Bicarbonate-dependent effect of hydrogen sulfide on vascular contractility in rat aortic rings

Abstract

Hydrogen sulfide (H2S), an endogenous gaseous mediator, produces both vasorelaxation and vasoconstriction at different concentrations. We found in the present study that NaHS, an H2S donor, produced stronger vasorelaxant and weaker vasoconstrictive effects in HEPES solution compared with those achieved in Krebs solution. We further screened the buffer components and found that bicarbonate (HCO3−) was the ion to influence the effect of H2S. After examining the vasorelaxant effects of acetylcholine, a vasodilator by releasing nitric oxide, and isoprenaline, a β-adrenoceptor agonist, in HEPES and Krebs buffers, we found the HCO3−-dependent effect was specific to H2S. Blockade of anion exchanger-2 activity with 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid (DIDS) or with HCO3−-free solution abolished the vasoconstrictive effect of NaHS. Moreover, NaHS decreased nitric oxide level in the rat aorta in HCO3−-containing buffer, but this effect was abolished by HCO3−-free buffer or DIDS. In summary, we found for the first time that H2S stimulates anion exchanger to transport extracellular HCO3−in exchange for intracellular superoxide anions, which may further inactivate nitric oxide and induces vasoconstriction.