Key result
Exogenous estrogen preserves distal pulmonary arterial mechanics and prevents pulmonary hypertension in rats.
Why the study?
The impact of 17b-estradiol on pulmonary arterial hypertension is unclear due to conflicting evidence and limitations of prior endpoints that do not fully capture RV afterload.
Does exogenous estrogen preserve distal pulmonary arterial mechanics and prevent pulmonary hypertension in rats?
Does exogenous estrogen preserve distal pulmonary arterial mechanics and prevent pulmonary hypertension in rats?
Exogenous estrogen appears to preserve distal pulmonary arterial mechanics and prevent pulmonary hypertension in a rat model, providing insight into its protective effects in PAH.
May inform estrogen-based PAH therapies; hypothesis-generating in rats and leaves open human translation.
To the Editor: 17b-estradiol (E2), the most abundant female sex steroid, has been implicated in the development and progression of pulmonary arterial hypertension (PAH) (1, 2).Although some studies have found that E2 drives PAH progression, others have found a protective effect (3-6).The majority of these studies used right ventricular (RV) end systolic or mean pulmonary artery (PA) pressure as the primary metric of pulmonary vascular function and RV afterload.However, these endpoints are affected by RV function and do not fully capture RV afterload (7, 8).
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Philip et al. (2019) conducted a letter in Pulmonary arterial hypertension. 17b-estradiol (E2) vs. Vehicle (OVX+Veh) was evaluated on Pulmonary vascular function. Exogenous estrogen preserves distal pulmonary arterial mechanics and prevents pulmonary hypertension in rats.
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