Background: Soluble endoglin (sENG) has been implicated in the abnormal blood pressure response that occurs in mothers who develop preeclampsia on exposure to the hemodynamic stress of pregnancy. Elevated sENG has also been related to resting levels of blood pressure in young adults with a family history of pregnancy complications.
Hypothesis: We tested the hypothesis that sENG predicts blood pressure response to the hemodynamic stress of exercise in young adults born following pregnancy complications but that this association also exists more generally in young adults.
Methods: We recruited 128 young adults aged 24±4 years (range: 19-38 years) across a range of blood pressures and gestational ages. We completed multimodal assessment, including resting clinic and 24-hour ambulatory blood pressure monitoring, anthropometry, blood sampling, and cardiopulmonary exercise testing, throughout which blood pressures were measured. Enzyme-linked immunosorbent assays (ELISAs) were conducted in duplicate for vascular endothelial growth factor (VEGF), human soluble endoglin, and soluble fms-like tyrosine kinase-1 (sFlt-1).
Results: sENG levels were higher in preterm-born adults as compared to those born at term (8.12±1.4 and 4.55±0.85 ng/mL, p<0.001). However, in multivariate regression analysis, sENG was an independent predictor for resting and 24-hour average systolic (p<0.05) and diastolic blood pressure (p<0.01) across the whole cohort. In addition, sENG was a strong predictor of peak exercise diastolic blood pressure in all young adults when adjusting for age, sex and body mass index (β=0.74, p<0.001) and remained an independent predictor when also adjusting for gestational age, education, smoking and alcohol intake (β=0.40, p<0.001).
Conclusion: sENG is elevated in those with a history of pregnancy complications but is also an independent predictor of blood pressure response to exercise in young adults across a broad range of resting blood pressure levels and birth histories. sENG pathways may warrant further investigation as mediators in abnormal blood pressure responses to hemodynamic stress.