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国际生理学与病理学期刊
SJR: 0.116

ISSN 打印: 2155-014X
ISSN 在线: 2155-0158

Archives: Volume 1, 2010 to Volume 9, 2018

国际生理学与病理学期刊

DOI: 10.1615/IntJPhysPathophys.v3.i2.50
pages 149-160

Mechanisms of Hydrogen Sulfide Effects on Contractile Activity of Vascular Smooth Muscle in Rats

Olena M. Semenykhina
Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine
Olga V. Bazilyuk
Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine
Yulia P. Korkach
Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine
Vadim F. Sagach
Bogomolets Institute of Physiology, National Academy of Sciences of Ukraine, Kyiv, Ukraine

ABSTRACT

Effects of hydrogen sulfide (H2S) of different origin on the contractile activity of the vascular smooth muscles (VSM) were studied. The precursor of endogenous H2S synthesis (L-cysteine) and its exogenous donor sodium hydrosulfide (NaHS) were shown to change the tension of isolated from the aorta and portal vein rings in a concentration-related way. NaHS caused contractile responses in both vessels at 10−5 mol / l, while at higher concentrations (10−4 − 10−3 mol / l) it induced their relaxation. The VSM of the portal vein turned out to be the most sensitive to such influences. It has been shown that NaHS-evoked relaxation of the VSM was endothelium-independent. Removing of adventitia from the aorta significantly reduced the relaxation effects, as well as it resulted in a complete disappearance of the responses to NaHS-and L-cysteine administration, respectively, compared with the similar effects observed in the preparations with intact vascular adventitia. It has been shown that H2S-evoked relaxation of the VSM from the thoracic aorta was due to activating adenosine triphosphate-dependent potassium channels. That fact was proved by the fact that the blocker glibenclamide (10−5 mol / l) failed to cause the VSM relaxation.


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