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Keywords:

  • blood pressure;
  • hydrogen sulfide;
  • nitric oxide;
  • smooth muscle cells;
  • vasorelaxation

Hydrogen sulfide (H2S) has been traditionally viewed as a toxic gas. It is also, however, endogenously generated from cysteine metabolism. We attempted to assess the physiological role of H2S in the regulation of vascular contractility, the modulation of H2S production in vascular tissues, and the underlying mechanisms. Intravenous bolus injection of H2S transiently decreased blood pressure of rats by 12–30 mmHg, which was antagonized by prior blockade of KATP channels. H2S relaxed rat aortic tissues in vitro in a KATP channel-dependent manner. In isolated vascular smooth muscle cells (SMCs), H2S directly increased KATP channel currents and hyperpolarized membrane. The expression of H2S-generating enzyme was identified in vascular SMCs, but not in endothelium. The endogenous production of H2S from different vascular tissues was also directly measured with the abundant level in the order of tail artery, aorta and mesenteric artery. Most importantly, H2S production from vascular tissues was enhanced by nitric oxide. Our results demonstrate that H2S is an important endogenous vasoactive factor and the first identified gaseous opener of KATP channels in vascular SMCs.