Hydrogen sulfide, renin, and regulating the second messenger cAMP. focus on 'hydrogen sulfide regulates cAMP homeostasis and renin degranulation in As4.1 and rat renin-rich kidney cell'

摘要

the nonessential amino acid cysteine is catabolized by desul-furation, thereby releasing sulfur in a reduced oxidation state and generating sulfane sulfur or hydrogen sulfide (EfeS). H2S can be further oxidized to sulfate (10), a form of sulfur that can be excreted by the kidney. H2S can be produced within many mammalian cell types, and consequently this gaseous metabolite has received increasing interest as a possible signaling molecule, especially because it has physical characteristics akin to those of the more widely studied receptor-independent gasotransmitters nitric oxide and carbon monoxide (10). H2S has been reported to exist in as high as micromolar concentrations in various mammalian tissues, including the brain, kidney, liver, skin, lymphocytes, and vascular smooth muscle (10). Endogenous H2S production is primarily the result of two enzymes: cystathione (3-synthase and cystathione 7-lyase.