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H2S-induced vasorelaxation and underlying cellular and molecular…
H2S-induced vasorelaxation and underlying cellular and molecular mechanisms
Introduction
H2S & vascular smooth muscle cells
H2S induced a concentration-dependent relaxation of rat aortic tissues that was not affected by vascular denervation.
The vasorelaxant potency of H2S was attenuated by the removal of the endothelium.
The vasorelaxant effect of H2S was also significantly attenuated when Ca2+-free bath solution was used.
pretreatment of aortic tissues with H2S reduced the relaxant response of vascular tissues to SNP
H2S toxic gas
major toxic effects are the toxication of central nervous system and the inhibition of the respiratory system
H2S can also be produced endogenously from l-cysteine by (CBS) and/or (CSE)
tissue content of H2S in the brain has been determined to be between 50 and 160 μM
In both the aorta and portal vein of rats, H2S induced a dose-dependent relaxation, but other thiol-containing endogenous substances such as cysteine and glutathione did not have any vasorelaxant effect
vascular effects of H2S
the activation of ATP-sensitive K+ (KATP) channels in vascular smooth muscle cells (SMCs) might play an important role
The interaction of H2S with different cellular signaling pathways in vascular SMCs, including cGMP and oxygen-derived free radicals, has not been systematically examined
RESULTS
Vasorelaxation induced by NaHS and H2S gas.
vasorelaxation induced by both NaHS and H2S could be reversed by removing the chemicals
Effect of denervation on H2S-induced vasorelaxation.
cumulative effect of H2S at different concentrations was examined on denervated or endothelium-free aortic tissues
Interaction of H2S and endothelium on H2S-induced vasorelaxation.
removal of the endothelium with saponin treatment
The coapplication of the Ca2+-dependent K+ (KCa) channel blockers apamin and charybdotoxin
Involvement of the cGMP pathway in H2S-induced vasorelaxation.
whether the H2S-induced vasorelaxation was mediated by this pathway
the soluble guanylyl cyclase (sGC) inhibitors ODQ and NS-2028，respectively
the H2S-induced relaxation was potentiated by ODQ or NS-2028.
Influence of extracellular [Ca2+] entry on H2S-induced vasorelaxation.
whether the H2S-induced relaxation was mediated by an extracellular [Ca2+]-dependent mechanism
either using a calcium-free bath solution or with the normal bath solution but in the presence of nifedipine, a voltage-gated Ca2+ channel inhibitor
Interaction between H2S and SNP on vascular contractility.