PMID- 20980409
OWN - NLM
STAT- MEDLINE
DCOM- 20110209
LR  - 20240323
IS  - 1522-1466 (Electronic)
IS  - 0363-6127 (Print)
IS  - 1522-1466 (Linking)
VI  - 300
IP  - 1
DP  - 2011 Jan
TI  - Chronic vasodilation produces plasma volume expansion and hemodilution in rats: 
      consequences of decreased effective arterial blood volume.
PG  - F113-8
LID - 10.1152/ajprenal.00478.2010 [doi]
AB  - 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.
FAU - Fekete, Andrea
AU  - Fekete A
AD  - Department of Physiology and Functional Genomics, University of Florida, PO Box 
      100274, Gainesville, FL 32610, USA.
FAU - Sasser, Jennifer M
AU  - Sasser JM
FAU - Baylis, Chris
AU  - Baylis C
LA  - eng
GR  - R01 DK056843/DK/NIDDK NIH HHS/United States
GR  - T32 HL083810/HL/NHLBI NIH HHS/United States
GR  - R01-HD-041571/HD/NICHD NIH HHS/United States
GR  - R01-DK-56843/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
DEP - 20101027
PL  - United States
TA  - Am J Physiol Renal Physiol
JT  - American journal of physiology. Renal physiology
JID - 100901990
RN  - 0 (RNA, Messenger)
RN  - 0 (Vasodilator Agents)
RN  - EC 3.1.4.35 (Cyclic Nucleotide Phosphodiesterases, Type 5)
RN  - I9ZF7L6G2L (Nifedipine)
RN  - M0KG633D4F (Sodium Nitrite)
SB  - IM
MH  - Animals
MH  - Blood Pressure/drug effects
MH  - Blood Volume/*physiology
MH  - Cyclic Nucleotide Phosphodiesterases, Type 5/metabolism
MH  - Female
MH  - Hemodilution
MH  - Nifedipine/pharmacology
MH  - Osmolar Concentration
MH  - Plasma Volume/drug effects/*physiology
MH  - Pregnancy/*physiology
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sodium Nitrite/pharmacology
MH  - Vasodilation/*physiology
MH  - Vasodilator Agents/pharmacology
PMC - PMC3023232
EDAT- 2010/10/29 06:00
MHDA- 2011/02/10 06:00
PMCR- 2012/01/01
CRDT- 2010/10/29 06:00
PHST- 2010/10/29 06:00 [entrez]
PHST- 2010/10/29 06:00 [pubmed]
PHST- 2011/02/10 06:00 [medline]
PHST- 2012/01/01 00:00 [pmc-release]
AID - ajprenal.00478.2010 [pii]
AID - F-00478-2010 [pii]
AID - 10.1152/ajprenal.00478.2010 [doi]
PST - ppublish
SO  - Am J Physiol Renal Physiol. 2011 Jan;300(1):F113-8. doi: 
      10.1152/ajprenal.00478.2010. Epub 2010 Oct 27.