Abstract
Aims: Hydrogen sulfide (H2S) at low concentrations serves as a physiological endogenous vasodilator molecule, while at higher concentrations it can trigger cytotoxic effects. The aim of our study was to elucidate the potential mechanisms responsible for the effects of H2S on vascular tone. Main methods: We measured the vascular tone in vitro in precontracted rat thoracic aortic rings and we have tested the effect of different oxygen levels and a variety of inhibitors affecting known vasodilatory pathways. We have also compared the vascular effect of high concentrations of H2S to those of pharmacological inhibitors of oxidative phosphorylation. Furthermore, we measured adenosine triphosphate (ATP)-levels in the same vascular tissues. Key findings: We have found that in rat aortic rings: (1) H2S decreases ATP levels; (2) relaxations to H2S depend on the ambient oxygen concentration; (3) prostaglandins do not take part in the H2S induced relaxations; (4) the 3':5'-cyclic guanosine monophosphate (cGMP)-nitric oxide (NO) pathway does not have a role in the relaxations (5) the role of KATP channels is limited, while Cl-/HCO3 - channels have a role in the relaxations. (6): We have observed that high concentrations of H2S relax the aortic rings in a fashion similar to sodium cyanide, and both agents reduce cellular ATP levels to a comparable degree. Significance: H2S, a new gasotransmitter of emerging importance, leads to relaxation via Cl-/HCO3 - channels and metabolic inhibition and the interactions of these two factors depend on the oxygen levels of the tissue.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 589-594 |
| Number of pages | 6 |
| Journal | Life Sciences |
| Volume | 83 |
| Issue number | 17-18 |
| DOIs | |
| State | Published - Oct 24 2008 |
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Keywords
- Hydrogen sulfide
- Oxidative phosphorylation
- Vasorelaxation
ASJC Scopus subject areas
- Pharmacology, Toxicology and Pharmaceutics(all)
- Biochemistry, Genetics and Molecular Biology(all)
Cite this
Hydrogen sulfide decreases adenosine triphosphate levels in aortic rings and leads to vasorelaxation via metabolic inhibition. / Kiss, Levente; Deitch, Edwin A.; Szabo, Csaba.
In: Life Sciences, Vol. 83, No. 17-18, 24.10.2008, p. 589-594.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Hydrogen sulfide decreases adenosine triphosphate levels in aortic rings and leads to vasorelaxation via metabolic inhibition
AU - Kiss, Levente
AU - Deitch, Edwin A.
AU - Szabo, Csaba
PY - 2008/10/24
Y1 - 2008/10/24
N2 - Aims: Hydrogen sulfide (H2S) at low concentrations serves as a physiological endogenous vasodilator molecule, while at higher concentrations it can trigger cytotoxic effects. The aim of our study was to elucidate the potential mechanisms responsible for the effects of H2S on vascular tone. Main methods: We measured the vascular tone in vitro in precontracted rat thoracic aortic rings and we have tested the effect of different oxygen levels and a variety of inhibitors affecting known vasodilatory pathways. We have also compared the vascular effect of high concentrations of H2S to those of pharmacological inhibitors of oxidative phosphorylation. Furthermore, we measured adenosine triphosphate (ATP)-levels in the same vascular tissues. Key findings: We have found that in rat aortic rings: (1) H2S decreases ATP levels; (2) relaxations to H2S depend on the ambient oxygen concentration; (3) prostaglandins do not take part in the H2S induced relaxations; (4) the 3':5'-cyclic guanosine monophosphate (cGMP)-nitric oxide (NO) pathway does not have a role in the relaxations (5) the role of KATP channels is limited, while Cl-/HCO3 - channels have a role in the relaxations. (6): We have observed that high concentrations of H2S relax the aortic rings in a fashion similar to sodium cyanide, and both agents reduce cellular ATP levels to a comparable degree. Significance: H2S, a new gasotransmitter of emerging importance, leads to relaxation via Cl-/HCO3 - channels and metabolic inhibition and the interactions of these two factors depend on the oxygen levels of the tissue.
AB - Aims: Hydrogen sulfide (H2S) at low concentrations serves as a physiological endogenous vasodilator molecule, while at higher concentrations it can trigger cytotoxic effects. The aim of our study was to elucidate the potential mechanisms responsible for the effects of H2S on vascular tone. Main methods: We measured the vascular tone in vitro in precontracted rat thoracic aortic rings and we have tested the effect of different oxygen levels and a variety of inhibitors affecting known vasodilatory pathways. We have also compared the vascular effect of high concentrations of H2S to those of pharmacological inhibitors of oxidative phosphorylation. Furthermore, we measured adenosine triphosphate (ATP)-levels in the same vascular tissues. Key findings: We have found that in rat aortic rings: (1) H2S decreases ATP levels; (2) relaxations to H2S depend on the ambient oxygen concentration; (3) prostaglandins do not take part in the H2S induced relaxations; (4) the 3':5'-cyclic guanosine monophosphate (cGMP)-nitric oxide (NO) pathway does not have a role in the relaxations (5) the role of KATP channels is limited, while Cl-/HCO3 - channels have a role in the relaxations. (6): We have observed that high concentrations of H2S relax the aortic rings in a fashion similar to sodium cyanide, and both agents reduce cellular ATP levels to a comparable degree. Significance: H2S, a new gasotransmitter of emerging importance, leads to relaxation via Cl-/HCO3 - channels and metabolic inhibition and the interactions of these two factors depend on the oxygen levels of the tissue.
KW - Hydrogen sulfide
KW - Oxidative phosphorylation
KW - Vasorelaxation
UR - http://www.scopus.com/inward/record.url?scp=53249087745&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=53249087745&partnerID=8YFLogxK
U2 - 10.1016/j.lfs.2008.08.006
DO - 10.1016/j.lfs.2008.08.006
M3 - Article
C2 - 18790700
AN - SCOPUS:53249087745
VL - 83
SP - 589
EP - 594
JO - Life Sciences
JF - Life Sciences
SN - 0024-3205
IS - 17-18
ER -