Endogenous hydrogen sulfide in the rostral ventrolateral medulla/Bötzinger complex downregulates ventilatory responses to hypoxia.

Respir Physiol Neurobiol. 2014 Jun 17. pii: S1569-9048(14)00154-2. doi: 10.1016/j.resp.2014.06.007. [Epub ahead of print] Donatti AF, Soriano RN, Sabino JP1 Branco LG. Previous studies using neonatal rat brainstem slices had shown that application of a compound that results in H2S production has a bilateral effect on the activity of the hypoglossal nerve rootlet, first decreasing and then increasing activity. These slices contained RVLM and BotC, so they thought that RVLM activity might be involved. In this paper, they decided to look at how hydrogen sulfide (H2S) regulates sympathetic nerve activity after activation in the RVLM. H2S is a common environmental toxin, and also acts as an endogenous neurotransmitter - so to study the effect of H2S in the RVLM, they did microinjections in to the region of the RVLM/BotC with Na2S to induce production of H2S or aminooxyacetate (AOA) to inhibit it via inhibition of cystathionine-B-synthase. They found that AOA injections up to 2pmol did nothing in normoxic rats, however in hypoxic rats, 1pmol injection of AOA was sufficient to increase breathing over the already increased hypoxia-inducd increase in respiration. On the other hand, 2pmol of Na2S could attenuate the increased respiration induced by exposure to hypoxia. When they measured the endogenous levels of H2S in rats experiencing hypoxia, they found it was lower than in normoxic rats. So my question is, I guess, is if this Na2S turns to H2S, doesn't that mean it's acting as a base. If that's true, is it reducing activation of chemoreceptors by decreasing free protons? It makes sense in my head, but I'm not a chemist. -DH