Sitdikova G F, Khaertdinov N N, Zefirov A L
Department of Human and Animal Physiology, Kazan (Privolzhskii) Federal University, Russia.
Bull Exp Biol Med. 2011 Jun;151(2):163-6. doi: 10.1007/s10517-011-1280-5.
The effects of sodium hydrosulfide NaHS, a donor of hydrogen sulfide H2S, on the force of muscle contraction were examined on isolated myocardial strips from frog ventricles. NaHS decreased the amplitude of muscle contractions in a dose-dependent manner under normal conditions and during inhibition of Ca channels with nifedipine. In contrast, under conditions of blockade of ATP-dependent potassium channels with glibenclamide, NaHS exerted a positive inotropic effect from the first minute of application. Neither blockade, nor activation of ATP-dependent K-channels with glibenclamide modulated the negative inotropic effect of NaHS. Inhibition of K-channels with tetraethylammonium (TEA) (3, 5, 10 mM) or 4-aminopyridine increased the amplitude of myocardial contractions. Preliminary application of 4-aminopyridine or TEA (3 mM) did not eliminate NaHS-induced negative inotropic effect, although higher TEA concentrations (5 or 10 mM) prevented it. The data indicate that the targets of H(2)S in frog myocardium are ATP-dependent, Ca-activated, and voltage-dependent K-channels.
在青蛙心室分离的心肌条上，研究了硫化氢（H₂S）供体硫氢化钠（NaHS）对肌肉收缩力的影响。在正常条件下以及用硝苯地平抑制钙通道期间，NaHS以剂量依赖的方式降低肌肉收缩幅度。相反，在用格列本脲阻断ATP依赖性钾通道的条件下，NaHS从应用的第一分钟起就发挥正性肌力作用。格列本脲对ATP依赖性钾通道的阻断或激活均未调节NaHS的负性肌力作用。用四乙铵（TEA）（3、5、10 mM）或4-氨基吡啶抑制钾通道可增加心肌收缩幅度。尽管较高浓度的TEA（5或10 mM）可防止这种情况，但预先应用4-氨基吡啶或TEA（3 mM）并不能消除NaHS诱导的负性肌力作用。数据表明，H₂S在青蛙心肌中的作用靶点是ATP依赖性、钙激活和电压依赖性钾通道。
