Hydrogen Sulfide as an Endothelium-Derived Hyperpolarizing Factor in Rodent Mesenteric Arteries

@inproceedings{2011HydrogenSA,
  title={Hydrogen Sulfide as an Endothelium-Derived Hyperpolarizing Factor in Rodent Mesenteric Arteries},
  author={},
  year={2011}
}
  • Published 2011
Hydrogen Sulfide as an Endothelium-Derived Hyperpolarizing Factor in Rodent Mesenteric Arteries To the Editor: We read with interest the article by Mustafa et al1 in Circulation Research in which the authors suggest that hydrogen sulfide is a major endothelium-derived hyperpolarizing factor (EDHF) that generates endothelial and vascular myocyte hyperpolarization and relaxation by predominantly activating ATP-sensitive potassium channels (KATP) through cysteine S-sulfhydration. As previously… CONTINUE READING

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However , it is important to stress that these data do not indicate that nitric oxide and prostacyclin pathways are poorly implicated because AChinduced relaxations involve various overlapping endothelial mechanisms such that when only one or two are inhibited , full ACh - mediated relaxations can still occur.2 In some vessels , nitric oxide or prostacyclin can produce vascular smooth muscle relaxation or hyperpolarization by activating KATP channels.2
We therefore suggest that the overall impairment of these two major vasorelaxant pathways can be reasonably explained by the gross increase in plasma levels of homocysteine observed in cystathionine -lyase knockout mice .
Homocysteine levels are elevated 10-fold in male cystathionine -lyase knockout animals and a staggering 60-fold in comparable female mice.8 Such hyperhomocysteinemia is known to generate oxidative stressdependent endothelial dysfunction associated not only with decreased nitric oxide availability9 but also with a reduction in EDHF - mediated responses by inhibiting activation of small and intermediate conductance calcium - activated potassium channels ( SKCa and IKCa ) .
We therefore suggest that the overall impairment of these two major vasorelaxant pathways can be reasonably explained by the gross increase in plasma levels of homocysteine observed in cystathionine -lyase knockout mice .
Homocysteine levels are elevated 10-fold in male cystathionine -lyase knockout animals and a staggering 60-fold in comparable female mice.8 Such hyperhomocysteinemia is known to generate oxidative stressdependent endothelial dysfunction associated not only with decreased nitric oxide availability9 but also with a reduction in EDHF - mediated responses by inhibiting activation of small and intermediate conductance calcium - activated potassium channels ( SKCa and IKCa ) .
Hydrogen Sulfide as an Endothelium - Derived Hyperpolarizing Factor in Rodent Mesenteric Arteries To the Editor : We read with interest the article by Mustafa et al1 in Circulation Research in which the authors suggest that hydrogen sulfide is a major endothelium - derived hyperpolarizing factor ( EDHF ) that generates endothelial and vascular myocyte hyperpolarization and relaxation by predominantly activating ATP - sensitive potassium channels ( KATP ) through cysteine S - sulfhydration .
Hydrogen Sulfide as an Endothelium - Derived Hyperpolarizing Factor in Rodent Mesenteric Arteries To the Editor : We read with interest the article by Mustafa et al1 in Circulation Research in which the authors suggest that hydrogen sulfide is a major endothelium - derived hyperpolarizing factor ( EDHF ) that generates endothelial and vascular myocyte hyperpolarization and relaxation by predominantly activating ATP - sensitive potassium channels ( KATP ) through cysteine S - sulfhydration .
However , it is important to stress that these data do not indicate that nitric oxide and prostacyclin pathways are poorly implicated because AChinduced relaxations involve various overlapping endothelial mechanisms such that when only one or two are inhibited , full ACh - mediated relaxations can still occur.2 In some vessels , nitric oxide or prostacyclin can produce vascular smooth muscle relaxation or hyperpolarization by activating KATP channels.2
Hydrogen Sulfide as an Endothelium - Derived Hyperpolarizing Factor in Rodent Mesenteric Arteries To the Editor : We read with interest the article by Mustafa et al1 in Circulation Research in which the authors suggest that hydrogen sulfide is a major endothelium - derived hyperpolarizing factor ( EDHF ) that generates endothelial and vascular myocyte hyperpolarization and relaxation by predominantly activating ATP - sensitive potassium channels ( KATP ) through cysteine S - sulfhydration .
Hydrogen Sulfide as an Endothelium - Derived Hyperpolarizing Factor in Rodent Mesenteric Arteries To the Editor : We read with interest the article by Mustafa et al1 in Circulation Research in which the authors suggest that hydrogen sulfide is a major endothelium - derived hyperpolarizing factor ( EDHF ) that generates endothelial and vascular myocyte hyperpolarization and relaxation by predominantly activating ATP - sensitive potassium channels ( KATP ) through cysteine S - sulfhydration .
Hydrogen Sulfide as an Endothelium - Derived Hyperpolarizing Factor in Rodent Mesenteric Arteries To the Editor : We read with interest the article by Mustafa et al1 in Circulation Research in which the authors suggest that hydrogen sulfide is a major endothelium - derived hyperpolarizing factor ( EDHF ) that generates endothelial and vascular myocyte hyperpolarization and relaxation by predominantly activating ATP - sensitive potassium channels ( KATP ) through cysteine S - sulfhydration .
Hydrogen Sulfide as an Endothelium - Derived Hyperpolarizing Factor in Rodent Mesenteric Arteries To the Editor : We read with interest the article by Mustafa et al1 in Circulation Research in which the authors suggest that hydrogen sulfide is a major endothelium - derived hyperpolarizing factor ( EDHF ) that generates endothelial and vascular myocyte hyperpolarization and relaxation by predominantly activating ATP - sensitive potassium channels ( KATP ) through cysteine S - sulfhydration .
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