The cardiovascular inhibition functions of hydrogen sulfide within the nucleus tractus solitarii are mediated by the activation of KATP channels and glutamate receptors mechanisms.

: Hydrogen sulfide (H2S), the colorless gas with the smell of rotten eggs, has been regarded as a novel gaseous signaling molecule. Although H2S has been proved been involved into the cardiovascular functions, the cardiovascular functions of H2S within the nucleus tractus solitarii (NTS) are not clear. Unilateral microinjection of NaHS (2 to 200 pmol), a H2S donor, into the NTS caused transient and dose-dependent hypotension and bradycardia (P<0.01). Microinjection of CBS allosteric activator S-ademetionine (SAM) into the NTS also produced significant decreases in BP (from 101 +/- 8 to 82 +/- 7 mmHg, P < 0.01) and HR (from 469 +/- 16 to 449 +/- 14 bpm, P<0.01), which was very similar to those of NaHS. Pretreatment with hydroxylamine, a CBS inhibitor, failed to affect the cardiovascular functions of intra-NTS NaHS. However, pretreatment with glibenclamide (10 nmol), a KATP channel blocker, eliminated the on BP (from -23 +/- 4 to -5 +/- 1 mmHg, P<0.01) and HR (from -24 +/- 2 to -5 +/- 1 bpm, P<0.01) by 78% and 79%, respectively, of intra-NTS NaHS (20 pmol). Likewise, pretreatment with kynurenic acid (Kyn, 5 nmol) also attenuated the effects of NaHS on BP (from -29 +/- 3 to -12 +/- 3 mmHg, P<0.01) and HR (from -19 +/- 2 to -9 +/- 2 bpm, P<0.01) by 59% and 53%, respectively, of intra-NTS NaHS (20 pmol). These data support the hypothesis that endogenous H2S produces cardiovascular inhibition functions in the NTS, mainly mediated by KATP channels regulation or/and glutamate receptors.