Decreased orthostatic adrenergic reactivity in non-dipping postural tachycardia syndrome

Whether non-dipping - the loss of the physiologic nocturnal drop in blood pressure - among patients with postural tachycardia syndrome (POTS) is secondary to autonomic neuropathy, a hyperadrenergic state, or other factors remains to be determined. In 51 patients with POTS (44 females), we retrospectively analyzed 24-hour ambulatory blood pressure recordings, laboratory indices of autonomic function, orthostatic norepinephrine response, 24-hour natriuresis and peak exercise oxygen consumption. Non-dipping (< 10% day-night drop in systolic blood pressure) was found in 55% (n = 28). Dippers and non-dippers did not differ in: 1) baseline characteristics including demographic and clinical profile, sleep duration, daytime blood pressure, 24-hour natriuresis, and peak exercise oxygen consumption; 2) severity of laboratory autonomic deficits (sudomotor, cardiovagal and adrenergic); 3) frequency of autonomic neuropathy (7/23 vs. 8/28, P = 0.885); 4) supine resting heart rate (75.3 ± 14.0 bpm vs. 74.0 ± 13.8 bpm, P = 0.532); or 5) supine plasma norepinephrine level (250.0 ± 94.9 pg/ml vs. 207.0 ± 86.8 pg/ml, P = 0.08). However, dippers differed significantly from non-dippers in that they had significantly greater orthostatic heart rate increment (43 ± 16 bpm vs. 35 ± 10 bpm, P = 0.007) and significantly greater orthostatic plasma norepinephrine increase (293 ± 136.6 pg/ml vs. 209 ± 91.1 pg/ml, P = 0.028). Our data indicate that in patients with POTS, a non-dipping blood pressure profile is associated with a reduced orthostatic sympathetic reactivity not accounted for by autonomic neuropathy.