We find that chronic exposure of human saphenous vein, atria and internal thoracic artery endothelium to the human immunodeficiency virus surface glycoprotein gp120, results in an increase in endothelial μ opioid receptor expression (52%). gp120 acts, in this regard, as a proinflammatory cytokine (e.g. interleukin-1-α) by increasing endothelial μ opioid receptor expression. In contrast, morphine decreases μ opioid receptor expression by 90% in a dose dependent fashion. Pretreatment of these tissues with the respective antagonists e.g., naloxone and anti-gp120 blocks the opiate decrease and increase gp120 induced increase in μ expression, respectively. Further, pretreatment of these endothelia with morphine inhibits gp120-stimulated μ transcript expression. Therefore, the immune down-regulating action of morphine may prevent viral replication because this process requires immune activation that can, in part, be provided for by gp120 proinflammatory actions.

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