP appears to be independent of PG synthesis. PGs, however, appear to be important for the maintenance of RBF and GFR during increased RVP. These findings suggest that different mechanisms are involved in the hemodynamic and natriuretic responses to arterial vs. venous pressure changes.
Authors:
M J Fiksen-Olsen; J C Romero
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The American journal of physiology     Volume:  260     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1991 Apr 
Date Detail:
Created Date:  1991-05-09     Completed Date:  1991-05-09     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  F525-9     Citation Subset:  IM    
Affiliation:
Department of Physiology and Biophysics, Mayo School of Medicine, Rochester, Minnesota 55905.
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MeSH Terms
Descriptor/Qualifier:
6-Ketoprostaglandin F1 alpha / urine
Animals
Blood Flow Velocity
Blood Pressure
Dinoprostone / urine
Dogs
Female
Glomerular Filtration Rate
Indomethacin / pharmacology
Kidney / blood supply*
Male
Meclofenamic Acid / pharmacology
Natriuresis
Prostaglandin Antagonists / pharmacology
Prostaglandins / physiology*
Renal Veins / physiology*
Renin / blood
Venous Pressure*
Grant Support
ID/Acronym/Agency:
HL-16496/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Prostaglandin Antagonists; 0/Prostaglandins; 363-24-6/Dinoprostone; 53-86-1/Indomethacin; 58962-34-8/6-Ketoprostaglandin F1 alpha; 644-62-2/Meclofenamic Acid; EC 3.4.23.15/Renin

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


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