SLC9C1 and hydrops fetalis: Experimental studies suggested that the use of SGLT2 inhibited NHE and protected HF; when cardiac cytoplasmic Na+ and Ca2+ concentrations and mitochondrial Ca2+ were measured fluorometrically in isolated ventricular myocytes from rabbits and rats, the results evidenced that empagliflozin directly inhibited NHE flux, caused by a reduction in cytoplasmic Na+ and Ca2+ concentrations and an increase in mitochondrial Ca2 [118].