Effects of Peripheral Chemoreceptors Deactivation on Sympathetic Activity in Heart Transplant Recipients

Heart transplantation initially normalizes sympathetic hyperactivity directed at the muscle circulation. However, sympathetic activity increases with time after transplantation and the exact mechanisms responsible for sympathetic control in heart transplant recipients remain unclear. We examined the effects of peripheral chemoreflex deactivation caused by breathing 100% oxygen on muscle sympathetic nerve activity (expressed as number of burst per minute and mean burst amplitude), heart rate, and mean blood pressure in 13 heart transplant recipients, 13 patients with essential hypertension, and 10 controls. Heart transplant recipients disclosed the highest sympathetic activity, whereas it did not differ between controls and patients with essential hypertension (5116 versus 3714 versus 3912 burst/min, respectively; P0.05). Breathing 100% oxygen, in comparison with 21% oxygen, reduced sympathetic activity (44 versus 12 burst/min, P0.01; 859 versus1018% of amplitude at baseline, P0.001) and mean blood pressure (45 versus 36 mm Hg; P0.05) in heart transplant recipients, decreased sympathetic activity (44 versus 03 burst/min, P0.05; 9016 versus1019% of amplitude at baseline, P0.05) in patients with essential hypertension, but did not reduce sympathetic activity (24 versus 33 burst/min, PNS; 9511 versus 9513% of amplitude at baseline, PNS) in control subjects. The sympathetic response to hyperoxia was more marked in heart transplant recipients than in controls (859 versus 9511% of baseline amplitude; P0.05). The decrease in sympathetic activity was most evident in patients with the longest time after heart transplantation (r0.75, P0.01). In conclusion, tonic chemoreflex activation increases resting muscle sympathetic nerve activity and favors blood pressure elevation after heart transplantation. (Hypertension. 2005;45:894-900.)