Evidence that NaHS inhibits the tachycardic responses induced by stimulation of the preganglionic sympathetic outflow in pithed rats

In anesthetized rats, i.v. administration of NaHS, a donor of H 2 S, elicited dose‐dependent bradycardia, although the mechanisms are unknown. In this regard, we hypothesized that the inhibition of the cardioaccelerator sympathetic outflow may be partially involved. Thus, this study was designed to determine the potential capability of NaHS to mediate inhibition of the tachycardic responses induced by preganglionic sympathetic stimulation (C7‐T1). For this purpose, Wistar rats were anesthetized, pithed and cannulated for drug administration. In animals pre‐treated with gallamine, the effect of i.v. infusion of NaHS (310 and 560 μg/kg min) or its vehicle (phosphate buffer saline; 0.02 ml/min) was determined on the tachycardic responses induced by: (1) sympathetic stimulation (0.1–3.2 Hz); or (2) i.v. bolus injections of exogenous noradrenaline (0.03–3 μg/kg). The tachycardic responses induced by preganglionic sympathetic stimulation were dose‐dependently inhibited by i.v. infusion of NaHS (310 and 560 μg/kg min), but not by vehicle, particularly at high frequencies. In marked contrast, the tachycardic responses to exogenous noradrenaline were not inhibited by the above doses of NaHS or its vehicle. These results, taken together, demonstrate that NaHS inhibited the tachycardic responses induced by preganglionic sympathetic outflow by a prejunctional mechanism. This is the first evidence demonstrating this effect by NaHS that may contribute, at least in part, to the bradycardia induced by NaHS. Support or Funding Information The authors acknowledge to Conacyt (Grant No. 252702) for their financial support.