Endogenous H2S opposes vasoconstriction in conjunction with NO in rat aorta

Hydrogen sulfide (H 2 S) is an endogenous vasodilator produced in the vasculature by cystathionine γ‐lyase (CSE) from L‐cysteine (Cys). Studies suggest interaction between NO and H 2 S to potentiate each other's effects. We hypothesized that H 2 S‐induced relaxation in rat aorta requires activation of nitric oxide synthase (NOS). In aortic ring segments, U46619‐contraction was reversed by Cys (1 μM). Inhibiting CSE with β‐cyano‐alanine, (BCA, 100 μM) diminished Cys‐induced dilation by 50%. Inhibiting NOS (L‐NNA, 100 μM) or disrupting the endothelium lowered Cys ‐ induced dilation by 80% and 85% respectively, suggesting Cys ‐ induced dilation is mediated in part through NOS. CSE inhibition diminished acetylcholine (ACH)‐induced dilation by 40% whereas either L‐NNA or endothelium disruption completely abolished dilation. U‐46619 induced greater contraction in BCA treated arteries vs. controls suggesting endogenous H 2 S opposes contraction. Endothelium disruption or inhibition of both NOS and CSE also increased contraction by U‐46619. H 2 S production measured in aortic segments was diminished by BCA and augmented by NOS inhibition. In aorta, CSE was primarily expressed in the endothelium. Our results indicate that ACH stimulates H 2 S production in the endothelium by CSE and dilation to H 2 S requires NOS. Furthermore, basal production of H 2 S appears to be inhibited by NOS.