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Sulfur dioxide: a physiologic endothelium-derived relaxing factor.
Xin-Bao Wang1, Hong Cui2, Jun-Bao Du3
1Department of Pediatrics, Beijing Friendship Hospital, Capital Medical University, Beijing, PR China.
Histology and Histopathology
|July 7, 2016
Summary
Sulfur dioxide (SO₂), a gasotransmitter, demonstrates endothelium-dependent vasodilation by opening potassium channels. This suggests SO₂ may be a novel endothelium-derived relaxant factor, potentially revolutionizing cardiovascular research.
Area of Science:
- Cardiovascular Physiology
- Gasotransmitter Signaling
Background:
- Nitric oxide (NO) was the first identified endothelium-derived relaxant factor (EDRF).
- Endogenous sulfur dioxide (SO₂) is increasingly recognized for its physiological roles, particularly in the cardiovascular system.
Approach:
- Investigated the vasodilatory effects of SO₂ at low concentrations.
- Examined the mechanisms of SO₂-induced vasodilation, including potassium channel activity and signaling pathways.
Key Points:
- SO₂ exhibits endothelium-dependent vasodilation, similar to NO.
- Vasodilation involves the opening of potassium channels (ATP-sensitive and calcium-activated) and vascular smooth muscle hyperpolarization.
- The 3'-5'-cyclic guanosine monophosphate pathway and nitric oxide synthase activation are implicated in SO₂'s EDRF-like effects.
- Gaseous SO₂ is more potent than its derivatives (bisulfite, sulfite).
Conclusions:
- SO₂ acts as an endothelium-derived relaxant factor.
- SO₂ may represent a new frontier in understanding and treating cardiovascular diseases.
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