Hypertension induced by aortic coarctation above the renal arteries is associated with immune cell infiltration of the kidneys
Hypertension induced by aortic coarctation above the renal arteries is associated with immune cell infiltration of the kidneys
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DOI：
10.1016/j.amjhyper.2005.05.034
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发表时间：
2005-11-01
影响因子：
3.2
通讯作者：
Vaziri, ND
中科院分区：
文献类型：
--
作者：
Rodriguez-Iturbe, B;Quiroz, Y;Vaziri, ND
背景：在几乎所有的高血压动物模型（HTN）中，活化T细胞和巨噬细胞的肾小管间质浸润都不可避免地存在，并在动脉压升高中起作用。肾动脉压升高在这种炎症过程的发病机制中的作用，如果有的话，是不确定的。同样不清楚的是，细胞浸润是由肾脏免疫细胞的局部激活引起的，还是由全身循环中白细胞激活引起的。方法：我们研究了Sprague-Dawley大鼠肾动脉上方腹主动脉缩窄（带状）导致近端严重HTN而远端不严重HTN的外周血白细胞活化和肾脏细胞浸润情况。结果：与假手术对照组相比，主动脉束带组在未暴露于HTN的肾脏中表现出活化T细胞、巨噬细胞、血管紧张素- ii阳性细胞、白细胞功能相关抗原-1整合素表达细胞的小管间质积累，硝基酪氨酸丰度增加（一种氧化应激指标），巨噬细胞趋化蛋白-1增加。这些发现与主动脉带状动物循环白细胞的激活有关。结论：在缩窄诱导的HTN和其他高血压疾病中，增加的气压力学应力并不是T细胞和巨噬细胞在肾脏中积累的必要条件。相反，肾灌注不足和随之而来的肾素-血管紧张素系统的激活可能通过促进局部诱导趋化剂和炎症细胞因子介导这一过程。在该模型中观察到的小管间质炎症与全身循环中的白细胞活化有关。Am J Hypertens 2005；[j] .中华高血压杂志，2005。
Background: Renal tubulointerstitial infiltration of activated T cells and macrophages is invariably present and plays a role in elevation of arterial pressure in nearly all animal models of hypertension (HTN). The role, if any, of elevated renal arterial pressure in the pathogenesis of this inflammatory process is uncertain. Also unclear is whether the cellular infiltration is caused by the local activation of immune cells in the kidney or a consequence of leukocyte activation in the systemic circulation.Methods: We studied activation of peripheral blood leukocytes and cellular infiltration in the kidneys of Sprague-Dawley rats with abdominal aorta coarctation (banding) above renal arteries, which causes severe HTN proximal but not distal to coarctation.Results: Compared with the sham operated controls' the aorta-banded group exhibited tubulointerstitial accumulation of activated T cells, macrophages, angiotensin-II positive cells, leukocyte function-associated antigen-1 integrin expressing cells, increased nitrotyrosine abundance (a measure of oxidative stress), and increased macrophage chemoattractant protein-1 in the kidneys which are not exposed to HTN in this model. These findings were associated with the activation of the circulating leukocytes in the aorta-banded animals.Conclusions: Increased baromechanical stress is not a requisite for accumulation of T cells and macrophages in the kidney in the coarctation-induced HTN and possibly in other hypertensive disorders. On the contrary, renal hypoperfusion and the consequent activation of renin-angiotensin system may mediate this process by promoting local induction of chemoattractant and inflammatory cytokines. The observed tubulointerstitial inflammation in this model is associated with leukocyte activation in the systemic circulation. Am J Hypertens 2005; 18:1449 -1456 (D 2005 American Journal of Hypertension, Ltd.