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To understand the relationship between putative neurohormonal factors operative in hypertension and coronary artery calcification (CAC), the relevant cellular actions of angiotensin (Ang II) and endothelin-1 (ET-1) are reviewed. There is compelling evidence to implicate ET-1 in CAC. ET-1 increases phosphate transport with a 42 to 73% increase in Vmax. Increased cellular phosphate may induce CAC through increased Ca x phosphate product, transformation of vascular smooth muscle cells into a bone-producing phenotype or cell apoptosis that releases procalcific substances. ET-1 is increased in several models of vascular calcification. ET-1 inhibits inhibitors of calcification, matrix Gla and osteoprotegerin, while enhancing pro-calcific factors such as BMP-2 and osteopontin. In contrast, Ang II inhibits phosphate transport decreasing Vmax by 38% and increases matrix Gla. Ang II also stimulates bone resorption. Vascular calcification is reduced by ET-1 A receptor antagonists and to a greater extent than angiotensin receptor blockade although both agents reduce blood pressure

Endothelin but Not Angiotensin II May Mediate Hypertension-Induced Coronary Vascular Calcification in Chronic Kidney Disease