Investigation of interactions of hydrogenous sulfide with endogenous mediators in isolated rabbit gastric fundus

The aim of this study is to investigate the effects of H2S in rabbit gastric fundus on electrical field stimulation (EFS)-mediated cholinergic transmission and for the evaluation of interaction with NO, in the presence of NOS inhibitor, L-NAME, on EFS-mediated cholinergic neurotransmission. In the experiments, in order to record isometric contractions, 2.5-3 kg of 20 albino rabbits gastric smooth muscle strips were placed into an organ bath containing Krebs solution after being connected to an isometric force transducer. Guanethidine and indometacin had no effect on EFS-mediated cholinergic contraction responses while atropin totally abolished, neostigmine increased and ?-gonotoxin GVIA significantly diminished the responses. Nitric oxide synthase inhibitor, L-NAME increased the EFS-mediated contraction responses. These results show that EFS-mediated contraction responses obtained from gastric fundus depend on neural stimulation and are originated from cholinergic neurons. In the presence of guanethidine and indometacin, while NaHS and L-cysteine diminished EFS-mediated cholinergic contraction responses depending on concentration, PAG had no effect. In the presence of L-NAME, inhibitor effect of NAHS and L-cysteine showed no difference. However, in the presence of L-NAME, the reversal of inhibitor effect significantly increased. In gastric fundus strips contracted by noradrenaline, while NaHS and L-cysteine caused a significant relaxation, PAG had no relaxant effect. Since the inhibitor effect NaHS and L-cysteine on EFS-mediated cholinergic contraction responses were seen on also noradrenalin-contracted tissues, the effects are thought to occur via a postsnaptic mechanism. Although H2S effect on EFS-mediated neurogenic contraction responses reversed 55% depending on time, since no reversal was seen in noradrenalin-contracted tissues and the reversal increased in the presence of L-NAME, it is considered that H2S has an effect on neurotransmitter release from neural endings and has an interaction with NO.