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Modulation of gap-junction-dependent arterial relaxation by ascorbic acid.

David H Edwards¹, Andrew T Chaytor, Linda M Bakker

¹Department of Diagnostic Radiology, Wales Heart Research Institute, Cardiff University, Cardiff, UK.

Journal of Vascular Research

|June 26, 2007

Summary

Ascorbic acid (AA) preserves arterial electrotonic signaling through gap junctions, enhancing endothelium-dependent relaxation. This previously unrecognized ability of AA supports cell coupling when it is otherwise impaired.

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Area of Science:

Cardiovascular Physiology
Endothelial Function
Cellular Electrophysiology

Background:

Endothelium-dependent relaxation is crucial for vascular health.
Gap junctions mediate intercellular communication in the arterial wall.
The role of ascorbic acid (AA) in regulating these processes is not fully understood.

Purpose of the Study:

To investigate if ascorbic acid (AA) influences endothelium-dependent relaxation.
To determine if AA modulates the spread of endothelial hyperpolarization via gap junctions.

Main Methods:

Myography and sharp electrode techniques were used on isolated rabbit iliac arteries.
Gap junction blockers and connexin-mimetic peptides were employed.
Nitric oxide (NO) synthase and cyclooxygenase blockade were performed.

Main Results:

AA prevented gap junction blockers from inhibiting endothelium-dependent relaxations and smooth muscle hyperpolarizations.
AA counteracted the effects of peptides that attenuate hyperpolarization spread.
AA did not enhance relaxation mediated by residual NO.

Conclusions:

Ascorbic acid (AA) preserves electrotonic signaling through myoendothelial and smooth muscle gap junctions.
AA modulates arterial function by maintaining cell coupling under depressed conditions.
The mechanism does not involve increased 'residual' NO activity.