Table 1.

Comparison of phenotype and biochemistry between pulmonary hypertension and preeclampsia.

	Pulmonary hypertension	Preeclampsia
Local vascular resistance	Increased pulmonary vascular resistance Increased mean pulmonary arterial pressure (>20 mm Hg)	Increased uteroplacental vascular resistance Reduced uteroplacental blood flow
Systemic blood pressure		Elevated systolic and diastolic blood pressure (>140 and >90 mmHg, respectively
Vascular remodeling	Increased vascular remodeling due to intimal and medial hypertrophy, fibrosis, inflammation, etc.	Reduced vascular remodeling due to impaired endovascular trophoblast invasion and subsequent failure to replace vascular smooth muscle cells (VSMCs) and endothelial cells
Complications	Right ventricular overload and heart failure	Intrauterine growth restriction Proteinuria Uteroplacental and other maternal organ dysfunction
Endothelin-1	Increased circulating endothelin-1	Increased circulating endothelin-1
Hypoxia, hypoxia inducible factor (HIFs) and microRNA-210 (miR-210)	Hypoxia is a major contributor to Group III pulmonary hypertension resulting from lung disease and/or hypoxia Increased incidence at high altitude Increased expression of HIFs in pulmonary arteries Increased expression of miR-210 in pulmonary arteries	Hypoxia is a major contributor to preeclampsia Increased incidence at high altitude Increased expression of HIFs in uteroplacental tissues Increased expression of miR-210 in uteroplacental tissues
Reactive oxygen species (ROS) and oxidative stress	Increased ROS and oxidative stress in pulmonary arteries (some studies suggest decreased ROS and oxidative stress)	Increased ROS and oxidative stress in uteroplacental tissues
ER stress and the unfolded protein response (UPR)	Increased ER stress and activation of the UPR in pulmonary arteries	Increased ER stress and activation of the UPR in uteroplacental tissues