Endothelin receptor type A (ETA) (ETA)

The Endothelin receptor type A (ETA), encoded by the EDNRA gene, is a G protein-coupled receptor (GPCR) that mediates the potent vasoconstrictive and mitogenic effects of endothelin-1 (ET-1). In the uterus, ETA receptors are densely expressed in the myometrium, where their activation leads to strong smooth muscle contractions via the Gq/11-phospholipase C-inositol trisphosphate (IP3) pathway (UniProt: P25101). This pathway is critical in both normal physiological labor and pathological states such as preeclampsia, where elevated ET-1 levels contribute to systemic hypertension and placental dysfunction (PubMed: 25600494). ETA receptor antagonists, such as ambrisentan and macitentan, are clinically established for treating pulmonary arterial hypertension by reducing vascular resistance and inhibiting smooth muscle hypertrophy (StatPearls: NBK537027). In the context of uterine health, the pathway is a subject of research for managing dysmenorrhea and preterm labor, although its clinical application is limited by the high risk of teratogenicity associated with endothelin system modulation. Beyond contraction, the ETA receptor is involved in cell proliferation and fibrosis, making it a target of interest in oncology and chronic kidney disease.

Other names

EDNRAEndothelin A receptorET-AhET-AREndothelin-1 receptor

Competitive antagonism of the endothelin receptor type A, which inhibits the Gq-protein signaling pathway and prevents endothelin-1-induced calcium mobilization and smooth muscle contraction.