UT-A expression in pars recta from a rat model of chronic renal failure

被引:0
|
作者
Zotta, Elsa [1 ]
Ochoa, Federico [1 ]
Tironi Farinati, Carla [1 ]
Damiano, Alicia [1 ]
Silberstein, Claudia [1 ]
Levy Yeyati, Nesmo [1 ]
Ibarra, Cristina [1 ]
机构
[1] Univ Buenos Aires, Fac Med, Dept Physiol, Physiopathogeny Lab, RA-1121 Buenos Aires, DF, Argentina
关键词
Chronic renal failure; Fractional excretion of urea; Urea secretion; UT-A2; transporter;
D O I
暂无
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Background: Urea transport depends on the diffusion through cell membrane and the facilitated urea transport. Two groups of urea transporters (UT-A and UT-B) have been identified in mammals, and both are involved in intrarenal recycling of urea. The aim of our study was to examine the renal urea handling in rats with chronic renal failure (CRF). Methods: CRF rats were induced by 5/6 nephrectomy followed by a high-protein (HP) diet to increase the progressive loss of renal function for 5 months. Functional studies on water and urea handling were performed. RTPCR, immunoblotting and immunohistochemistry were used to identify UT-A proteins in remnant kidney. Results: A significant decrease in creatinine clearance consistent with development of CRF was observed. The remnant kidneys were hypertrophied, and total renal mass was increased. Urine production increased markedly, whereas urine osmolality and solute-free water reabsorption decreased significantly. Fractional urea excretion was increased reaching values of 105% +/- 8%. UT-A protein was localized in pars recta by immunohistochemical studies, and it was identified as UT-A2 in outer medulla from remnant kidneys by RT-PCR and immunoblotting. Conclusion: In uremic rats, an urea transporter type UT-A2 was expressed in the pars recta, suggesting a possible relation with the fractional urea excretion increase. This expression may be a consequence of an adaptive mechanism in the handling of urea during development of CRF. Further studies will be necessary to elucidate the contribution of this mechanism to renal damage observed in the progression of CRF.
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页码:947 / 958
页数:12
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