Three experiments with New Zealand albino rabbits examined the role of anterior and posterior cingulate cortex in Pavlovian conditioning. Tones served as conditioned stimuli, and paraorbital electric shock served as the unconditioned stimulus. Anterior cingulate lesions attenuated conditioned heart rate (HR) decelerations, relative to posterior cingulate or sham lesions, but enhanced the magnitude of the bradycardiac component of the orienting reflex. Posterior cingulate lesions enhanced the bradycardiac component of the conditioned response, particularly late in training, relative to anterior or sham lesions. Somatomotor eye-blink conditioning, shock thresholds, and HR unconditioned responses were unaffected by cingulate lesions. Electrical stimulation of cingulate cortex revealed effective sites for eliciting heart rate and blood pressure (BP) changes only in anterior cingulate cortex. Relatively large (70-100 beats per minute) HR decelerations accompanied by small (1-5-mm Hg) BP depressor responses were elicited by stimulation of this area; the HR decreases were abolished by atropine methyl nitrate but were unaffected by either propranolol hydrochloride or phentolamine hydrochloride. These results are discussed in terms of cingulate involvement in the mediation of the cardiovascular component of a response pattern related to stimulus processing.