We find that chronic exposure of human saphenous vein, atria and internal t
horacic artery endothelium to the human immunodeficiency virus surface glyc
oprotein gp120, results in an increase in endothelial mu opioid receptor ex
pression (52%). gp120 acts, in this regard, as a proinflammatory cytokine (
e.g. interleukin-1-alpha) by increasing endothelial mu opioid receptor expr
ession. In contrast, morphine decreases mu opioid receptor expression by 90
% in a dose dependent fashion. Pretreatment of these tissues with the respe
ctive antagonists e.g., naloxone and anti-gp120 blocks the opiate decrease
and increase gp120 induced increase in CL expression, respectively. Further
, pretreatment of these endothelia with morphine inhibits gp120-stimulated
mu transcript expression. Therefore, the immune down-regulating action of m
orphine may prevent viral replication because this process requires immune
activation that can, in part, be provided for by gp120 proinflammarory acti
ons.