Sympathetic nerve activity in response to hypotensive stress in the postural tachycardia syndrome

Increased central sympathetic activity and/or deficient peripheral sympathetic nerve function are among the proposed pathophysiological changes in patients with the postural tachycardia syndrome (POTS). Little is known about sympathetic nerve outflow and its role in hemodynamic control in this disorder.

We recorded peroneal muscle sympathetic nerve activity in 9 POTS patients and 9 control subjects at rest and during a nitroprusside-induced hypotensive stimulus. Baseline blood pressure (BP) and heart rate were significantly higher in POTS patients than in controls. At rest, the burst frequency was similar in POTS patients and controls (18.1+/-6.2 and 20.1+/-7.9 bursts/min, respectively; P=NS), whereas the burst incidence was significantly lower (23.1+/-6.8 versus 32.2+/-11.4 bursts/100 heartbeats, P<0.05). Nitroprusside increased sympathetic outflow significantly more in POTS patients than in controls despite a similar BP decrease (burst frequency 20.4+/-7.5 versus 12.1+/-4.1 bursts/min, P=0.008, and burst incidence 21.8+/-8.4 versus 14.4+/-5.2 bursts/100 heartbeats, P=0.03). The change in mean burst area, a measure of the number of actively firing sympathetic neurons, was similar in patients and controls (117+/-15% versus 114+/-21%, P=NS).

At rest, the tachycardia and normal burst frequency result in normal or even elevated BP in POTS patients. During a hypotensive stimulus, cardiovascular homeostasis is maintained by the increased sympathetic outflow and normal heart rate response despite the lack of concomitant increase in mean burst area that is most likely due to sympathetic denervation.