Captopril inhibits the production of tumor necrosis factor-α by human mononuclear cells in patients with congestive heart failure

• Published in: Clinica chimica acta 2001-02, Vol.304 (1), p.85-90
• Main Authors: Zhao, Shui-Ping, Xie, Xiao-Mei
• Format: Article
• Language: English
• Subjects: Adult; Aged; Biological and medical sciences; Captopril; Captopril - pharmacology; Captopril - therapeutic use; Cardiology. Vascular system; Cardiovascular system; Congestive heart failure; Female; Heart; Heart Failure - drug therapy; Heart Failure - metabolism; Heart failure, cardiogenic pulmonary edema, cardiac enlargement; Humans; Male; Medical sciences; Middle Aged; Miscellaneous; Monocytes - drug effects; Monocytes - metabolism; Pharmacology. Drug treatments; Tumor Necrosis Factor-alpha - antagonists & inhibitors; Tumor Necrosis Factor-alpha - biosynthesis; Tumor necrosis factor-α
• ISSN: 0009-8981; 1873-3492
• DOI: 10.1016/S0009-8981(00)00405-8

To study the effects of captopril on tumor necrosis factor-α produced by peripheral blood mononuclear cells (PBMC) of patients with congestive heart failure (CHF), we determined the TNF-α concentrations of culture supernatants of PBMC with and without catopril in 74 CHF patients with various heart diseases. The results showed that the supernatants concentrations of TNF-α in cultured PBMC (PBMC-TNF-α) were significantly increased in non-cachetic and cachetic CHF patients, and even higher in cachetic CHF patients, as compared with the controls (i.e., patients with New York Heart Association CHF classification I). The PBMC-TNF-α was significantly inhibited by captopril. These results demonstrate that the expression of TNF-α in PBMC is increased and can be inhibited by captopril in patients with CHF, especially in those accompanied by cachexia. This suggests that the immunomodulatory effects of captopril may contribute to its beneficial effects in heart failure patients.