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Anti‐Inflammatory Effects of ACE Inhibition Persist Following Withdrawal of Treatment
Author(s) -
Hale Taben Mary,
Tu Danni,
Shahid Wafa,
Biwer Lauren A
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.1133.7
Subject(s) - enalapril , monocyte , nitric oxide synthase , medicine , ace inhibitor , nitric oxide , cytokine , endocrinology , inflammation , immune system , chemokine , angiotensin converting enzyme , granulocyte , ventricular remodeling , pharmacology , immunology , myocardial infarction , blood pressure
Transient (2‐wk tx + 2‐wk washout) angiotensin converting enzyme (ACE) inhibition induces persistent changes that result in a preservation of cardiac function and fewer infiltrating macrophages after 10 days of nitric oxide synthase inhibition (L‐NAME) – despite evidence of infarction. In the present study we investigated whether prior ACE inhibition (enalapril) would yield a modified immune response during L‐NAME‐induced pathological remodeling. We performed a time course analysis of left ventricular (LV) inflammatory cytokines and macrophage infiltration during L‐NAME (L) treatment in SHR that were previously treated with placebo (C+L) or enalapril (E+L) for 2wks followed by 2‐wk washout. L‐NAME equivalently increased arterial pressure, regardless of pre‐treatment. Distinct patterns of cytokine levels were observed in C+L vs E+L. In C+L, but not E+L LV there was an early (day 3) and sustained increase in monocyte chemoattractant protein‐1 and granulocyte macrophage colony stimulating factor that resulted in a significant increase in macrophage infiltration on day 7 of L‐NAME treatment. This is the first evidence that transient pre‐treatment with an ACE inhibitor can produce long‐term changes in L‐NAME‐induced immune responses. Further studies will determine whether this reduced macrophage recruitment will result in attenuation of post‐infarct remodeling.