Increased central arterial stiffness explains baroreflex dysfunction in spinal cord injury.

After cervical spinal cord injury (SCI), orthostatic hypotension and intolerance commonly ensue. The cardiovagal baroreflex plays an important role in the acute regulation of blood pressure (BP) and is associated with the onset of presyncope. The cardiovagal baroreflex is dysfunctional after SCI; however, this may be influenced by either increased stiffening of the arteries containing the stretch-receptors (which has been shown in SCI) or a more downstream neural mechanism (i.e., solitary nucleus, sinoatrial node). Identifying where along this pathway baroreflex dysfunction occurs may highlight a potential therapeutic target. This study examined the relationship between spontaneous cardiovagal baroreflex sensitivity (BRS) and common carotid artery (CCA) stiffness in those with high level SCI before and after midodrine (alpha1-agonist) administration, as well as in able-bodied controls, to evaluate: (1) the role arterial stiffening plays mediating baroreflex function after SCI and (2) the effect of normalizing BP on these parameters. Three to five min recordings of beat-by-beat BP and heart rate, as well as 30 sec duration recordings of CCA diameter were used for analysis. All participants were tested supine and during upright-tilt. Arterial stiffness (β-stiffness index) was elevated in those with SCI when upright (+12%; p<0.05). Further, β-stiffness index was negatively related to reduced BRS in those with SCI when upright (R2=0.55; p<0.05), but not in able-bodied persons. Normalizing BP did not improve BRS or CCA stiffness. This study clearly shows that reduced BRS is closely related to increased arterial stiffness in the population with SCI.