Sulfur dioxide: a physiologic endothelium-derived relaxing factor

Abstract

The gasotransmitter nitric oxide was classified as the first endothelium-derived relaxant factor, and opened a new era in cardiovascular research. Another small gas, sulfur dioxide (SO₂), can also be generated endogenously in mammals. Recent studies have shown that SO₂ may play important roles in the cardiovascular system. At low concentrations, the vasodilatory effect of SO₂ is endothelium-dependent. The vasodilation induced by an endothelium-derived relaxant factor is achieved by the opening of potassium channels, and hyperpolarization of the membranes of vascular smooth muscle cells. This feature is in accordance with that of SO₂. The vasodilatory effect of SO₂ is related to the opening of adenosine triphosphate-sensitive potassium channels and high-conductance calcium-activated potassium channels. The 3'-5'-cyclic guanosine monophosphate pathway and activation of nitric oxide synthase are also involved in the endothelium-derived relaxant factor effect of SO₂. The vasodilatory effect of gaseous SO₂ is much stronger than that of its derivatives (bisulfite and sulfite). It is suggested that SO₂ may be a candidate endothelium-derived relaxant factor, which could lead to a new era of research into cardiovascular disease in mammals.