TY - JOUR
T1 - Lateralization of expression of neural sympathetic activity to the vessels and effects of carotid baroreceptor stimulation
AU - Diedrich, Andreá
AU - Porta, Alberto
AU - Barbic, Franca
AU - Brychta, Robert J.
AU - Bonizzi, Pietro
AU - Diedrich, Laura
AU - Cerutti, Sergio
AU - Robertson, David
AU - Furlan, Raffaello
PY - 2009/6
Y1 - 2009/6
N2 - Human studies suggest that cardiovascular neural sympathetic control is predominantly modulated by the right cerebral hemisphere. It is unknown whether post-ganglionic sympathetic activity [muscle sympathetic nerve activity (MSNA)] shows any functional asymmetry. Eight right-handed volunteers (3 women and 5 men, 32 ± 2 yr of age) underwent ECG, beat-by-beat blood pressure, respiratory activity, and simultaneous right and left MSNA recordings during spontaneous and controlled breathing (CB, 15 breaths/min, 0.25 Hz). Dynamic carotid baroreceptor stimulation was obtained by 0.1-Hz sinusoidal suction, from 0 to -50 mmHg, randomly applied to the right, left, and combined right and left sides of the neck during CB. Laterality was assessed by changes in the MSNA burst rate (in bursts/min, and bursts/100 beats), strength [amplitude (A) and area (AA)], and the oscillatory component at 0.1 Hz during baroreceptor stimulation. Amplitude parameters were normalized by CB burst mean amplitude and area of the same side. At rest, the right and left MSNA burst rate and total MSNA activity were similar. Conversely, the right MSNA normalized burst A N (1.36 ± 0.18) and AA N (1.31 ± 0.16) were larger than the left MSNA A N (1.04 ± 0.09) and AA N (1.02 ± 0.08). Unilateral and bilateral carotid baroreflex stimulation abolished the right prevalence of A N and AA N. In conclusion, the right lateralization of sympathetic activity to the vessels is indicated by normalized burst strength parameters of bilateral MSNA recordings at rest during spontaneous breathing. Carotid baroreceptor stimulation disrupted such expression of MSNA lateralization possibly by disturbing the synchronizing action of right cerebral hemisphere.
AB - Human studies suggest that cardiovascular neural sympathetic control is predominantly modulated by the right cerebral hemisphere. It is unknown whether post-ganglionic sympathetic activity [muscle sympathetic nerve activity (MSNA)] shows any functional asymmetry. Eight right-handed volunteers (3 women and 5 men, 32 ± 2 yr of age) underwent ECG, beat-by-beat blood pressure, respiratory activity, and simultaneous right and left MSNA recordings during spontaneous and controlled breathing (CB, 15 breaths/min, 0.25 Hz). Dynamic carotid baroreceptor stimulation was obtained by 0.1-Hz sinusoidal suction, from 0 to -50 mmHg, randomly applied to the right, left, and combined right and left sides of the neck during CB. Laterality was assessed by changes in the MSNA burst rate (in bursts/min, and bursts/100 beats), strength [amplitude (A) and area (AA)], and the oscillatory component at 0.1 Hz during baroreceptor stimulation. Amplitude parameters were normalized by CB burst mean amplitude and area of the same side. At rest, the right and left MSNA burst rate and total MSNA activity were similar. Conversely, the right MSNA normalized burst A N (1.36 ± 0.18) and AA N (1.31 ± 0.16) were larger than the left MSNA A N (1.04 ± 0.09) and AA N (1.02 ± 0.08). Unilateral and bilateral carotid baroreflex stimulation abolished the right prevalence of A N and AA N. In conclusion, the right lateralization of sympathetic activity to the vessels is indicated by normalized burst strength parameters of bilateral MSNA recordings at rest during spontaneous breathing. Carotid baroreceptor stimulation disrupted such expression of MSNA lateralization possibly by disturbing the synchronizing action of right cerebral hemisphere.
KW - Area
KW - Burst amplitude
KW - Laterality
KW - Muscle sympathetic nerve activity recording
KW - Sympathetic control of circulation
UR - http://www.scopus.com/inward/record.url?scp=66949154672&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=66949154672&partnerID=8YFLogxK
U2 - 10.1152/ajpheart.01045.2008
DO - 10.1152/ajpheart.01045.2008
M3 - Article
C2 - 19363133
AN - SCOPUS:66949154672
VL - 296
JO - American Journal of Physiology
JF - American Journal of Physiology
SN - 0363-6119
IS - 6
ER -