Amphetamine enhances natural killer cytotoxic activity via beta-adrenergic mechanism.

Although addiction to amphetamine (AMPH) is a serious social and medical problem, the data concerning AMPH - immune interactions are still not numerous. To analyze the mechanism of AMPH-induced changes in the function of the immune system, rats were pretreated with beta-adrenergic receptor antagonist propranolol (PROP; 5 mg/kg, i.p.) prior to AMPH (1 mg/kg, i.p.) administration. Natural Killer cells cytotoxicity (NKCC) ((51)Cr-release assay), the number of LGLs (NK cells) (Timonen method), leukocytes, lymphocytes and monocytes, and plasma corticosterone level (CORT) (RIA) were evaluated in the peripheral blood and spleen. In the peripheral blood increases in NKCC (+331 Delta %), as well as in LGL (+33 Delta %) and monocyte (+65 Delta %) number observed after AMPH were partially inhibited by PROP (respectively by 30%, 19%, and 30%) in contrast to lymphopenia (-19 Delta %) and granulocytosis (+65 Delta %) which were not affected by beta-blockade. In the spleen AMPH-induced decreases in NKCC (-25 Delta %) and in all the leukocyte populations number (approximately -30 Delta %) were completely blocked by PROP. Plasma CORT level, highly elevated by AMPH (+337 Delta %), was attenuated nearly by 50% under beta-adrenergic blockade. These data indicate that AMPH-induced enhancement of cytotoxic activity of NK cell is related to beta-adrenergic mechanism.