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首页> 外文期刊>American Journal of Physiology >Effect of AT1 receptor antagonism on vascular and circulating inflammatory mediators in SHR: role of NF-kappaB/IkappaB system.
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Effect of AT1 receptor antagonism on vascular and circulating inflammatory mediators in SHR: role of NF-kappaB/IkappaB system.

机译：AT1受体拮抗作用对SHR中血管和循环炎症介质的影响：NF-κB/ IkappaB系统的作用。

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摘要

We investigated the role of angiotensin II in vascular and circulating inflammatory markers in spontaneously hypertensive rats (SHR). IL-1beta, IL-6, and TNF-alpha aortic mRNA expression and plasma levels were measured in adult SHR untreated or treated with the angiotensin II receptor antagonist candesartan (2 mg.kg(-1).day(-1)) or antihypertensive triple therapy (TT; in mg.kg(-1).day(-1): 20 hydralazine + 7 type 1 hydrochlorothiazide + 0.15 reserpine) for 10 wk. Likewise, aortic expression of NF-kappaB p50 subunit precursor p105 and its inhibitor (IkappaB) were measured. Age-matched Wistar-Kyoto rats (WKY) served as normotensive reference. High blood pressure levels were associated with increased (P < 0.05) aortic mRNA expression of IL-1beta, IL-6, and TNF-alpha. Hypertension was also accompanied by increased IL-1beta and IL-6 plasma levels. No differences were observed in circulating TNF-alpha levels between SHR and WKY. SHR presented elevated aortic mRNA expression of the transcription factor NF-kappaB and reduction in its inhibitor, IkappaB. Candesartan decreased (P < 0.05) blood pressure levels, aortic mRNA expression of IL-1beta, IL-6, and TNF-alpha, and (P < 0.05) IL-1beta and IL-6 plasma concentration. However, although arterial pressure decrease was comparable for the treatments, TT only partially reduced the increments in inflammatory markers. In fact, candesartan-treated rats showed significantly lower levels of circulating and vascular inflammatory markers than TT-treated animals. The treatments increased IkappaB mRNA expression similarly. However, only candesartan reduced NF-kappaB mRNA expression. In summary, 1) SHR presented a vascular inflammatory process; 2) angiotensin II, and increased hemodynamic forces associated with hypertension, seems to be involved in stimulation of inflammatory mediators through NF-kappaB system activation; and 3) reduction of inflammatory mediators produced by candesartan in SHR could be partially due to both downregulation of NF-kappaB and upregulation of IkappaB.
机译：我们调查了自发性高血压大鼠（SHR）中血管紧张素II在血管和循环炎症标记物中的作用。在未治疗或经血管紧张素II受体拮抗剂坎地沙坦（2 mg.kg（-1）.day（-1）或未治疗）的成年SHR中测量IL-1beta，IL-6和TNF-α主动脉mRNA表达和血浆水平抗高血压三联疗法（TT; mg.kg（-1）.day（-1）：20肼苯哒嗪+ 7型1氢氯噻嗪+ 0.15利血平）10周。同样，测量了NF-κBp50亚基前体p105及其抑制剂（IkappaB）的主动脉表达。年龄匹配的Wistar-Kyoto大鼠（WKY）作为血压正常参考。高血压水平与IL-1beta，IL-6和TNF-α的主动脉mRNA表达升高（P <0.05）有关。高血压还伴有IL-1beta和IL-6血浆水平升高。 SHR和WKY之间的循环TNF-α水平未见差异。 SHR表现出转录因子NF-kappaB的主动脉mRNA表达升高，并且其抑制剂IkappaB降低。坎地沙坦降低（P <0.05）血压水平，IL-1beta，IL-6和TNF-alpha的主动脉mRNA表达，以及（P <0.05）IL-1beta和IL-6血浆浓度。但是，尽管动脉压的下降与治疗相当，但TT仅部分减少了炎症标志物的增加。实际上，坎地沙坦治疗的大鼠的循环和血管炎性标志物水平明显低于TT治疗的动物。这些处理类似地增加了IkappaB mRNA的表达。但是，只有坎地沙坦降低了NF-κBmRNA的表达。总之，1）SHR表现为血管炎性过程; 2）血管紧张素II和与高血压相关的增加的血流动力学力似乎与通过NF-κB系统激活刺激炎症介质有关; 3）坎地沙坦在SHR中产生的炎性介质减少可能部分归因于NF-κB的下调和IkappB的上调。

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