Orthostatic hypotension (OH) is an important but often neglected clinical sign that can result from heterogeneous underlying pathophysiology. During the first few minutes following orthostasis, the 2 main variables governing blood pressure (BP) maintenance are the neurally mediated arterial baroreceptor control of sympathetic vasomotor tone of resistance and splanchnic capacitance vessels and the magnitude of central blood volume.1 Activation of the renin-angiotensin-aldosterone system and other endocrine systems mostly applies to prolonged orthostasis beyond the first few minutes.