The vasodilator response of nitric oxide (NO), hydrogen sulfide (H₂S) and sulfur dioxide (SO₂) were studied to
determine the significance of the actions and interactions of these gasotransmitters for controlling aortic tone in rats. The isometric tension of five separate sets of experiments was recorded. Sodium nitroprusside (SNP; NO donor), sodium disulphide (Na₂S; H₂S donor), SO₂ derivatives and their paired combinations were added to phenylephrine (PE)-induced contraction during the peak value. Then maximal relaxation rate was calculated four times at 5 min intervals. Tetraethylammonium (TEA) and Glibenclamide (GLIB) were applied for investigating the molecular mechanism of the gasses. While, in a separate set of experiments, we used either L-Arginine (L-Arg), L-Cysteine (L-Cyst) or L-nitroarginine methyl ester (L-NAME) before applying gasotransmitters. Highest and prolonged relaxation rate were recorded when SNP was combined with SO₂. The combination of Na₂S and SO₂-induced vasorelaxation was blocked by TEA and GLIB pretreatments. L-Cyst decreased relaxation compared to SNP and vice versa to SO₂ induced vasorelaxation. L-Arg markedly attenuated relaxation responses of Na₂S and SO₂ derivatives. Also, L-NAME delayed relaxation compared to Na₂S and SO₂. These results suggest that exogenous paired combinations of H₂S, NO and SO₂ will enhance and elongate the rate of aortic relaxation. Meanwhile, preincubation of aortic rings with precursors attenuate the dilatory effects of exogenous studied gases.