Role of nucleus tractus solitarii (nTS) hydrogen sulfide (H2S) in hindlimb unloaded rats

Abstract

Cardiovascular deconditioning alters central cardiorespiratory regulation and is mimicked by hindlimb unloading (HU). Preliminary data suggest the ventilatory response to hypoxia is augmented in HU rats. Furthermore, H2S from cystathionine beta synthase (CBS) augments excitatory neurotransmission in nTS, the initial site for cardiorespiratory sensory integration. Preliminary studies suggest nTS H2S augments phrenic (PNA) and splanchnic sympathetic (sSNA) nerve activity during acute hypoxia (AH) but its influence in HU rats is unknown. To test the hypothesis that increased endogenous H2S from CBS in the nTS enhances cardiorespiratory responses to AH after HU, we examined mean arterial pressure (MAP), PNA and sSNA responses to AH (2 min; 10% O2). Baseline cardiorespiratory parameters were similar in anesthetized control (C) and HU rats. Chemoreflex activation with AH increased PNA and sSNA and decreased MAP in both groups; the depressor response was less in HU rats. Bilateral nTS microinjection of the CBS inhibitor aminooxyacetate (AOA; 1 mM, 90 nl), to decrease H2S, increased baseline MAP and sSNA in both groups. In the presence of AOA, the increase in PNA amplitude to AH tended to be blunted in CC rats; this attenuation appeared to be less in HU. AOA did not alter the sSNA response to AH in CC rats, but reduced sSNA during AH after HU. These preliminary data suggest that CBS‐derived H2S in nTS augments cardiorespiratory responses to hypoxia and this modulation is diminished after HU. HL55306