In addition to nitric oxide and carbon monoxide, hydrogen sulfide (H
2S), synthesized enzymatically from l-cysteine or l-homocysteine, is the third gasotransmitter in mammals. Endogenous H
2S is involved in the regulation of many physiological processes, including vascular tone. Although initially
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In addition to nitric oxide and carbon monoxide, hydrogen sulfide (H
2S), synthesized enzymatically from l-cysteine or l-homocysteine, is the third gasotransmitter in mammals. Endogenous H
2S is involved in the regulation of many physiological processes, including vascular tone. Although initially it was suggested that in the vascular wall H
2S is synthesized only by smooth muscle cells and relaxes them by activating ATP-sensitive potassium channels, more recent studies indicate that H
2S is synthesized in endothelial cells as well. Endothelial H
2S production is stimulated by many factors, including acetylcholine, shear stress, adipose tissue hormone leptin, estrogens and plant flavonoids. In some vascular preparations H
2S plays a role of endothelium-derived hyperpolarizing factor by activating small and intermediate-conductance calcium-activated potassium channels. Endothelial H
2S signaling is up-regulated in some pathologies, such as obesity and cerebral ischemia-reperfusion. In addition, H
2S activates endothelial NO synthase and inhibits cGMP degradation by phosphodiesterase 5 thus potentiating the effect of NO-cGMP pathway. Moreover, H
2S-derived polysulfides directly activate protein kinase G. Finally, H
2S interacts with NO to form nitroxyl (HNO)—a potent vasorelaxant. H
2S appears to play an important and multidimensional role in endothelium-dependent vasorelaxation.
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