硫化氢的区域特异性和妊娠增强血管扩张作用

Obstetrics and gynecology research Pub Date : 2023-01-01 Epub Date: 2023-12-22 DOI:10.26502/ogr0145
Pankaj Yadav, Dong-Bao Chen, Sathish Kumar
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摘要

硫化氢(H2S)是一种心血管信号分子,可引起血管平滑肌细胞的血管扩张,但其机制尚不清楚。我们研究了 H2S 如何影响非妊娠大鼠和妊娠大鼠无内皮的肠系膜动脉和子宫动脉及其内在机制。在妊娠大鼠和非妊娠大鼠中,H2S 供体 GYY4137 和 NaHS 对子宫动脉的松弛作用大于对肠系膜动脉的松弛作用。GYY4137 和 NaHS 对妊娠大鼠和非妊娠大鼠子宫动脉的松弛作用更大。高细胞外 K+ 会抑制 NaHS 在妊娠子宫动脉中的松弛作用,这表明钾通道参与其中。电压门控钾通道阻滞剂不会影响 NaHS 松弛,ATP 敏感钾通道阻滞剂会降低 NaHS 松弛,而钙激活钾(BKCa)通道阻滞剂则会取消 NaHS 松弛。硫醇还原剂二硫苏糖醇也能阻止 NaHS 松弛。因此,H2S 在子宫动脉中具有区域特异性和妊娠增强血管舒张作用,主要由 BKCa 通道和硫化作用介导。
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Region-Specific and Pregnancy-Enhanced Vasodilator Effects of Hydrogen Sulfide.

Hydrogen sulfide (H2S) is a cardiovascular signaling molecule that causes vasodilation in vascular smooth muscle cells, but its mechanism is unclear. We examined how H2S affects mesenteric and uterine arteries without endothelium in nonpregnant and pregnant rats and the underlying mechanisms. H2S donors GYY4137 and NaHS relaxed uterine arteries more than mesenteric arteries in both pregnant and nonpregnant rats. GYY4137 and NaHS caused greater relaxation in the uterine artery of pregnant versus nonpregnant rats. High extracellular K+ abolished NaHS relaxation in pregnant uterine arteries, indicating potassium channel involvement. NaHS relaxation was unaffected by voltage-gated potassium channel blockers, reduced by ATP-sensitive potassium channel blockers, and abolished by calcium-activated potassium (BKCa) channel blockers. Thiol-reductant dithiothreitol also prevented NaHS relaxation. Thus, H2S has region-specific and pregnancy-enhanced vasodilator effects in the uterine arteries, mainly mediated by BKCa channels and sulfhydration.

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