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NaHS prejunctionally inhibits the cardioaccelerator sympathetic outflow in pithed rats. | LitMetric

NaHS prejunctionally inhibits the cardioaccelerator sympathetic outflow in pithed rats.

Eur J Pharmacol

Departamento de Farmacobiología, Cinvestav-Coapa, Czda. de los Tenorios 235, Col. Granjas-Coapa, Del. Tlalpan, C.P. 14330 México City, Mexico.

Published: March 2018

AI Article Synopsis

  • Hydrogen sulfide is identified as a gasotransmitter that may protect the heart from damage caused by ischemia-reperfusion and influences heart rate, possibly by inhibiting sympathetic nerve activity.
  • This study investigated the effects of sodium hydrosulfide (NaHS) on the heart rate responses in Wistar rats, focusing on its ability to suppress increased heart rates induced by sympathetic stimulation.
  • Results showed that NaHS effectively reduced heart rate increases from sympathetic stimulation, indicating its action through a prejunctional mechanism, but did not affect heart rate increases caused by noradrenaline or isoproterenol.

Article Abstract

Hydrogen sulfide is a gasotransmitter that mediates cardiovascular responses and could protect the heart from ischemia-reperfusion damage. Furthermore, this gas mediates bradycardia although the mechanisms involved remain elusive. In this regard, the inhibition of the cardiac sympathetic outflow may be partially involved. Thus, this study was designed to determine the capability of NaHS to inhibit the tachycardic responses induced by preganglionic stimulation of the cardioaccelerator sympathetic outflow. Wistar rats were anaesthetized with isoflurane, cannulated and pithed. Then, animals received gallamine and the effect of i.v. infusion of NaHS (310 and 560 μg/kg min) was evaluated on the tachycardic responses induced by (1) sympathetic stimulation (0.1-3.2 Hz) at C-T region of the vertebral column; or i.v. injections of (2) noradrenaline (0.03-3 μg/kg) and (3) isoproterenol (0.0003-0.1 μg/kg). Notably, NaHS significantly and dose-dependently inhibited the tachycardic responses induced by electrical stimulation of the preganglionic sympathetic outflow without significantly modify the tachycardic responses induced by either noradrenaline or isoproterenol. These results allow us to conclude that i.v. infusion of NaHS inhibited the tachycardic responses induced by stimulation of the cardioaccelerator sympathetic outflow by a prejunctional mechanism.

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Source
http://dx.doi.org/10.1016/j.ejphar.2018.01.030DOI Listing

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