Key result
Prior pre-eclampsia was associated with enhanced sensitivity to the pressor effects of endothelin-1 up to 16 months postpartum compared with normotensive pregnancy, mediated via ETB receptors.
Why the study?
Does endothelin type B (ETB) receptor dysfunction contribute to persistent microvascular dysfunction and future CVD risk in women with a history of pre-eclampsia?
Does endothelin type B (ETB) receptor dysfunction contribute to persistent microvascular dysfunction and future CVD risk in women with a history of pre-eclampsia?
Alterations in ETB receptor function may contribute to the pathogenesis of pre-eclampsia and subsequent cardiovascular disease risk, presenting a potential therapeutic target.
In a recent issue of Clinical Science, Stanhewicz et al. investigated persistent microvascular dysfunction in women up to 16 months postpartum. The authors found sensitivity to the pressor effects of endothelin-1 (ET-1) was enhanced when compared with women who had a normotensive pregnancy. Importantly, the authors demonstrated that this effect was mediated via the endothelin type B (ETB) receptors. Therefore, the present study highlights the possibility that alterations in the localization of the ETB receptor contributes to the pathogenesis of pre-eclampsia and future cardiovascular disease (CVD) risk. Currently, there is great interest in the role of the endothelin system in pre-eclampsia. Targetting the endothelin system, potentially by modulating upstream pathways to prevent ETB receptor dysfunction, may improve health outcomes for women and their offspring during pre-eclampsia and later life.
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Katrina M. Mirabito Colafella (2018) conducted an editorial in Pre-eclampsia and future cardiovascular disease (CVD) risk. Prior pre-eclampsia vs. Normotensive pregnancy was evaluated on Sensitivity to the pressor effects of endothelin-1 (ET-1). Prior pre-eclampsia was associated with enhanced sensitivity to the pressor effects of endothelin-1 up to 16 months postpartum compared with normotensive pregnancy, mediated via ETB receptors.
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