The present paper reviews the effects of stress on noradrenergic receptor function in the brain. Most forms of stress thus far examined have been found to reduce either the magnitude of the cAMP response to stimulation by catecholamines (CAs) and/or the density of beta adrenergic receptors in the brain. These effects (a) generally occur in the cerebral cortex, (b) are more marked after chronic than acute stress, (c) may be the result of excessive release of norepinephrine (NE), ACTH or serotonin (5-HT) and (d) may occur in neurons glia or both. The function of these receptor alterations is not known but is presumed to be related in some manner to adaptation to chronic stress. A review of similar changes occurring in peripheral organs after repeated stress or CA injections reveals that subsensitivity of beta adrenergic receptors can be associated with either decreases or increases in CA-stimulated organ output. The latter findings caution against concluding that there is a decreased postsynaptic noradrenergic function after adaptation to chronic stress. Instead they suggest that it may be more appropriate to view stress-induced receptor subsensitivity as part of a more complex pattern of adaptive changes which includes alterations in the size, number, efficiency and output of CA effector cells.