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Contribution of hydrogen sulfide to the control of coronary blood flow

Eli D Casalini1, Adam G Goodwill, Meredith K Owen

  • 1Department of Cellular and Integrative Physiology, Indiana University School of Medicine, Indianapolis, Indiana, USA.

Microcirculation (New York, N.Y. : 1994)
|September 17, 2013
PubMed

Insights

Exogenous hydrogen sulfide (H2S) causes significant coronary vasodilation by activating KATP channels. However, endogenous H2S does not appear to regulate coronary microvascular resistance.

Area of Science:

  • Cardiovascular Physiology
  • Hydrogen Sulfide Biology
  • Microcirculation Research

Background:

  • Hydrogen sulfide (H2S) is an endogenously produced gasotransmitter with known physiological roles.
  • Its precise mechanisms in regulating coronary microvascular resistance and myocardial perfusion remain incompletely understood.

Purpose of the Study:

  • To investigate how H2S influences coronary microvascular resistance and myocardial blood flow.
  • To elucidate the specific ion channels and pathways involved in H2S-mediated coronary vasodilation.
  • To determine the role of endogenous H2S in regulating coronary circulation.

Main Methods:

  • Experiments utilized isolated coronary arteries and open-chest anesthetized dogs.
  • Assessed the effects of exogenous H2S and its substrate l-cysteine on coronary tone and flow.
  • Investigated the involvement of Kv channels, KATP channels, and nitric oxide synthesis.

Main Results:

  • Intracoronary H2S significantly increased coronary blood flow in a dose-dependent manner.
  • This vasodilation was primarily mediated by the activation of KATP channels, not Kv channels.
  • Inhibition of nitric oxide synthesis did not affect H2S-induced vasodilation.
  • Endogenous H2S, via CSE, did not play a significant role in basal or ischemic coronary flow regulation.

Conclusions:

  • Exogenous H2S induces potent, endothelial-independent coronary vasodilation.
  • KATP channel activation is the predominant mechanism for H2S-mediated coronary dilation.
  • Endogenous H2S does not appear to have a significant functional role in regulating coronary microvascular resistance.
Abstract

Keywords:
K channelscoronary circulationreactive hyperemia

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