Mackovic-Basic M, Fan R, Kurtz I
Department of Medicine, Cedars Sinai Medical Center, University of California at Los Angeles School of Medicine 90048.
Am J Physiol. 1992 Aug;263(2 Pt 2):F328-34. doi: 10.1152/ajprenal.1992.263.2.F328.
Na(+)-H+ exchange in the rat proximal tubule luminal membrane increases approximately 30% within 15 min after the contralateral uninephrectomy. The present study was designed to test whether altered renal sympathetic nerve outflow to the remaining kidney is the underlying mechanism of increased antiport activity and whether suppression of Na(+)-H+ antiport activity by renal denervation inhibits renal hypertrophy in the remaining kidney after uninephrectomy. Sprague-Dawley rats were divided into four groups: 1) sham operated, 2) uninephrectomized, 3) uninephrectomized with prior denervation of the remaining kidney, and 4) contralateral renal denervation. Na(+)-H+ antiport activity (brush-border vesicles), Na(+)-K(+)-ATPase activity (basolateral vesicles), and kidney weight were measured days 1-7. On days 1 and 7, Na(+)-H+ antiport activity and Na(+)-K(+)-ATPase activities were significantly greater in uninephrectomized rats. Denervation of the remaining kidney before contralateral uninephrectomy prevented the stimulation of the antiporter and Na(+)-K(+)-ATPase activity, but failed to inhibit renal hypertrophy by day 7. In separate experiments, contralateral renal denervation alone without removal of the kidney stimulated the Na(+)-H+ antiporter and Na(+)-K(+)-ATPase activity. Kidney weight, however, remained unchanged. The results demonstrate a dissociation between the activation of the Na(+)-H+ antiporter and induction of renal hypertrophy in vivo.
大鼠近端肾小管腔膜中的钠氢交换在对侧肾切除术后15分钟内增加约30%。本研究旨在测试剩余肾脏肾交感神经传出的改变是否是反向转运活性增加的潜在机制,以及肾去神经支配对钠氢反向转运活性的抑制是否会抑制肾切除术后剩余肾脏的肾肥大。将Sprague-Dawley大鼠分为四组:1)假手术组,2)肾切除组,3)对剩余肾脏预先去神经支配的肾切除组,4)对侧肾去神经支配组。在第1至7天测量钠氢反向转运活性(刷状缘小泡)、钠钾ATP酶活性(基底外侧小泡)和肾脏重量。在第1天和第7天,肾切除大鼠的钠氢反向转运活性和钠钾ATP酶活性显著更高。在对侧肾切除术前对剩余肾脏进行去神经支配可防止反向转运体和钠钾ATP酶活性的刺激,但到第7天时未能抑制肾肥大。在单独的实验中,仅对侧肾去神经支配而不切除肾脏可刺激钠氢反向转运体和钠钾ATP酶活性。然而,肾脏重量保持不变。结果表明,体内钠氢反向转运体的激活与肾肥大的诱导之间存在分离。