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Glutathione reverses endothelial dysfunction and improves nitric oxide bioavailability
A Prasad1, N P Andrews, F A Padder
1Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892-1650, USA.
Journal of the American College of Cardiology
|August 10, 1999
Summary
Glutathione (GSH) supplementation enhances nitric oxide (NO) activity and improves blood vessel function in patients with atherosclerosis. This thiol therapy selectively targets endothelial dysfunction, offering a potential treatment for related cardiovascular conditions.
Area of Science:
- Cardiovascular Research
- Biochemistry
- Medical Science
Background:
- Endothelial dysfunction and reduced nitric oxide (NO) activity are key factors in atherosclerosis and unstable angina.
- Understanding mechanisms to improve NO bioavailability is crucial for managing cardiovascular disease.
Purpose of the Study:
- To investigate if glutathione (GSH) enhances endothelium-dependent vasomotion and NO activity in atherosclerosis.
- To determine the effect of GSH on acetylcholine (ACH)-mediated vasodilation and cyclic guanylate monophosphate (cGMP) levels.
Main Methods:
- Studied 17 patients with atherosclerosis or risk factors, measuring vasodilation with ACH, nitroglycerin, and sodium nitroprusside before and after GSH infusion.
- Measured femoral vein plasma cGMP levels during ACH infusion in 10 patients.
- Assessed femoral artery flow velocity and calculated the flow resistance index (FVRI).
Main Results:
- GSH significantly potentiated ACH-mediated vasodilation, decreasing FVRI by 47-56% before and 61-67% after supplementation (p=0.003).
- GSH increased femoral vein cGMP levels during ACH infusion from 17.6 to 23.3 pmol/ml (p=0.006).
- These improvements were observed specifically in patients with impaired endothelial function and did not affect endothelium-independent vasodilation.
Conclusions:
- Thiol supplementation with GSH selectively improves endothelial dysfunction in humans.
- GSH enhances NO activity, offering a targeted approach to improving vascular function in atherosclerosis.