Although all cells are variously affected by oxygen, a few have the responsibility of monitoring oxygen tensions and initiating key homeostatic responses when P O 2 falls to critical levels. These ʻoxygen-sensing' cells include the chemoreceptors in the gills (neuroepithelial cells), airways (neuroepithelial bodies) and vasculature (carotid bodies) that initiate cardiorespiratory reflexes, oxygen sensitive chromaffin cells associated with systemic veins or adrenal glands that regulate the rate

more »

... f catecholamine secretion, and vascular smooth muscle cells capable of increasing blood flow to systemic tissues, or decreasing it through the lungs. In spite of intense research, and enormous clinical applicability, there is little, if any, consensus regarding the mechanism of how these cells sense oxygen and transduce this into the appropriate physiological response. We have recently proposed that the metabolism of hydrogen sulfide (H 2 S) may serve as an ʻoxygen sensor' in vertebrate vascular smooth muscle and preliminary evidence suggests it has similar activity in gill chemoreceptors. In this proposed mechanism, the cellular concentration of H 2 S is determined by the simple balance between constitutive H 2 S production in the cytoplasm and H 2 S oxidation in the mitochondria; when tissue oxygen levels fall the rate of H 2 S oxidation decreases and the concentration of biologically active H 2 S in the tissue increases. This commentary briefly describes the oxygen-sensitive tissues in fish and mammals, delineates the current hypotheses of oxygen sensing by these tissues, and then critically evaluates the evidence for H 2 S metabolism in oxygen sensing.