The relationships between stress and hypertension have been evaluated extensively. Acutely, stress has been shown to increase blood pressure by increasing cardiac output and the heart rate without affecting total peripheral resistance. Acute stress has been found to increase levels of catecholamines, cortisol, vasopressin, endorphins and aldosterone, which may in part explain the increase in blood pressure. However, a primary role for the activation of the sympathetic nervous system has recently been suggested in several studies. Studies in the rat are beginning to determine specific central nervous system pathways which transform stressful stimuli into signals triggering a cardiovascular response without direct cortical participation. Furthermore, acute stress reduces renal sodium excretion, which contributes to an increase in blood pressure. Several studies suggest that prolonged stress may predispose people and animals to prolonged hypertension and certain populations are at risk for the development of stress-induced hypertension. It is likely that prolonged stress-induced hypertension is the result of neurohormonal trophic factors which cause vascular hypertrophy or atherosclerosis. Because stress can affect measurement of blood pressure due to the phenomenon of 'white-coat hypertension', ambulatory blood pressure monitoring is emerging as an important feature in the evaluation of patients with hypertension. Finally, relaxation techniques are being used increasingly in the treatment of patients with hypertension.