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Published on: September 28, 2015
Effects of angiotensin-II receptor blockers on experimental autoimmune myocarditis
Xuefei Liu1, Xinglei Zhu, Aiying Wang
1Department of Cardiology, Provincial Hospital Affiliated to Shandong University, 324 Jingwu Weiqi Road, Jinan, 250021, PR China.
Insights
Angiotensin-II type 1 receptor blockers (ARBs) like valsartan improve experimental autoimmune myocarditis (EAM) by modulating immune responses, not just lowering blood pressure. This suggests ARBs have immunomodulatory effects beneficial for EAM treatment.
Area of Science:
- Cardiovascular Research
- Immunology
- Pharmacology
Background:
- Angiotensin-II type 1 receptor blockers (ARBs) are established treatments for cardiovascular diseases.
- Emerging evidence highlights non-hemodynamic effects of ARBs.
- The study investigates ARBs' impact on experimental autoimmune myocarditis (EAM).
Purpose of the Study:
- To investigate the effects of ARBs on the development of EAM.
- To elucidate the underlying mechanisms of ARBs' action in EAM.
Main Methods:
- An EAM rat model was induced using porcine cardiac myosin.
- Valsartan was administered to EAM rats, with regular blood pressure monitoring.
- Cardiac function, myocarditis severity, T-cell proliferation, and cytokine profiles were assessed.
Main Results:
- Valsartan improved cardiac function and reduced myocarditis severity without altering blood pressure.
- Valsartan suppressed antigen-specific T-cell proliferation.
- Th1 cytokines (IFN-gamma, IL-2) decreased, while Th2 cytokines (IL-4, IL-10) increased.
Conclusions:
- Valsartan ameliorates EAM through mechanisms independent of blood pressure reduction.
- The immunomodulatory effects of ARBs, particularly on T-cell balance, contribute to their therapeutic benefits in EAM.
Background:
The effects of angiotensin-II type 1 receptor blockers (ARBs) on the treatment of hypertension, heart failure, and other cardiovascular diseases have been confirmed extensively. However, recent studies have emphasized the nonhemodynamic effects of these drugs. The purpose of this study was to investigate the effects of ARBs on the development of experimental autoimmune myocarditis (EAM), and to clarify the mechanisms involved.
Methods:
EAM model was induced in Lewis rats by injection of porcine cardiac myosin subcutaneously. We administered valsartan (a new ARB) to rats with EAM and measured blood pressure regularly. Echocardiography was performed to examine the cardiac function and heart structure of the rats. The severity of myocarditis was detected by histopathological evaluation. We evaluated antigen-specific T-cell proliferation responses to cardiac myosin by the lymphocyte proliferation assay and measured serum levels of Th1 and Th2 cytokines by enzyme-linked immunosorbent assay.
Results:
There was no significant difference in the blood pressure (BP) level between the groups and cardiac function of valsartan-treated rats was significantly improved compared with untreated rats. Valsartan markedly reduced the severity of myocardial lesions and suppressed lymphocyte proliferation in rats immunized with myosin. After drug administration, Th1 cytokines (IFN-gamma and IL-2) were significantly down-regulated, while Th2 cytokines (IL-4 and IL-10) were detected to undergo up-regulation.
Conclusions:
The results suggest that valsartan can ameliorate EAM independent of BP-lowering effects. Some of the beneficial effects of ARBs may be due to their immunomodulatory reactions in the modification of helper T-cell balance.
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