Sympathetic modulation of radial artery compliance in congestive heart failure

Animal studies have suggested that arterial compliance can be modulated by adrenergic influences. Whether this adrenergic modulation also occurs 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 pathophysiological conditions. We have found that cigarette smoking, ie, an action that produces a marked sympathetic activation, causes a significant reduction in radial artery compliance, as measured by an echotracking 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 pulse pressure, the reduction amounted to 35.7+/-4.8% (mean+/-SEM) and was independent of the smoking-related blood pressure increase. Furthermore, pharmacological stimulation of adrenergic receptors located in the arterial wall was also shown to affect arterial compliance because the radial artery compliance index was markedly reduced (-29.5+/-3.9%) during phenylephrine infusion in the brachial artery at doses devoid of any systemic blood pressure effect. Evidence was also obtained that the relationship between sympathetic activation and arterial compliance has pathophysiological relevance, because in 17 patients with congestive heart failure (New York Heart Association classes II through IV) there was a significant inverse correlation (r=.62, P<.01) between muscle 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 that induces a transient blockade of nerve conduction to the upper limb, markedly increases radial artery compliance (change in compliance index, +30.0+/-5.0%). Thus, at least at the radial artery level arterial compliance is under a pronounced tonic restraint by sympathetic influences and can be modulated in either direction by reflex or central alterations in sympathetic drive. This modulation has pathophysiological implications