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Abstract Hypertension (HTN) is common with coarctation of the aorta (CoA), a common congenital cardiovascular defect. Coarctation-induced mechanical stimuli can drive remodeling in the proximal aorta, resulting in stiffening and HTN. Natriuretic peptide receptor C (NPRC) expression is downregulated in proximal aortas of hypertensive CoA patients, and preclinical models show endothelial NPRC decreases with increasing coarctation severity.
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