In order to quantitate the effect of spinal anesthesia on adrenergic tone, plasma levels of norepinephrine (NE) and epincphrine (EPI) were measured by radioenzymatic assay in 24 patients prior to elective lower body surgical procedures. The subsequent neuroendocrine responses to surgical stress of 16 of these patients were then compared to those of 10 patients receiving inhalation anesthesia (halothane-nitrous oxide). High thoracic dermatome spinal anesthesia caused suppression of both arterial plasma NE and EPI and a fall of mean arterial pressure (MAP); in contrast, no changes of NE, EPI, or MAP were observed in patients receiving low spinal anesthesia. Overall, there was a relationship between the sensory dermatome anesthesia level and changes of both plasma NE (r = 0.71, P < 0.001) and EPI (r = 0.52, P < 0.02). In the inhalation anesthesia group, plasma NE increased during the operation and plasma levels of NE, EPI, growth hormone, and cortisol were elevated during the postoperative recovery period. These neuroendocrine responses to surgical stress were not observed in patients receiving either low or high spinal anesthesia. Thus, the effect of spinal anesthesia on adrenergic tone depends on the cord level of anesthesia and can be quantitated by measurement of plasma catecholamines. The neuroendocrine responses to surgical stress were prevented in patients who received low spinal anesthesia and who had no suppression of efferent adrenergic tone. These findings indicate that neural afferents from the site of tissue injury, which were blocked by low spinal anesthesia, mediated both the adrenergic and the hormonal responses to surgical stress in the inhalation anesthesia group.