Rettig R, Folberth C, Stauss H, Kopf D, Waldherr R, Unger T
Department of Pharmacology, University of Heidelberg, Federal Republic of Germany.
Am J Physiol. 1990 Mar;258(3 Pt 2):F606-11. doi: 10.1152/ajprenal.1990.258.3.F606.
We have previously shown that transplantation of kidneys from genetically hypertensive to normotensive rats result in hypertension in renal graft recipients. To investigate whether this posttransplantation hypertension may have been the result of damage to the renal graft by high perfusion pressure before transplantation, we normalized blood pressure throughout life in spontaneously hypertensive rat (SHR) kidney donors by continuous antihypertensive treatment with the angiotensin-converting enzyme inhibitor ramipril (1 mg.kg-1.day-1 in drinking fluid). When kidneys from these rats were transplanted at age 20 wk to age-matched bilaterally nephrectomized F1 hybrids bred from SHR and Wistar-Kyoto (WKY) parents, posttransplantation hypertension still developed. In contrast, blood pressure did not change significantly in recipients of kidneys from ramipril-treated WKY rats. In the initial phase, recipients of SHR kidneys had a lower body weight and higher plasma urea concentrations than recipients of WKY kidneys. However, in the chronic phase, there were no significant differences between the two groups with respect to daily water intake, plasma urea concentration, glomerular filtration rate, renal blood flow, and weight of transplanted kidneys; no histological differences were observed between renal grafts from WKY and SHR donors, except for structural vascular hypertrophy in the latter group. We conclude that posttransplantation hypertension in recipients of SHR kidney grafts also develops, when the grafts have not been subjected to high renal perfusion pressure before transplantation. Our data support the hypothesis that SHR kidneys carry a primary defect, which can induce hypertension in renal graft recipients.
我们之前已经表明，将基因性高血压大鼠的肾脏移植给血压正常的大鼠会导致肾移植受体出现高血压。为了研究这种移植后高血压是否可能是移植前高灌注压力对肾移植造成损伤的结果，我们通过用血管紧张素转换酶抑制剂雷米普利（饮水中1毫克·千克⁻¹·天⁻¹）进行持续抗高血压治疗，使自发性高血压大鼠（SHR）肾脏供体终生血压正常化。当这些大鼠的肾脏在20周龄时移植给年龄匹配的、由SHR和Wistar-Kyoto（WKY）亲本培育的双侧肾切除的F1杂种时，移植后高血压仍然会发生。相比之下，接受雷米普利治疗的WKY大鼠肾脏受体的血压没有显著变化。在初始阶段，SHR肾脏受体的体重低于WKY肾脏受体，血浆尿素浓度高于WKY肾脏受体。然而，在慢性阶段，两组在每日饮水量、血浆尿素浓度、肾小球滤过率、肾血流量和移植肾脏重量方面没有显著差异；除了后一组存在结构性血管肥大外，未观察到WKY和SHR供体的肾移植之间存在组织学差异。我们得出结论，当移植前肾移植未受到高肾灌注压力时，SHR肾移植受体的移植后高血压也会发生。我们的数据支持这样的假设，即SHR肾脏存在原发性缺陷，可在肾移植受体中诱发高血压。
