The impact of hydrogen sulfide (H₂S) on neurotransmitter release from the cat carotid body

Abstract

Do cat carotid bodies (CBs) increase their release of acetylcholine and ATP in response to H(2)S? 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(2)S, an H(2)S donor. H(2)S, 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(2)S synthesizing enzyme, and for a subunit of the K(ATP) channel. The data suggest that Na(2)S 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(2)S levels rise, the glomus cells responding very actively to hypoxia may be protected from over-exertion by the H(2)S opening of the K(ATP) channels.