UT-A urea transporter protein in heart - Increased abundance during uremia, hypertension, and heart failure

Urea transporters have been cloned from kidney medulla (UT-A) and erythrocy tes (UT-B). We determined whether UT-A proteins could be detected in heart and whether their abundance was altered by uremia or hypertension or in hum an heart failure. In normal rat heart, bands were detected at 56, 51, and 3 9 kDa. In uremic rats, the abundance of the 56-kDa protein increased 1.9-fo ld compared with pair-fed, sham-operated rats, whereas the 51- and 39-kDa p roteins were unchanged. We also detected UT-A2 mRNA in hearts from control and uremic rats. Because uremia is accompanied by hypertension, the effects of hypertension per se were studied in uninephrectomized deoxycorticostero ne acetate salt-treated rats, where the abundance of the 56-kDa protein inc reased 2-fold versus controls, and in angiotensin II-infused rats, where th e abundance of the 56 kDa protein increased 1.8-fold versus controls. The 5 1- and 39-kDa proteins were unchanged in both hypertensive models. In human left ventricle myocardium, UT-A proteins were detected at 97, 56, and 51 k Da. In failing left ventricle (taken at transplant, New York Heart Associat ion class IV), the abundance of the 56-kDa protein increased 1.4-fold, and the 51-kDa protein increased 4.3-fold versus nonfailing left ventricle (don or hearts). We conclude that (1) multiple UT-A proteins are detected in rat and human heart; (2) the 56-kDa protein is upregulated in rat heart in ure mia or models of hypertension; and (3) the rat results can be extended to h uman heart, where 56- and 51-kDa proteins are increased during heart failur e.