Hydrogen Sulfide-Induced Vasodilation: The Involvement of Vascular Potassium Channels

Abstract

Hydrogen sulfide (H2S) has been highlighted as an important gasotransmitter in mammals. A growing number of studies have indicated that H2S plays a key role in the pathophysiology of vascular diseases and physiological vascular homeostasis. Alteration in H2S biogenesis has been reported in a variety of vascular diseases and H2S supplementation exerts effects of vasodilation. Accumulating evidence has shown vascular potassium channels activation is involved in H2S-induced vasodilation. This review aimed to summarize and discuss the role of H2S in the regulation of vascular tone, especially by interaction with different vascular potassium channels and the underlying mechanisms.

Elevated plasma sulfides are associated with cognitive dysfunction and brain atrophy in human Alzheimer's disease and related dementias

“…While it is tempting to regard plasma sulfides exclusively as toxic species based on this and our previous report [ 93 ], sulfides have also been shown to be protective in vascular disease [ 78 ], where free sulfide preserves brain vasomotion [ 80 ], protects against global and focal cerebral ischemic injury [ 81 , 82 ] and is involved in blood brain barrier integrity [ 83 , 84 ]. Thus, it is highly likely that some sulfide species are neuro-protective, and that elevated hydrogen sulfide with limited generation of acid-labile and bound sulfides is adaptive, but that accumulation of bound (and possibly acid labile) sulfides become cytotoxic.…”

“…Sulfides are protective in vascular disease [ 78 ], with decreased levels of bound, acid labile and total sulfides predicting cardiovascular disease risk [ 79 ]. Studies have demonstrated that hydrogen sulfide is produced by cerebral microvessels; we and others have also previously described that free sulfide preserves brain vasomotion [ 80 ], protects against global and focal cerebral ischemic injury [ 81 , 82 ], and participates in blood brain barrier integrity [ 83 , 84 ].…”

Treatment of refractory shock with vitamin B12: A narrative review

“…Impaired mitochondrial function occurs as hydrogen sulfide exerts toxic effects on cytochrome c oxidase, an enzyme in mitochondrial aerobic metabolism 13 . Vascular smooth muscle relaxation occurs as a result of activation of adenosine triphosphate–sensitive potassium channels and inhibition of angiotensin‐converting enzyme at the vascular endothelium 13,14 . The effect of hydroxocobalamin on hydrogen sulfide action is less clear than with NO, but it is proposed that hydroxocobalamin may scavenge circulating hydrogen sulfide as seen in animal models of hydrogen sulfide toxicity 15 …”

“…13 Vascular smooth muscle relaxation occurs as a result of activation of adenosine triphosphate-sensitive potassium channels and inhibition of angiotensin-converting enzyme at the vascular endothelium. 13,14 The effect of hydroxocobalamin on hydrogen sulfide action is less clear than with NO, but it is proposed that hydroxocobalamin may scavenge circulating hydrogen sulfide as seen in animal models of hydrogen sulfide toxicity. 15 Hydroxocobalamin is one of several vitamers of vitamin B 12 .…”

Hydrogen Sulfide and Oxygen Homeostasis in Atherosclerosis: A Systematic Review from Molecular Biology to Therapeutic Perspectives

“…Recent studies have demonstrated that H 2 S plays a crucial role in regulating various aspects of cardiovascular health, including blood pressure, vascular tone, inflammation, and oxidative stress [29]. H 2 S has been shown to promote vasodilation by activating potassium channels and inhibiting calcium channels in vascular smooth muscle cells [30]. Moreover, H 2 S has been found to regulate endothelial function by stimulating the release of nitric oxide (NO), a potent vasodilator that plays a key role in maintaining vascular homeostasis.…”