Quan X J, Wang L L, Dai F, Luo H S, Wang J H
Department of Gastroenterology, the Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710004, China.
Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan 430060, China.
Zhonghua Yi Xue Za Zhi. 2020 Apr 14;100(14):1095-1101. doi: 10.3760/cma.j.cn112137-20191016-02237.
To investigate the role of nitric oxide (NO) in hydrogen sulfide (H(2)S)-induced inhibition upon colonic smooth muscle contraction. Immunohistochemistry was applied to observe the distribution of H(2)S-producing enzymes CBS and CSE in adult male Wistar rats. Organ bath system was used to observe the spontaneous contraction of colonic smooth muscle. Patch clamp technique was applied to record currents of L-type calcium channel (I(Ca,L)) in smooth muscle cells. Specific immunoreactivity for CSE and CBS was observed in mucosa, smooth muscle and enteric plexus of rat proximal colon. NaHS elicited relaxation in a concentration-dependent manner upon muscle contraction in the presence of tetrodotoxin. The NaHS IC(50) of LM was 917.6 μmol/L (95% 776.3-1 085 μmol/L, 6) and the NaHS IC(50) of CM was 730.4 μmol/L (95% 592.2-900.8 μmol/L, 6). The SNP-induced relaxation in muscle strips was partially reversed by NaHS (0.05). Instead, the relaxation caused by NaHS was decreased by the sGC inhibitor ODQ but affected neither by NO precursor L-arginine, the NO inhibitor L-NNA nor the competitive cGMP antagonist PET-cGMP. NaHS (100 μmol/L) increased I(Ca,L) while NaHS (300 μmol/L) decreased the peak I(Ca,L) with modifying the ion channel characteristics (0.05). Exogenous hydrogen sulfide might have a dual effect on colonic motility and its inhibitory effect might be independent of NO signaling system. L-type calcium channel may play an important role during the process of H(2)S modulating colonic contraction.
探讨一氧化氮（NO）在硫化氢（H₂S）诱导的结肠平滑肌收缩抑制中的作用。应用免疫组织化学法观察成年雄性Wistar大鼠中产生H₂S的酶CBS和CSE的分布。采用器官浴系统观察结肠平滑肌的自发收缩。应用膜片钳技术记录平滑肌细胞中L型钙通道（I(Ca,L)）的电流。在大鼠近端结肠的黏膜、平滑肌和肠神经丛中观察到CSE和CBS的特异性免疫反应性。在存在河豚毒素的情况下，NaHS以浓度依赖性方式引起肌肉收缩松弛。LM的NaHS IC₅₀为917.6 μmol/L（95% 776.3 - 1085 μmol/L，6），CM的NaHS IC₅₀为730.4 μmol/L（95% 592.2 - 900.8 μmol/L，6）。SNP诱导的肌条松弛被NaHS部分逆转（0.05）。相反，NaHS引起的松弛被sGC抑制剂ODQ降低，但不受NO前体L-精氨酸、NO抑制剂L-NNA或竞争性cGMP拮抗剂PET-cGMP的影响。NaHS（100 μmol/L）增加I(Ca,L)，而NaHS（300 μmol/L）通过改变离子通道特性降低I(Ca,L)峰值（0.05）。外源性硫化氢可能对结肠运动具有双重作用，其抑制作用可能独立于NO信号系统。L型钙通道可能在H₂S调节结肠收缩过程中起重要作用。
