Bronchodilatory Effect of Hydrogen Sulfide in Rat

The aims of present study were to elucidate the effect of NaHS as a H2S donor on precontracted rat trachea smooth muscle, role of epithelium and nitric oxide in this action. Tracheal rings from male adult Wistar rats were isolated and mounted in an organ bath containing Krebs–Henseleit solution under 1.5 g resting tension and contractions were recorded isometrically. After equilibrium period (60 min), cumulative concentrations of NaHS (0.2-1.2 mM) were applied on the tracheal basal tone or on the plateau of contractions induced by KCl (60 mM) or carbachol (CCh, 0.55 μM) in the absence and presence of certain antagonists and inhibitors. The tracheal basal tone was unaffected by NaHS but tracheal contractions induced by KCl and CCh were attenuated by NaHS in a concentration-dependent manner (P< 0.001). Removing the tracheal epithelial did not attenuate the NaHS spasmolytic effect in the tissue precontracted by KCl and CCh. The bronchodilatory effect was unaffected by tissue incubation (30 min, 1 μM) with, glibenclamide, propranolol, indomethacin, methylene blue (10 μM), and L-NAME (300 μM). It seems that bronchodilatory effect of H2S was not mediated by KATP channels, β-adrenoceptors, epithelium and production of nitric oxide, cGMP and prostaglandins. Since CCh and KCl activate Ca2+ influx and CCh promotes Ca2+ from intracellular pool as well, therefore, we may conclude that the relaxant effect of NaHS was mediated by the Ca2+ influx blockade and cholinergic receptors inactivation. This preliminary study shows the possible therapeutical property of H2S in obstructive pulmonary diseases.