高血压和衰老大鼠肠道局部ace样活性和皮质酮生成

H. Salmenkari, M. Holappa, A. Siltari, R. Korpela, H. Vapaatalo
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摘要

肾素血管紧张素系统(RAS)参与炎症过程,作为促炎或抗炎介质。RAS的成分,如血管紧张素转换酶(ACE),已经在肠道上皮局部检测到。此外,抗炎类固醇,皮质酮,在肠道中产生。高血压和衰老引起血管内皮低度炎症。目前尚不清楚它们是否会在肠道中引起类似的低度炎症,以及低度炎症是否会引起ACE的激活和皮质酮分泌的升高。在9周龄和26周龄自发性高血压大鼠(SHR)及其正常Wistar-Kyoto (WK)对照的回肠和结肠中测量这两个变量。通过组织匀浆样品中由海马基-组氨酸-亮氨酸生成组氨酸来测量ace活性,发现幼龄动物的回肠和结肠中ace活性相似,尽管幼龄正常动物的回肠表现出最低水平。在老龄动物中,回肠的ACE活性高于结肠,特别是在血压正常的大鼠中。体外培养90分钟后,以回肠或结肠上清液中的皮质酮浓度来测定皮质酮的产生。在SHR和WK中,回肠的皮质酮产量高于结肠。没有明确的证据表明年龄依赖性或高血压对肠道测量变量的影响。因此,在衰老或高血压中假定的肠道低度炎症并不是一个足够强的刺激来提高皮质酮的产生或激活ACE。
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Local Intestinal ACE-Like Activity and Corticosterone Production in Hypertensive and Aging Rats
The renin angiotensin system (RAS) participates in inflammatory processes, as either a pro-inflammatory or an anti-inflammatory mediator. Components of RAS, such as angiotensin-converting enzyme (ACE), have been detected locally in the gut epithelium. In addition, the anti-inflammatory steroid, corticosterone, is produced in the gut. Hypertension and aging evoke a low-grade inflammatory process in the vascular endothelium. It is not known whether they induce a similar low-grade inflammation in the intestine and if the low-grade inflammation would evoke an activation of ACE and an elevation of corticosterone production. These two variables were measured in ileum and colon of 9- and 26-week old spontaneously hypertensive rats (SHR) and their normotensive Wistar-Kyoto (WK) controls. ACE-activity, measured via the formation of histidyl-leucine from hippuryl-histidyl-leucine in the tissue homogenate samples, was similar in the ileum and colon of young animals although the ileum of the young normotensive animals displayed the lowest level. In the old animals, the ACE activity was higher in the ileum than in the colon, especially in normotensive rats. Corticosterone production was measured as corticosterone concentration in the supernatants of ileum or colon after a 90-min ex vivo incubation. Corticosterone production was higher in ileum than in colon in both SHR and WK. No clear evidence was seen for age-dependency or for an effect of hypertension in the measured variables in the intestine. Thus, the putative low-grade inflammation in the intestine in aging or hypertension is not a strong enough stimulus to elevate corticosterone production or activate ACE.
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