A statistically and clinically significant reduction in arterial pressure occurs following a single bout of low intensity, short duration aerobic exercise in individuals with hypertension. The reduction in arterial pressure is most often associated with a decrease in total peripheral resistance, peripheral sympathetic nerve activity, and plasma norepinephrine concentration; however, cardiac output is often elevated without a change in heart rate. The purpose of this article is to review the literature and propose a model that analyzes the components contributing to the postexercise reduction in arterial pressure. The model implicates an attenuated vascular response to catecholamine stimulation and an enhanced inhibitory cardiopulmonary reflex response. Recent evidence has shown that a single bout of dynamic exercise significantly attenuated the vasoconstrictor response to phenylephrine in an isolated aortic ring preparation and in the intact conscious rabbit and rat. This suggests that the ability of the vasculature to respond to a change in sympathetic nerve activity or catecholamine stimulus after exercise is significantly attenuated. Since the blood vessel is less responsive to catecholamine stimulation after exercise, a higher level of sympathetic nerve activity may be required to maintain arterial pressure. However, a single bout of dynamic exercise sufficient to produce postexertional hypotension also lowers both the concomitant plasma norepinephrine concentration and postganglionic muscle sympathetic nerve activity. These effects may explain the significant reduction in total peripheral resistance associated with dynamic exercise. The reduction in sympathetic activity appears to be mediated by a postexercise facilitation of inhibitory cardiopulmonary reflexes.