UT‐B Deficient Mice Develop Cardiac Hypertrophy and Cardiac Dysfunction Associated with Aging

Urea transporter B (UT‐B) is a urea transporter protein expressed in kidney, heart, testis, etc. To determine whether UT‐B could play an important role in cardiac function, we evaluated the morphological and functional difference between wild‐type mice and UT‐B null mice by histological analysis, electrocardiogram and left ventricular (LV) hemodynamics measurement. RT‐PCR and immunofluorescence showed UT‐B expression in cardiomyocytes in wild‐type mice and no UT‐B expression in UT‐B null mice. Urea concentration in heart tissue and serum were significantly higher in UT‐B null mice than that in wild‐type mice , and became much higher with aging. Aging UT‐B null mice had significant cardiac hypertrophy with severe interstitium fibrosis compared to age‐matched wild‐type mice. M‐model echocardiographic images of hearts showed increased AWd, AWs, PWd and PWs in 52‐weeks‐old UT‐B null mice compared with age‐matched wild‐type mice. But LVDd and LVDs in UT‐B null mice did not differ from those of wild‐type mice (P > 0.05). E/A ratio was decreased and LVEDP was increased in UT‐B null mice. Our results provide the first evidence that UT‐B deletion causes accumulation of urea in heart tissue, cardiac hypertrophy and progressive cardiac dysfunction in mice, which suggests that UT‐B play an important role in cardiac function. This work was supported by grants from the National Natural Science Foundation of China (30370572).