Captopril inhibits the production of tumor necrosis factor-alpha by human mononuclear cells in patients with congestive heart failure.
To study the effects of captopril on tumor necrosis factor-alpha produced by peripheral blood mononuclear cells (PBMC) of patients with congestive heart failure (CHF), we determined the TNF-alpha 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-alpha in cultured PBMC (PBMC-TNF-alpha) 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-alpha was significantly inhibited by captopril. These results demonstrate that the expression of TNF-alpha 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.
Zhao
S P
SP
Department of Cardiology, Second Affiliated Hospital of Human Medical University, ChangSha 410011, China.
Xie
X M
XM
D000328:Adult; D000368:Aged; D002216:Captopril / Q000494:pharmacology* / Q000627:therapeutic use; D005260:Female; D006333:Heart Failure / Q000188:drug therapy / Q000378:metabolism*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000187:drug effects* / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors* / Q000096:biosynthesis
D014409:Tumor Necrosis Factor-alpha; D002216:Captopril