We have studied the mechanisms contributing to the characteristic cardiovascular response produced after lesions of the A1 noradrenaline cell area in the ventrolateral medulla of the rabbit, at and below the level of the obex. Forty-five minutes after the A1 lesions there were dramatic increases in plasma adrenaline and plasma vasopressin (AVP) levels, which rose more than forty-fold, accompanied by smaller increases in plasma noradrenaline concentration and plasma renin activity (PRA) which were approximately doubled. Administration of an AVP antagonist did not effect the pressor response to A1 lesions but did reduce the bradycardia whereas administration of phentolamine, an alpha adrenoceptor blocker, completely prevented the increase in blood pressure after lesions. Administration of propranolol and methylscopolamine together, reduced the magnitude of the bradycardia by blocking cardiac efferent mechanisms mediating baroreceptor reflexes, but left a persistent residual fall in heart rate which was independent of baroreflexes; on the other hand when the AVP antagonist was given simultaneously with propranolol and methylscopolamine the bradycardia was completely abolished. Furthermore, infusion of AVP producing plasma levels similar to those seen after A1 lesions, caused a fall in heart rate and cardiac output with only a minor degree of vasoconstriction and no change in mean arterial pressure. An inhibitor of angiotensin converting enzyme had no effect on either heart rate or blood pressure. The rise in blood pressure observed after lesions of the A1 noradrenaline cell region is principally due to activation of the sympatho-adrenal system. The bradycardia is partly reflex due to stimulation of arterial baroreceptors. There is a marked rise in plasma AVP which exerts a minor vasoconstrictor effect but contributes directly and more substantially to the fall in heart rate.