Animal studies have suggested that arterial compliance can be modulate
d by adrenergic influences. Whether this adrenergic modulation also oc
curs in humans is still a matter of debate. In the present article we
address this issue by examining the relationships between sympathetic
tone and arterial compliance in a variety of physiological and pathoph
ysiological conditions. We have found that cigarette smoking, ie, an a
ction that produces a marked sympathetic activation, causes a signific
ant reduction in radial artery compliance, as measured by an echotrack
ing device capable of providing continuous beat-to-beat evaluation of
this hemodynamic variable. When expressed as compliance index, ie, as
the ratio between the area under the compliance-pressure curve and pul
se pressure, the reduction amounted to 35.7+/-4.8% (mean+/-SEM) and wa
s independent of the smoking-related blood pressure increase. Furtherm
ore, pharmacological stimulation of adrenergic receptors located in th
e arterial wall was also shown to affect arterial compliance because t
he radial artery compliance index was markedly reduced (-29.5+/-3.9%)
during phenylephrine infusion in the brachial artery at doses devoid o
f any systemic blood pressure effect. Evidence was also obtained that
the relationship between sympathetic activation and arterial complianc
e has pathophysiological relevance, because in 17 patients with conges
tive heart failure (New York Heart Association classes II through IV)
there was a significant inverse correlation (r=.62, P<.01) between mus
cle sympathetic nerve activity (directly measured by microneurography
in the peroneal nerve) and radial artery compliance. Finally, we have
recently observed that anesthesia of the brachial plexus, a maneuver t
hat induces a transient blockade of nerve conduction to the upper limb
, markedly increases radial artery compliance (change in compliance in
dex, +30.0+/-5.0%). Thus, at least at the radial artery level arterial
compliance is under a pronounced tonic restraint by sympathetic influ
ences and can be modulated in either direction by reflex or central al
terations in sympathetic drive. This modulation has pathophysiological
implications.