There is evidence that some anesthetic agents cause central sympathetic nervous activation by mechanisms that remain obscure. There is, however, the finding that all such agents tested to date cause inhibition or loss of the barostatic reflexes, while agents which do not interfere with these reflexes fail to cause sympathetic excitation. Since sympathetic activation during the administration of an anesthetic has valuable hemodynamic consequences, we believe an understanding of the mode of action of such agents to be important. The previous work has deficiences which the proposed study seeks to correct: the experiments were performed with a single basal anesthetic (nitrous oxide), and the nervous impulses were recorded from a single locus (cervical sympathetic) which does not supply fibers either to the myocardium or to major blood vessels. In addition, the carotid sinus reflex was elicited by electrical stimulation of the central end of a divided sinus nerve, which is unphysiological and also difficult to interpret. In this application we propose to learn: 1) (by decerebration) whether the response is complete within the medulla; 2) whether the response occurs in the absence of a basal anesthetic; 3) whether the parasympathetic component of the barostatic reflexes is affected in the same manner as the sympathetic; 4) whether the autonomic responses are generalized; and 5) (by carotid sinus perfusion) whether non-excitatory anesthetics "sensitize" the barostatic reflexes, thus accounting for the presence simultaneously of arterial hypotension, depressed sympathetic nervous activity and active barostatic reflexes.