Social stress in mammals has repeatedly been shown to cause substantial alterations in the distribution pattern of immune cells in the peripheral blood. The studies described here investigated the role of adrenergic mechanisms in mediating stressor-induced changes in blood leukocyte numbers using a social confrontation procedure in the rat. Experimental manipulations were carried out to eliminate the stress-associated release of adrenal hormones or to block the binding of endogenous catecholamines to alpha- and beta-adrenergic receptors. Adrenalectomy completely abolished the stressor-induced decreases in circulating numbers of T helper cells (CD4+), cytotoxic T cells (CD8+) and B cells but was ineffective in preventing neutrophil granulocytosis, monocytosis and an increase in natural killer (NK) cells. Treatment with the alpha-adrenergic antagonist phentolamine (PHE) was highly effective in preventing granulocytosis and partially blocked lymphopenia, but failed to abolish monocytosis and an increase in NK cells. Treatment with the beta-adrenergic antagonists propranolol (PROP) or nadolol (NAD) entirely blocked the increases in monocytes and NK cells. In addition, beta-adrenergic blockade also significantly reduced neutrophilia, with PROP being more effective than NAD. The results presented here provide evidence that catecholamines play an important role in the redistribution of blood leukocytes during social stress. In particular, the mobilization of cells of the innate immune response seems to be regulated by adrenergic mechanisms.