Document Detail

Contribution of nitric oxide to arterial pressure and heart rate variability in rats submitted to high-sodium intake.
MedLine Citation:
PMID:  11566899     Owner:  NLM     Status:  MEDLINE    
The aim of this study was to determine the contribution of NO to arterial pressure and heart rate variability in normotensive rats subjected to high sodium intake. Arterial pressure, heart rate, and arterial pressure and heart rate variability, baroreflex sensitivity, and pressure responsiveness were measured in male Wistar rats treated for 6 weeks (control and high sodium [1%] intake groups), before and after acute NO synthesis blockade. After treatment, no changes were observed in arterial pressure or heart rate. Arterial pressure variability was increased after sodium intake; however, heart rate variability and baroreflex sensitivity were not modified in high-sodium rats. NO synthase blockade increased arterial pressure in both groups but was higher in the high-sodium group (from 110+/-5 to 162+/-1.5 mm Hg) compared with the control group (from 109+/-6.7 to 144+/-10 mm Hg). The increase in arterial pressure was accompanied by a decrease in heart rate (from 354+/-28 to 303+/-25 bpm in control rats and from 380+/-34 to 298+/-30 bpm in high-sodium rats). NO synthase blockade increased the tachycardic response to sodium nitroprusside in high-sodium rats. Arterial pressure variability, evaluated by a nonlinear method (3D return maps), showed a larger reduction in response to NO synthase inhibition in the high-sodium group (from 162+/-26 to 34.8+/-8.6 for general index of beat-to-beat blood pressure variability) than in the control group (from 58+/-9.6 to 36+/-4.7 for general index of beat-to-beat blood pressure variability). Heart rate variability, evaluated by the SD of the R-R intervals, was not changed in control rats but was increased by NO synthase inhibition in the high-sodium rats (from 9.5+/-0.2 to 21.9+/-1.7 milliseconds). These findings suggest an important role for increased NO production in adaptation to high-sodium intake. The increase in NO system sensitivity in high-sodium intake may contribute to changes in the autonomic nervous system regulating heart rate and, especially, arterial pressure variability.
S Lacchini; E L Ferlin; R S Moraes; J P Ribeiro; M C Irigoyen
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Hypertension     Volume:  38     ISSN:  1524-4563     ISO Abbreviation:  Hypertension     Publication Date:  2001 Sep 
Date Detail:
Created Date:  2001-09-21     Completed Date:  2001-10-18     Revised Date:  2005-11-17    
Medline Journal Info:
Nlm Unique ID:  7906255     Medline TA:  Hypertension     Country:  United States    
Other Details:
Languages:  eng     Pagination:  326-31     Citation Subset:  IM    
Laboratory of Genetics and Molecular Cardiology, Hypertension Unit, Heart Institute (InCor), University of São Paulo, São Paulo, Brazil.
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MeSH Terms
Baroreflex / drug effects
Blood Pressure / drug effects*,  physiology
Chlorides / blood
Dose-Response Relationship, Drug
Enzyme Inhibitors / pharmacology
Heart Rate / drug effects*,  physiology
Nitric Oxide / antagonists & inhibitors,  physiology*
Nitric Oxide Synthase / antagonists & inhibitors
Nitroarginine / pharmacology
Nitroprusside / pharmacology
Phenylephrine / pharmacology
Potassium / blood
Rats, Wistar
Sodium / blood
Sodium, Dietary / administration & dosage*
Vasoconstrictor Agents / pharmacology
Vasodilator Agents / pharmacology
Reg. No./Substance:
0/Chlorides; 0/Enzyme Inhibitors; 0/Sodium, Dietary; 0/Vasoconstrictor Agents; 0/Vasodilator Agents; 10102-43-9/Nitric Oxide; 15078-28-1/Nitroprusside; 2149-70-4/Nitroarginine; 59-42-7/Phenylephrine; 7440-09-7/Potassium; 7440-23-5/Sodium; EC Oxide Synthase

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