| Summary: | Objectives: This study examined the dose-dependent actions of hydrogen sulfide donor sodium hydrosulphide (NaHS) on isometric contractions and ion transport in rat aorta smooth muscle cells (SMC).
Methods: Isometric contraction was measured in ring aortas segments from male Wistar rats. Activity of Na+/K+-pump and Na+,K+,2Cl-cotransport was measured in cultured endothelial and smooth muscle cells from the rat aorta as ouabain-sensitive and ouabain-resistant, bumetanide-sensitive components of the 86Rb influx, respectively.
Results: NaHS exhibited the bimodal action on contractions triggered by modest depolarization ([K+]o=30 mM). At 10−4 M, NaHS augmented contractions of intact and endothelium-denuded strips by ~ 15% and 25%, respectively, whereas at concentration of 10−3 M it decreased contractile responses by more than two-fold. Contractions evoked by 10−4 M NaHS were completely abolished by bumetanide, a potent inhibitor of Na+,K+,2Cl-cotransport, whereas the inhibition seen at 10−3 M NaHS was suppressed in the presence of K+ channel blocker TEA. In cultured SMC, 5×10−5 M NaHS increased Na+,K+,2Cl- - cotransport without any effect on the activity of this carrier in endothelial cells. In depolarized SMC, 45Ca influx was enhanced in the presence of 10−4 M NaHS and suppressed under elevation of [NaHS] up to 10−3 M. 45Ca influx triggered by 10−4 M NaHS was abolished by bumetanide and L-type Ca2+ channel blocker nicardipine.
Conclusions: Our results strongly suggest that contractions of rat aortic rings triggered by low doses of NaHS are mediated by activation of Na+,K+,2Cl-cotransport and Ca2+ influx via L-type channels.
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