The effect of hydrogen sulfide on the contractility of cerebral arterioles. A pilot study

Background and Aims: Endogenous gaseous substances, such as NO and CO have been found to be effective vasodilators earlier. H2S has been identified as an additional one, however, for that substance both vasodilatory and vasoconstrictor responses have been described in different vascular territories. Our aim was to examine the effect of hydrogen sulfide on the tone of cerebral arterioles and some aspects of its mechanism. Methods: The work was performed on excised rat anterior cerebral artery segments in vitro (diameter range 150-250 mu m), using a pressure myograph system. We used NaHS as exogenous H2S donor, propargylglycine (PAG) to abolish the endogenous synthesis of hydrogen sulfide and 4,4'-Diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS) to examine the potential role of Cl-/HCO3-. exchanger in the effects of H2S. The time course of the events after application of exogenous H2S was also evaluated. Results: Our findings revealed that in these pathologically important vessels (1) endogenously produced H2S is not a vasodilator, but a moderate vasoconstrictor, (2) H2S has a biphasic effect: low concentrations are moderate vasoconstrictors, while at higher concentrations the initial contraction is followed by dilatation; (3) that vasodilation is prevented by DIDS (4,4'-Diisothiocyanatostilbene-2,2'-disulfonic acid disodium, an inhibitor of the Cl-/HCO3 exchanger). Conclusion: These studies confirm that H2S should be taken into consideration as a modulator of cerebral arteriolar tone in mammals.

Automated summary

This study investigated the effect of hydrogen sulfide on cerebral arteriolar tone and its mechanism. The results showed that endogenously produced hydrogen sulfide is a moderate vasoconstrictor in these important vessels. Hydrogen sulfide exhibits a biphasic effect, with low concentrations causing moderate vasoconstriction and higher concentrations leading to initial contraction followed by dilation. The vasodilation effect is prevented by inhibition of the Cl-/HCO3- exchanger.