Early and delayed orthostatic hypotension

The circulatory adjustments to upright posture are mediated by nerves and hormones and occur in a time-dependent manner to counteract the gravitational pooling of blood below the heart. Central command, otolith (vestibular) signaling, and arterial baroreflexes produce rapid activation of sympathetic vasomotor outflow, compensatory vasoconstriction, and tachycardia.1,2 The continued loss of plasma into the interstitial space reduces intravascular volume.3 Low-pressure baroreceptors in veins and atria trigger volume expansion and vasoconstriction. Central neurons in the hypothalamus release vasopressin, the antidiuretic hormone, from the neurohypophysis.4,5 In the periphery, renin release by the kidney activates angiotensin and aldosterone secretion to retain sodium and water. These overlapping volume expansion and vasoconstrictor responses are finely tuned to maintain orthostatic pressure and allow us to remain standing.