Hydrogen sulphide induces vasoconstriction of rat coronary artery via activation of Ca2+ influx

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Hydrogen sulphide (H2S) exhibits a dual modulation of isolated artery tension. This study investigated the vasoconstrictive effect of sulphur sodium hydride (NaHS), a donor of gaseous H2S, on rat coronary artery.


The contractile response of isolated arteries was recorded using a wire myograph. Fluo-3/AM was used to load vascular smooth muscle, and intracellular calcium was determined using confocal laser microscopy. The protein expression of Rho kinase was examined using Western blot.


NaHS induced concentration-dependent contractions of rat coronary artery, and the contraction reached approx. 65% of 60 mm KCl-induced contraction. The NaHS-induced contraction was elevated following the removal of endothelium or the use of the nitric oxide synthase inhibitor L-NAME. The cyclooxygenase inhibitor indomethacin reduced NaHS-induced contraction. The Rho kinase inhibitor Y-27632 significantly attenuated NaHS-induced vasoconstriction. Furthermore, NaHS elevated the protein expression of Rho kinase. NaHS-induced contraction was completely abolished in a Ca2+-free solution and suppressed by the Ca2+ influx blocker nifedipine (100 nm). NaHS also significantly increased the change rate of Ca2+ fluorescence intensity. However, treatment with a Cl−/HCO3− exchanger blocker, K+ channel blockers, the mitogen-activated protein kinase inhibitor U-0126 or cyclic adenosine monophosphate did not affect contraction. Species-dependent differences in NaHS-induced vasoconstriction were observed because these effects were only modest in dog coronary artery and absent in rabbit coronary artery.


NaHS induces the contraction of rat coronary artery, which is dependent on the activation of Ca2+ influx. Rho kinase likely participates in the vasoconstriction.

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