Hydrogen sulphide induces vasoconstriction of rat coronary artery via activation of Ca(2+) influx

Abstract

Aim: 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.

Methods: 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.

Results: 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 Ca(2+)-free solution and suppressed by the Ca(2+) influx blocker nifedipine (100 nm). NaHS also significantly increased the change rate of Ca(2+) fluorescence intensity. However, treatment with a Cl(-)/HCO(3-) 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.

Conclusions: NaHS induces the contraction of rat coronary artery, which is dependent on the activation of Ca(2+) influx. Rho kinase likely participates in the vasoconstriction.

Keywords: Ca2+ influx; coronary artery; hydrogen sulphide; rat; vasoconstriction.