| Chronic vasodilation produces plasma volume expansion and hemodilution in rats: consequences of decreased effective arterial blood volume. | |
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MedLine Citation:
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PMID: 20980409 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Andrea Fekete; Jennifer M Sasser; Chris Baylis |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2010-10-27 |
Journal Detail:
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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:
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Created Date: 2011-01-07 Completed Date: 2011-02-09 Revised Date: 2012-01-02 |
Medline Journal Info:
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Nlm Unique ID: 100901990 Medline TA: Am J Physiol Renal Physiol Country: United States |
Other Details:
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Languages: eng Pagination: F113-8 Citation Subset: IM |
Affiliation:
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Department of Physiology and Functional Genomics, University of Florida, PO Box 100274, Gainesville, FL 32610, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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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:
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R01-DK-56843/DK/NIDDK NIH HHS; R01-HD-041571/HD/NICHD NIH HHS; T32 HL083810/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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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 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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