The renin angiotensin system (RAS) participates in inflammatory processes,\nas either a pro-inflammatory or an anti-inflammatory mediator. Components\nof RAS, such as angiotensin-converting enzyme (ACE), have been detected\nlocally in the gut epithelium. In addition, the anti-inflammatory steroid, corticosterone,\nis produced in the gut. Hypertension and aging evoke a low-grade\ninflammatory process in the vascular endothelium. It is not known whether\nthey induce a similar low-grade inflammation in the intestine and if the\nlow-grade inflammation would evoke an activation of ACE and an elevation\nof corticosterone production. These two variables were measured in ileum and\ncolon of 9- and 26-week old spontaneously hypertensive rats (SHR) and their\nnormotensive Wistar-Kyoto (WK) controls. ACE-activity, measured via the\nformation of histidyl-leucine from hippuryl-histidyl-leucine in the tissue homogenate\nsamples, was similar in the ileum and colon of young animals although\nthe ileum of the young normotensive animals displayed the lowest\nlevel. In the old animals, the ACE activity was higher in the ileum than in the\ncolon, especially in normotensive rats. Corticosterone production was measured\nas corticosterone concentration in the supernatants of ileum or colon after\na 90-min ex vivo incubation. Corticosterone production was higher in ileum\nthan in colon in both SHR and WK. No clear evidence was seen for\nage-dependency or for an effect of hypertension in the measured variables in\nthe intestine. Thus, the putative low-grade inflammation in the intestine in\naging or hypertension is not a strong enough stimulus to elevate corticosterone\nproduction or activate ACE.
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