The impact of hydrogen sulfide (H ₂S) on neurotransmitter release from the cat carotid body

Do cat carotid bodies (CBs) increase their release of acetylcholine and ATP in response to H ₂S? Two CBs, incubated in a Krebs Ringer bicarbonate solution at 37°C, exhibited a normal response to hypoxia-increased release of acetylcholine (ACh) and ATP. They were challenged with several concentrations of Na ₂S, an H ₂S donor. H ₂S, a new gasotransmitter, is reported to open K _ATP channels. Under normoxic conditions the CBs reduced their release of ACh and ATP below control values. They responded identically to pinacidil, a well-known K _ATP channel opener. CB glomus cells exhibited a positive immunohistochemical signal for cystathione-β-synthetase, a H ₂S synthesizing enzyme, and for a subunit of the K _ATP channel. The data suggest that Na ₂S may have opened the glomus cells' K _ATP channels, hyperpolarizing the cells, thus reducing their tonic release of ACh and ATP. Since during hypoxia H ₂S levels rise, the glomus cells responding very actively to hypoxia may be protected from over-exertion by the H ₂S opening of the K _ATP channels.