Li FF, et al. – Here, researchers hypothesized that dysregulated IKCa and SKCa channels may be involved in the pathogenesis of preeclampsia (PE) mediated by the impaired nitric oxide (NO) system on chorionic plate resistance arteries (CPAs). This examination gives evidence that dysregulated IKCa and SKCa channels could contribute to the fetal pathogenesis of PE through direct promotion of vascular constriction of CPAs and through influencing functions of NO and activities of NOS.

Methods

• In this research, the location of IKCa and SKCa channels, activities of NO synthases (NOS), and expression levels of these molecules were studied on CPAs from 30 normal pregnancies and 30 PE.
• The vasodilating function of CPAs was measured under openers or blockers of IKCa/SKCa channels in the presence or absence of NO donor or inhibitor.

Results

• In this study, IKCa and SKCa channels were located both on endothelium and on smooth muscles of CPAs and the expressions of them were downregulated in PE women comparing to those in normal pregnant women.
• The protein expressions of endothelial NOS (eNOS) and inducible NOS (iNOS) were downregulated on CPAs in PE accompanied by reduced activity of eNOS.
• Notably, the vasodilatory functions mediated by IKCa/SKCachannels and by NO were aberrant on preeclamptic CPAs.
• In addition, IKCa and SKCa channels were responsible for nitric oxide (NO)–attributable vasorelaxation and activity modulation of NO synthases.