Abd Elmoneim H, Sharabi F, Mohy El Din M, Louedec L, Norel X, Senbel A
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Alexandria University, Egypt.
Laboratory for Vascular Translational Sciences, INSERM U1148, CHU X Bichat, Université Paris 13, Paris, France.
Life Sci. 2017 Nov 15;189:39-43. doi: 10.1016/j.lfs.2017.09.013. Epub 2017 Sep 14.
Hydrogen sulfide (HS) is a newly-introduced gasotransmitter in penile tissues. However, its exact mechanism of action in mediating penile erection is not fully elucidated. The major aim of this study was to examine the role of different K channels in mediating the responses to HS in the corpus cavernosum.
Tension studies using isolated rat corpus cavernosum strips were conducted. Endogenous HS production was measured using polarographic technique. Results are expressed as mean±SEM.
l-Cysteine (10M) stimulated rat corpus cavernosum to produce HS. Blockade of CSE by BCA (10M) reduced the concentration of HS produced from rat corpus cavernosum significantly. Addition of TEA (10M) or 4-AP (10M) didn't have a significant effect on the concentration of HS produced. l-Cysteine (10-10M) elicited a concentration-dependent relaxation response which was significantly reduced by blockade of CSE using BCA (10M). TEA (10M), 4-AP (10M) and TEA (10M) attenuated l-cysteine-induced relaxation significantly. At 10M, l-cysteine resulted in percentage relaxation of 1.55±0.63, 10.94±1.93 and 1.93±0.80 in presence of TEA (10M), 4-AP (10M) and TEA (10M) respectively compared to 23.78±2.71 as control. Both glibenclamide (10M) and BaCl (3×10M) failed to reduce these relaxations significantly.
HS-induced relaxation of rat corpus cavernosum may be mediated - at least in part - through BK and K channels not by K and K channels. It also seems that K-channels do not contribute to the synthesis of HS.
硫化氢（HS）是一种新发现的在阴茎组织中的气体信号分子。然而，其介导阴茎勃起的确切作用机制尚未完全阐明。本研究的主要目的是探讨不同钾通道在介导海绵体对HS反应中的作用。
采用离体大鼠海绵体条进行张力研究。用极谱技术测定内源性HS的产生。结果以平均值±标准误表示。
L-半胱氨酸（10μM）刺激大鼠海绵体产生HS。BCA（10μM）对胱硫醚-γ-裂解酶（CSE）的阻断显著降低了大鼠海绵体产生的HS浓度。加入TEA（10μM）或4-氨基吡啶（4-AP，10μM）对产生的HS浓度没有显著影响。L-半胱氨酸（10 - 10μM）引起浓度依赖性舒张反应，使用BCA（10μM）阻断CSE可使其显著降低。TEA（10μM）、4-AP（10μM）和TEA（10μM）显著减弱L-半胱氨酸诱导的舒张。在10μM时，与作为对照的23.78±2.71相比，L-半胱氨酸在存在TEA（10μM）、4-AP（10μM）和TEA（10μM）时分别导致舒张百分比为1.55±0.63、10.94±1.93和1.93±0.80。格列本脲（10μM）和氯化钡（3×10μM）均未能显著降低这些舒张。
HS诱导的大鼠海绵体舒张可能至少部分通过大电导钙激活钾（BK）通道和钾通道介导，而非通过钾通道和钾通道。似乎钾通道对HS的合成没有贡献。
