Contribution of nitric oxide to arterial pressure and heart rate variability in rats submitted to high-sodium intake.
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.
Lacchini
S
S
Laboratory of Genetics and Molecular Cardiology, Hypertension Unit, Heart Institute (InCor), University of São Paulo, São Paulo, Brazil.
Ferlin
E L
EL
Moraes
R S
RS
Ribeiro
J P
JP
Irigoyen
M C
MC
D000818:Animals; D017704:Baroreflex / Q000187:drug effects; D001794:Blood Pressure / Q000187:drug effects* / Q000502:physiology; D002712:Chlorides / Q000097:blood; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects* / Q000502:physiology; D008297:Male; D009569:Nitric Oxide / Q000037:antagonists & inhibitors / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D019335:Nitroarginine / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011188:Potassium / Q000097:blood; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000097:blood; D012982:Sodium, Dietary / Q000008:administration & dosage*; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
D002712:Chlorides; D004791:Enzyme Inhibitors; D012982:Sodium, Dietary; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009599:Nitroprusside; D010656:Phenylephrine; D019335:Nitroarginine; D009569:Nitric Oxide; D012964:Sodium; D019001:Nitric Oxide Synthase; D011188:Potassium