科研之友
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Elevated C-reactive protein (CRP) may contribute to elevated arterial pressure in angiotensin (Ang) II-dependent hypertension. However, the in vivo effects of Ang H and of mineralocorticoid receptor (MR) antagonism on CRP during Ang II-dependent hypertension have not been examined. In addition, urinary CRP excretion as a method to monitor the progression of Ang II-induced inflammation has not been evaluated. Urine samples were collected from 3 groups (n = 10/group) of rats: normotensive control, Ang II-infused (60 ng/minute), and Ang II + eplerenone (epl; 25 mg/day). A diet containing epl (0.1%) was provided after I week of Ang II infusion. After 28 days, Ang II increased systolic blood pressure (SBP) from 136 +/- 5 to 207 +/- 8 mm Hg; this response in SBP was not altered after MR antagonism (215 +/- 6 mm Hg). Ang II infusion increased plasma CRP from 14 +/- 2 to 26 +/- 3 mu g/mL and increased urinary immunoreactive CRP (irCRP) excretion nearly 8-fold (143 +/- 26 vs. 1102 +/- 115 ng/day). Treatment with eplerenone reduced plasma CRP by 25% and urinary irCRP by 34% in Ang II-infused rats, suggesting that aldosterone contributes to the CRP-associated inflammatory response in Ang II-dependent hypertension. The increase in SBP preceded the increase in irCRP excretion by at least 4 days, suggesting that CRP does not significantly contribute to increased arterial BP in Ang II-dependent hypertension. The blockade of MR reduced plasma CRP and urinary irCRP excretion, demonstrating the contribution of aldosterone to the Ang II-induced generation of CRP. Furthermore, urinary CRP may serve as a noninvasive index for monitoring cardiovascular inflammation during hypertension. J Am Soc Hypertens 2009;3(3):184-191.
- 出版日期2009-6
