ZFIN ID: ZDB-PUB-080622-25
Hydrogen Sulfide as an Oxygen Sensor in Trout Gill Chemoreceptors
Olson, K.R., Healy, M.J., Qin, Z., Skovgaard, N., Vulesevic, B., Duff, D.W., Whitfield, N.L., Yang, G., Wang, R., and Perry, S.F.
Date: 2008
Source: American journal of physiology. Regulatory, integrative and comparative physiology   295(2): R669-R680 (Journal)
Registered Authors: Perry, Steve F.
Keywords: none
MeSH Terms:
  • Animals
  • Cells, Cultured
  • Chemoreceptor Cells/drug effects
  • Chemoreceptor Cells/metabolism*
  • Chemoreceptor Cells/physiopathology
  • Cystathionine beta-Synthase/antagonists & inhibitors
  • Cystathionine beta-Synthase/metabolism
  • Cystathionine gamma-Lyase/antagonists & inhibitors
  • Cystathionine gamma-Lyase/metabolism
  • Disease Models, Animal
  • Dose-Response Relationship, Drug
  • Enzyme Inhibitors/pharmacology
  • Female
  • Gills/drug effects
  • Gills/enzymology
  • Gills/metabolism*
  • Gills/physiopathology
  • Heart Rate
  • Hydrogen Sulfide/administration & dosage
  • Hydrogen Sulfide/blood
  • Hydrogen Sulfide/metabolism*
  • Hypoxia/genetics
  • Hypoxia/metabolism*
  • Hypoxia/physiopathology
  • Injections
  • Ion-Selective Electrodes
  • Male
  • Membrane Potentials
  • Mitochondria/metabolism
  • Neuroepithelial Cells/metabolism
  • Oncorhynchus mykiss
  • Oxygen/metabolism*
  • Polarography
  • RNA, Messenger/metabolism
  • Receptors, Cell Surface
  • Reflex
  • Respiratory Mechanics
  • Signal Transduction*/drug effects
  • Zebrafish
PubMed: 18565835 Full text @ Am. J. Physiol. Regul. Integr. Comp. Physiol.
Oxygen chemoreceptors elicit cardiorespiratory reflexes in all vertebrates but consensus on oxygen sensing-signal transduction mechanism(s) is lacking. We recently proposed that hydrogen sulfide (H2S) metabolism is involved in O2 sensing in vascular smooth muscle. Here, we examined the possibility that H2S is an O2 sensor in trout chemoreceptors where the first pair of gills is a primary site of aquatic O2 sensing and the homolog of the mammalian carotid body. Intrabuccal injection of H2S in unanesthetized trout produced a dose-dependent bradycardia and increased ventilatory frequency and amplitude similar to the hypoxic response. Removal of the first, but not second, pair of gills significantly inhibited H2S-mediated bradycardia, consistent with the loss of aquatic chemoreceptors. mRNA for H2S synthesizing enzymes, CBS and CSE, was present in branchial tissue. Homogenized gills produced H2S enzymatically and H2S production was inhibited by O2, whereas mitochondrial H2S consumption was O2-dependent. Ambient hypoxia did not affect plasma H2S in unanesthetized trout, but produced a PO2-dependent increase in a sulfide moiety suggestive of increased H2S production. In isolated zebrafish neuroepithelial cells, the putative chemoreceptive cells of fish, both hypoxia and H2S produced a similar ~10 mV depolarization. These studies are consistent with H2S involvement in O2 sensing/signal transduction pathway(s) in chemoreceptive cells as previously demonstrated in vascular smooth muscle. This novel mechanism, whereby [H2S] is governed by the balance between constitutive production and oxidation, tightly couples tissue [H2S] to PO2 and may provide an exquisitely sensitive, yet simple, O2 sensor in a variety of tissues. Key words: fish gill, neuroepithelial cell, cardiovascular reflexes, respiratory reflexes.