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Nitric oxide does not mediate flow induced endothelium dependent arterial dilatation in the cat
A M Melkumyants1, S A Balashov, A N Klimachev
1Department of Circulation Biomechanics and Control, Cardiology Research Centre, Moscow, Russia.
Insights
Flow-induced arterial dilation is not mediated by nitric oxide (NO) derived from L-arginine. Inhibition of NO synthesis did not affect flow-induced dilation, suggesting an alternative pathway for this vascular response.
Area of Science:
- Cardiovascular Physiology
- Endothelial Function
- Nitric Oxide Biology
Background:
- Endothelium-derived nitric oxide (NO) plays a crucial role in vascular homeostasis.
- Flow-induced dilation is a key mechanism regulating blood flow in conduit arteries.
- The precise mediators of flow-induced dilation remain an area of active investigation.
Purpose of the Study:
- To investigate whether endothelium-derived nitric oxide (NO) produced from L-arginine mediates flow-induced dilation in conduit arteries.
- To differentiate the role of NO from other vasodilatory mechanisms in response to increased blood flow.
Main Methods:
- Feline femoral artery diameter changes were measured in response to increased blood flow, acetylcholine, and ATP.
- Endothelium-derived NO synthesis was inhibited using NG-nitro-L-arginine methyl ester and NG-monomethyl-L-arginine.
- Vascular responses were assessed before and after NO synthesis inhibition in anesthetized cats.
Main Results:
- Inhibition of NO synthesis increased systemic arterial pressure and constricted the femoral artery.
- Acetylcholine and ATP-induced vasodilation were significantly reduced after NO synthesis inhibition.
- Crucially, the dilator response to increased blood flow rate remained unaffected by NO synthesis inhibition.
Conclusions:
- Flow-induced, endothelium-dependent arterial dilation is not mediated by nitric oxide derived from L-arginine.
- If NO is released during increased flow, its source is distinct from the L-arginine pathway.
- These findings suggest alternative signaling pathways contribute to flow-mediated vascular regulation.
Objective:
The aim was to determine whether the endothelium derived nitric oxide formed from L-arginine is the factor which mediates flow induced dilatation of conduit arteries.
Methods:
Changes in diameter of feline femoral artery caused by blood flow rate increases, acetylcholine, and ATP were recorded during perfusion with blood in situ before and after the inhibition of endothelium derived nitric oxide synthesis by NG-nitro-L-arginine methyl ester and NG-monomethyl-L-arginine. Fourteen anaesthetised cats of either sex, weight 2.6-3.9 kg, were used for the studies.
Results:
Intravenous administration of NG-nitro-L-arginine methyl ester and NG-monoethyl-L-arginine in doses 10 and 30 mg.kg-1 evoked a rise in mean systemic arterial pressure, constriction of the femoral artery, and considerable decrease in acetylcholine and ATP induced dilatation. However, it did not affect the dilator response induced by increased blood flow rate.
Conclusions:
Flow induced endothelium dependent arterial dilatation is not mediated by nitric oxide or, if nitric oxide is still released in response to flow rate increase, it has a source distinct from L-arginine.