Experimental observations on the biological signifi cance of hydrogen sulfide in carotid body chemoreception

Abstract

The cascade of transduction of hypoxia and hypercapnia, the natural stimuli to chemoreceptor cells, is incompletely understood. A particular gap in that knowledge is the role played by second messengers, or in a most ample term, of modulators. A recently described modulator of chemoreceptor cell responses is the gaseous transmitter hydrogen sulfide, which has been proposed as a specific activator of the hypoxic responses in the carotid body, both at the level of the chemoreceptor cell response or at the level of the global output of the organ. Since sulfide behaves in this regard as cAMP, we explored the possibility that sulfide effects were mediated by the more classical messenger. Data indicate that exogenous and endogenous sulfide inhibits adenyl cyclase finding additionally that inhibition of adenylyl cyclase does not modify chemoreceptor cell responses elicited by sulfide. We have also observed that transient receptor potential cation channels A1 (TRPA1) are not regulated by sulfide in chemoreceptor cells.