Hydrogen Sulfide (H2S): A Physiologic Mediator of Carotid Body Response to Hypoxia
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Carotid bodies are sensory organs for monitoring arterial blood O2 levels. Nitric oxide and carbon monoxide function as inhibitory gasotransmitters in the carotid body. Hydrogen sulfide (H2S) is another emerging gasotransmitter. The purpose of this article is to review recent studies addressing the role of H2S in carotid body.Cystathionine γ-lyase (CSE) and cystathionine β synthase (CBS) are the two major enzymes that catalyze the formation of endogenous H2S. Both CSE and CBS are expressed in glomus cells, the putative site of sensorytransduction in the carotid body. Hypoxia increases H2S generation in the carotid body. CSE knockout mice displayed absence of hypoxia-evoked H2S generation and severely impaired sensory excitation by low O2. Pharmacological inhibitors of CSE as well as CBS showed a similar phenotype in mice and rats. Like hypoxia, H2S donors stimulated the carotid body sensory activity and this response required Ca2+ influx via voltage-gated Ca2+ channels. Evidence is emerging implicating Ca2+ activated K+ channels in glomus cells as potential targets of H2S.
KeywordsHypoxia Gasotransmitters K+ channels Voltage-activated Ca2+ channels Glomus cells
N.R.P gratefully acknowledges the collaborations of Drs. S.H. Snyder, G. K. Kumar, Y.J. Peng and M.M. Gadalla. Research from author’s laboratory is supported by grants HL-76537, HL-90554, and HL-86493 from the National Institutes of Health.