NOS3 and coronary vasospasm: This concept has been described in a patient with frequent coronary artery spasms caused by a genetic defect in y+LAT expression, a major transporter for cationic amino acids, that may cause increased ADMA levels in the cytosol of endothelial cells and eNOS inhibition or uncoupling, all of which was corrected by administration of high-dose l-arginine, probably by CAT-1/l-arginine-driven export of ADMA from endothelial cells and recoupling of eNOS (Closs et al, 2012).