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The hemodynamic response to nitrite is acute and dependent upon tissue perfusion
Luke S Dunaway1, Khatera Saii2, Anthea LoBue3
1Robert M. Berne Cardiovascular Research Center, University of Virginia School of Medicine, Germany.
Nitric Oxide : Biology and Chemistry
|August 3, 2024
Summary
Nitrite administration acutely improved tissue perfusion and lowered blood pressure in mice lacking endothelial nitric oxide synthase (eNOS), suggesting nitrite
Area of Science:
- Vascular biology
- Cardiovascular physiology
- Nitric oxide signaling
Background:
- Nitric oxide (NO) produced by endothelial nitric oxide synthase (eNOS) regulates vascular tone.
- Hypoxia may facilitate nitrite-derived NO formation, impacting blood flow.
- eNOS knockout (KO) mice exhibit reduced tissue perfusion compared to wild-type (WT) mice.
Purpose of the Study:
- To investigate the effects of nitrite administration on tissue perfusion and systemic hemodynamics in WT and eNOS KO mice.
- To determine if nitrite can restore normal blood flow and pressure in a model of hypoperfusion.
Main Methods:
- Laser speckle contrast imaging was used to assess tissue perfusion.
- Sodium nitrite was administered intraperitoneally to mice over 4 consecutive days.
- Systemic blood pressure was measured using invasive Millar catheterization.
Main Results:
- Nitrite administration dose-dependently increased peripheral blood flow in eNOS KO mice but not WT mice.
- These perfusion changes were transient, lasting less than 24 hours.
- High-dose nitrite acutely decreased blood pressure in eNOS KO mice, inversely correlating with baseline perfusion.
Conclusions:
- Nitrite administration can acutely reverse hypoperfusion and hypertension in eNOS deficient mice.
- The vasodilatory effects of nitrite appear dependent on the presence of tissue hypoperfusion.
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