Hydrogen Sulfide and Endothelium-Dependent Vasorelaxation

Molecules

Jerzy Bełtowski¹  Anna Jamroz-Wiśniewska² 

[1] Department of Pathophysiology, Medical University, 20-150 Lublin, Poland;Department of Neurology, Medical University, 20-090 Lublin, Poland; E-Mail:

关键词: hydrogen sulfide;    endothelium-derived hyperpolarizing factor;    potassium channels;    nitric oxide;    cyclic GMP;    protein kinase G;    nitroxyl;    perivascular sensory neurons;   

DOI  :  10.3390/molecules191221183

来源: mdpi

【 摘 要 】

In addition to nitric oxide and carbon monoxide, hydrogen sulfide (H₂S), synthesized enzymatically from l-cysteine or l-homocysteine, is the third gasotransmitter in mammals. Endogenous H₂S is involved in the regulation of many physiological processes, including vascular tone. Although initially it was suggested that in the vascular wall H₂S is synthesized only by smooth muscle cells and relaxes them by activating ATP-sensitive potassium channels, more recent studies indicate that H₂S is synthesized in endothelial cells as well. Endothelial H₂S production is stimulated by many factors, including acetylcholine, shear stress, adipose tissue hormone leptin, estrogens and plant flavonoids. In some vascular preparations H₂S plays a role of endothelium-derived hyperpolarizing factor by activating small and intermediate-conductance calcium-activated potassium channels. Endothelial H₂S signaling is up-regulated in some pathologies, such as obesity and cerebral ischemia-reperfusion. In addition, H₂S activates endothelial NO synthase and inhibits cGMP degradation by phosphodiesterase 5 thus potentiating the effect of NO-cGMP pathway. Moreover, H₂S-derived polysulfides directly activate protein kinase G. Finally, H₂S interacts with NO to form nitroxyl (HNO)—a potent vasorelaxant. H₂S appears to play an important and multidimensional role in endothelium-dependent vasorelaxation.

【 授权许可】

CC BY   
© 2014 by the authors; licensee MDPI, Basel, Switzerland.