Hydrogen Sulfide as an Oxygen Sensor in Trout Chemoreceptors

Oxygen (O 2 ) sensing chemoreceptors elicit cardiorespiratory reflexes in all vertebrates but the oxygen sensing‐signal transduction mechanism(s) is unknown. Here we examined the possibility that H 2 S is an O 2 sensor in rainbow trout where the first pair of gill arches is a primary site of chemoreception and the homolog of the mammalian carotid body. In unanesthetized trout, ambient hypoxia produced a PO 2 ‐dependent increase in plasma [H 2 S] indicative of inverse coupling of PO 2 and H 2 S. mRNA for the H 2 S synthesizing enzymes CBS and CSE was present in gill tissue and gills produced H 2 S enzymatically. Intrabuccal injection of H 2 S in unanesthetized trout produced a dose‐dependent bradycardia and increased ventilatory frequency and amplitude similar to hypoxia. Removal of the first but not second gill arches inhibited H 2 S‐mediated bradycardia, consistent with the hypothesized loss of aquatic chemoreceptor function. In isolated zebrafish neuroepithelial cells, the putative chemoreceptive cells of fish, hypoxia and H 2 S produced a similar ~10 mV depolarization. This suggests that H 2 S is involved in the O 2 sensing/signal transduction pathway in chemoreceptive cells as it is in vascular smooth muscle. This mechanism, whereby [H 2 S] is governed by the balance between constitutive production and oxidation, tightly couples tissue [H 2 S] to PO 2 and may provide an exquisitely sensitive O 2 sensor in a variety of tissues. Support: NSF IOS 0641436 & NSERC