A more recent version of this article appeared on July 20, 2001

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(Circulation Research. 2001;0:hh1401.093293.)
© 2001 American Heart Association, Inc.

Article

UT-A Urea Transporter Protein in Heart

Increased Abundance During Uremia, Hypertension, and Heart Failure

Presented in part at Experimental Biology ’99, Washington, DC, April 17–21, 1999, the 33rd Annual Meeting of the American Society of Nephrology, Toronto, Ontario, Canada, October 13–16, 2000, and Experimental Biology 2001, Orlando, Fla, March 31–April 4, 2001, and published in abstract form (FASEB J. 1999;13:A392; J Am Soc Nephrol. 2000;11:24A; and FASEB J. 2001;15:A852).

Rafael Duchesne, Janet D. Klein, Jeffrey B. Velotta, John J. Doran, Patricia Rouillard, Brian R. Roberts, Alicia A. McDonough Jeff M. Sands

From the Renal Division, Department of Medicine (R.D., J.D.K., J.J.D., P.R., B.R.R., J.M.S.) and Department of Physiology (J.M.S.), Emory University School of Medicine, Atlanta, Ga, and Department of Physiology and Biophysics (J.B.V., A.A.M.), USC Keck School of Medicine, Los Angeles, Calif.

Correspondence to Dr Jeff M. Sands, Emory University School of Medicine, Renal Division, WMRB Room 338, 1639 Pierce Dr NE, Atlanta, GA 30322. E-mail jsands{at}emory.edu

Abstract

Abstract—Urea transporters have been cloned from kidney medulla (UT-A) and erythrocytes (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 human heart failure. In normal rat heart, bands were detected at 56, 51, and 39 kDa. In uremic rats, the abundance of the 56-kDa protein increased 1.9-fold compared with pair-fed, sham-operated rats, whereas the 51- and 39-kDa proteins 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 deoxycorticosterone acetate salt–treated rats, where the abundance of the 56-kDa protein increased 2-fold versus controls, and in angiotensin II–infused rats, where the abundance of the 56 kDa protein increased 1.8-fold versus controls. The 51- 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 kDa. In failing left ventricle (taken at transplant, New York Heart Association 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 (donor 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 uremia or models of hypertension; and (3) the rat results can be extended to human heart, where 56- and 51-kDa proteins are increased during heart failure.

Key Words: urea • cardiac hypertrophy • polyamine • human heart failure • rat models

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