Calcium entry blockers increase interleukin-10 production in endotoxemia

Csaba Szabó, György Haskó, Zollán H. Németh, E. Sylvester Vizi

    Research output: Contribution to journalArticle

    34 Scopus citations

    Abstract

    Intracellular calcium is an important mediator of the cellular response in endotoxemia and shock. Here we investigated the effects of verapamil and diltiazem, two calcium entry blockers, on endotoxin (bacterial lipopolysaccharide, LPS)-induced production of pro- and anti-inflammatory cytokines and of nitric oxide in mice. LPS-induced interleukin-10 plasma levels were significantly enhanced, and circulating tumor necrosis factor-α concentrations were significantly suppressed in animals pretreated intraperitoneally with verapamil (10 mg/kg) or diltiazem (20 mg/kg). However, LPS-induced interleukin-6 levels were unaffected by the calcium antagonists. Similarly, LPS-induced production of nitrite/nitrate (breakdown products of nitric oxide) was not affected by verapamil and diltiazem. We conclude that calcium entry blockers selectively modulate the production of some pro- and anti-inflammatory mediators in endotoxemia. These effects may contribute to the cytoprotective and anti-inflammatory effects of calcium entry blockers in shock and trauma.

    Original languageEnglish (US)
    Pages (from-to)304-307
    Number of pages4
    JournalShock
    Volume7
    Issue number4
    DOIs
    StatePublished - 1997

    ASJC Scopus subject areas

    • Emergency Medicine
    • Critical Care and Intensive Care Medicine

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    Szabó, C., Haskó, G., Németh, Z. H., & Sylvester Vizi, E. (1997). Calcium entry blockers increase interleukin-10 production in endotoxemia. Shock, 7(4), 304-307. https://doi.org/10.1097/00024382-199704000-00011