Both the sympathetic nervous system and the renin–angiotensin–aldosterone system (RAAS) have central roles in vascular adaptive processes. Stimulation of the 2 systems has been demonstrated in a range of cardiovascular disorders, including congestive heart failure and hypertension. However, elucidation regarding the interactions of the many factors involved in these 2 systems is lacking. Angiotensin-converting enzyme inhibitors have been used to reveal the contribution of some elements in the RAAS. Until relatively recently, little was known about the specific disturbances of the sympathetic nervous system in cardiovascular disease. Plasma norepinephrine levels, an indicator of sympathetic activity, have limited value because they are affected by various physiologic processes in addition to sympathetic activation. Newer approaches to the assessment of neurohormonal activity include the determination of the power content of heart-rate variability. More specific probes may lead to a better comprehension of neurohormonal physiology in health and disease and underlie future therapeutic advances targeted to prevention and treatment of specific syndromes.