Abstract

Objective To observe the cardiovascular functions of hydrogen sulfide (H2S) within the caudal ventrolateral medulla (CVLM) and to explore its mechanisms in rats. Methods Sixty-seven male SD rats were employed in present study. Among them, 34 rats were randomized into control group (aCSF, 100 nL, n = 6), NaHS group (sodium hydrosulfide, NaHS, 2, 20 or 200 pmol, n = 7 for each dose), S-ademetionine (SAM, 10 nmol, n = 7). In 33 rats, hydroxylamine (HA, n = 7), kynurenic acid (KYN, n = 7) or glibenclamide (GLI, n = 7) were prior applied before NaHS (20 pmol) was microinjected into the CVLM. Results Unilateral microinjection of NaHS (2 to 200 pmol), a H2S donor, into the CVLM caused the transient and dose-dependent hypotension and bradycardia (P Conclusion These data support the hypothesis that endogenous H2S produces cardiovascular inhibition functions in the CVLM, mainly mediated by KATP channels opening mechanism.

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