Endothelin-1 (ET-1), secreted by vascular endothelial cells, was initially considered a pathogenic factor for hypertension due to its potent vasoconstrictive effect. However, it was later discovered that ET-1 synthesized and secreted in the kidney exhibits diuretic and natriuretic effects, suggesting a potential antihypertensive role. ET-1 regulates electrolyte balance by stimulating two G protein-coupled receptors, endothelin receptor A and endothelin receptor B. In this article, we review the regulation of renal NaCl reabsorption by ET-1 and the underlying mechanisms, highlighting the significant role of ET-1 in the regulation of blood pressure.