RT Journal Article
ID 1205251850e3452b
A1 Semenykhina, Olena M.
A1 Bazilyuk, Olga V.
A1 Korkach, Yulia P.
A1 Sagach, Vadim F.
T1 Mechanisms of Hydrogen Sulfide Effects on Contractile Activity of Vascular Smooth Muscle in Rats
JF International Journal of Physiology and Pathophysiology
JO IJPP
YR 2012
FD 2012-06-09
VO 3
IS 2
SP 149
OP 160
K1 hydrogen sulfide
K1 L-cysteine
K1 NaHS
K1 glibenclamide
K1 aorta
K1 portal vein
K1 endothelium
K1 adventitia
AB 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.
PB Begell House
LK https://www.dl.begellhouse.com/journals/6ec4ba27650016b1,551b155962667b02,1205251850e3452b.html