Numerical data used to generate figures and table for the manuscript "Signal transduction pathway mediating carotid body dependent sympathetic activation and hypertension by chronic intermittent hypoxia"

Patients with obstructive sleep apnea (OSA) experience chronic intermittent hypoxia (CIH). OSA patients and CIH-treated rodents exhibit overactive sympathetic nervous system and hypertension, mediated through hyperactive carotid body (CB) chemoreflex. Activation of olfactory receptor 78 (Olfr78) by hydrogen sulfide (H₂S) is implicated in CB activation and sympathetic nerve responses to CIH, but the downstream signaling pathways remain unknown. Given that odorant receptor signaling is coupled to adenylyl cyclase 3 (Adcy3), we hypothesized that Adcy3-dependent cAMP contributes to CB and sympathetic responses to CIH. Our findings show that CIH increases cAMP levels in the CB, a response absent in <i>Adcy3</i>, <i>Cth </i>(encoding CSE), and <i>Olfr78</i> null mice. CBs from <i>Cth </i>and <i>Olfr78</i> mutant mice lacked persulfidation response to CIH, indicating that Adcy3 activation requires Olfr78 activation by H₂S in CIH. CIH also enhanced glomus cell Ca²⁺ influx, an effect absent in <i>Cnga2</i> (encoding cyclic nucleotide gated channel alpha2 subunit) and <i>Adcy3</i> mutants, suggesting that CIH-induced cAMP mediates enhanced Ca²⁺ responses through cyclic nucleotide-gated channels. Furthermore, <i>Adcy3</i> null mice did not exhibit neither CB activation nor sympathetic activation by CIH. These results demonstrate that Adcy3-dependent cAMP is a downstream signaling pathway to H₂S/Olfr78, mediating CIH-induced CB activation and sympathetic activity and hypertension.