Endothelial dysfunction is a hallmark of preeclampsia and the role of nitric oxide (NO) has been extensively studied in this pregnancy complication. In recent years, hydrogen sulphide (H2S) has arisen as a new gasotransmitter with an impact on endothelial function. However, the involvement of H2S in the pathophysiology of preeclampsia is not fully understood, and only a few studies with limited sample size have investigated circulating levels of H2S in preeclamptic patients. Moreover, H2S levels have not been previously evaluated in gestational hypertension. Furthermore, the relationship between H2S and NO in these hypertensive disorders of pregnancy has yet to be determined. We measured H2S levels in plasma of 120 healthy pregnant women, 88 gestational hypertensive and 62 preeclamptic women. We also measured plasma nitrite in a subset of patients and carried out correlation analysis between plasma H2S and nitrite in these three groups. We found that plasma H2S was elevated in preeclampsia and further increased in gestational hypertension compared to healthy pregnancy. Plasma nitrite was reduced in gestational hypertension and preeclampsia, and these levels were negatively correlated with H2S in both gestational hypertension and preeclampsia, but not in healthy pregnancy. Our results indicate that increases in H2S may represent a mechanism triggered as an attempt to compensate reduced NO in gestational hypertension and preeclampsia. Future studies are warranted to investigate the mechanisms underlying H2S/NO interaction on mediating endothelial dysfunction in these hypertensive disorders of pregnancy.
Aim: This work examined whether ARG1 (rs2781659, rs2781667, rs2246012 and rs17599586) and ARG2 (rs3742879 and rs10483801) single-nucleotide polymorphisms (SNPs) are associated with antihypertensive therapy responsiveness in preeclampsia (PE) and their effects on arginase isoforms and nitrite concentrations in responsive and nonresponsive patients. Methods: SNP genotypes were determined by TaqMan assays. Plasma arginase levels were measured by ELISA and nitrite concentrations were measured using an ozone-based chemiluminescence assay. Results: The G allele for ARG2 rs3742879 (A>G) was less frequent in nonresponsive compared with responsive patients (15.5% vs 24.7%) and the G carriers of the nonresponsive subgroup had lower arginase 2 (9.2 ± 7.5 ng/ml vs 19.1 ± 17.3 ng/ml) and higher nitrite concentrations (110.2 ± 52.8 nM vs 78.5 ± 37.9 nM) than carriers of the AA genotype (all p < 0.05). Conclusion: ARG2 SNP rs3742879 is associated with diminished arginase 2 levels and increased nitric oxide formation in nonresponsive PE patients.
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