Document Detail


Chronic vasodilation produces plasma volume expansion and hemodilution in rats: consequences of decreased effective arterial blood volume.
MedLine Citation:
PMID:  20980409     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Plasma volume (PV) expansion is required for optimal pregnancy outcomes; however, the mechanisms responsible for sodium and water retention in pregnancy remain undefined. This study was designed to test the "arterial underfill hypothesis" of pregnancy which proposes that an enlarged vascular compartment (due to systemic vasodilation and shunting of blood to the placenta) results in renal sodium and water retention and PV expansion. We produced chronic vasodilation by 14 days administration of nifedipine (NIF; 10 mg·kg(-1)·day(-1)) or sodium nitrite (NaNO2; 70 mg·kg(-1)·day(-1)) to normal, nonpregnant female Sprague-Dawley rats. Mean arterial pressure, monitored by telemetry, was reduced by both NIF and NaNO2 but was unchanged in control rats. At day 14, vasodilator treatment lowered hematocrit and increased PV (determined by Evans blue dye dilution). Plasma osmolarity (Posm), sodium (PNa), and total protein concentrations all fell. These responses resemble the responses to normal pregnancy with hemodilution, marked PV expansion, and decreased Posm and PNa. Our previous work indicates a role of increased inner medullary phosphodiesterase-5 (PDE5) in the sodium retention of pregnancy. Here, we found that inner medullary PDE5A mRNA and protein expression were increased by both NIF and NaNO2 treatment vs. control; however, neither renal cortical nor aortic PDE5 expression was changed by vasodilator treatment. We suggest that a primary, persistent vasodilation drives increased inner medullary PDE5 expression which facilitates continual renal Na retention causing "refilling" of the vasculature and volume expansion.
Authors:
Andrea Fekete; Jennifer M Sasser; Chris Baylis
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-10-27
Journal Detail:
Title:  American journal of physiology. Renal physiology     Volume:  300     ISSN:  1522-1466     ISO Abbreviation:  Am. J. Physiol. Renal Physiol.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2011-01-07     Completed Date:  2011-02-09     Revised Date:  2013-07-03    
Medline Journal Info:
Nlm Unique ID:  100901990     Medline TA:  Am J Physiol Renal Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  F113-8     Citation Subset:  IM    
Affiliation:
Department of Physiology and Functional Genomics, University of Florida, PO Box 100274, Gainesville, FL 32610, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Pressure / drug effects
Blood Volume / physiology*
Cyclic Nucleotide Phosphodiesterases, Type 5 / metabolism
Female
Hemodilution
Nifedipine / pharmacology
Osmolar Concentration
Plasma Volume / drug effects,  physiology*
Pregnancy / physiology*
RNA, Messenger / metabolism
Rats
Rats, Sprague-Dawley
Sodium Nitrite / pharmacology
Vasodilation / physiology*
Vasodilator Agents / pharmacology
Grant Support
ID/Acronym/Agency:
R01-DK-56843/DK/NIDDK NIH HHS; R01-HD-041571/HD/NICHD NIH HHS; T32 HL083810/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/RNA, Messenger; 0/Vasodilator Agents; 21829-25-4/Nifedipine; 7632-00-0/Sodium Nitrite; EC 3.1.4.35/Cyclic Nucleotide Phosphodiesterases, Type 5
Comments/Corrections

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


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