Valente Raphael C, Capella Luiz S, Nascimento Clarissa R, Braga Filipe, Echevarria-Lima Juliana, Lopes Aníbal G, Capella Márcia A M
Instituto de Bioquímica Médica, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Pflugers Arch. 2008 May;456(2):359-68. doi: 10.1007/s00424-007-0397-x. Epub 2007 Dec 4.
Although the kidney is a major target in hypertension, several studies have correlated important immune alterations with the development of hypertension in spontaneously hypertensive rats (SHR), like increased secretion of pro-inflammatory cytokines, inflammatory infiltration in kidneys and thymic atrophy. Because adenosine-triphosphate-binding cassette sub-family B member 1 (ABCB1; P-glycoprotein) and adenosine-triphosphate-binding cassette sub-family C member 1 (ABCC1; multidrug resistance protein 1), two proteins first described in multidrug resistant tumors, physiologically transport several immune mediators and are required for the adequate functioning of the immune system, we aimed to measure the expression and activity of these proteins in peripheral blood mononuclear cells (PBMC), thymocytes, and also kidneys of normotensive Wistar Kyoto rats and SHR. Our results showed that ABCB1, but not ABCC1, activity was diminished (nearly 50%) in PBMC. Moreover, Abcb1b gene was downregulated in PBMC and kidney of SHR and this was not counterbalanced by an upregulation of its homolog Abcb1a, suggesting that the diminished activity is due to downregulation of the gene. No alteration was detected in ABCB1 activity in SHR thymocytes, indicating that this downregulation occurs after lymphocytes leave the primary lymphoid organs. Even though it is not known at present which parameter(s) is(are) responsible for this downregulation, it may contribute for the altered immune response observed in hypertension and to possible altered drug disposition in hypertensive individuals, resulting in greater drug interaction and increased drug toxicity.
尽管肾脏是高血压的主要靶器官,但多项研究已将重要的免疫改变与自发性高血压大鼠(SHR)高血压的发展相关联,如促炎细胞因子分泌增加、肾脏炎症浸润和胸腺萎缩。由于三磷酸腺苷结合盒亚家族B成员1(ABCB1;P-糖蛋白)和三磷酸腺苷结合盒亚家族C成员1(ABCC1;多药耐药蛋白1)这两种最初在多药耐药肿瘤中发现的蛋白质,在生理上转运多种免疫介质且是免疫系统正常运作所必需的,我们旨在测量这些蛋白质在正常血压的Wistar Kyoto大鼠和SHR的外周血单核细胞(PBMC)、胸腺细胞以及肾脏中的表达和活性。我们的结果表明,PBMC中ABCB1的活性降低(近50%),而ABCC1的活性未降低。此外,SHR的PBMC和肾脏中Abcb1b基因下调,且其同源物Abcb1a的上调并未对此起到平衡作用,这表明活性降低是由于基因下调所致。在SHR胸腺细胞中未检测到ABCB1活性改变,这表明这种下调发生在淋巴细胞离开初级淋巴器官之后。尽管目前尚不清楚是哪个参数导致了这种下调,但它可能导致高血压中观察到的免疫反应改变以及高血压个体中可能的药物处置改变,从而导致更大的药物相互作用和增加的药物毒性。