Evidence assembled in this review indicates that sympathetic nervous system dysfunction is crucial in the development of
heart failure and
essential hypertension. This takes the form of persistent and adverse activation of sympathetic outflows to the heart and kidneys in both conditions. An important goal for clinical scientists is translation of the knowledge of pathophysiology, such as this, into better treatment for patients. The achievement of this 'mechanisms to management' transition is at different stages of development with regard to the two disorders. Clinical translation is mature in
cardiac failure, knowledge of cardiac neural pathophysiology having led to the introduction of
beta-adrenergic blockers, an effective
therapy. With
essential hypertension perhaps we are on the cusp of effective translation, with recent successful testing of selective
catheter-based renal sympathetic nerve ablation in patients with resistant
hypertension, an intervention firmly based on the demonstration of activation of the renal sympathetic outflow. Additional evidence in this regard is provided by the results of pilot studies exploring the possibility to reduce blood pressure in resistant hypertensives through electrical stimulation of the area of carotid baroreceptors. Despite the general importance of the sympathetic nervous system in blood pressure regulation, and the specific demonstration that the blood pressure elevation in
essential hypertension is commonly initiated and sustained by sympathetic nervous activation, drugs antagonizing this system are currently underutilized in the care of patients with
hypertension. Use of beta-
adrenergic blocking drugs is waning, given the propensity of this
drug class to have adverse metabolic effects, including predisposition to diabetes development. The blood pressure lowering achieved with carotid baroreceptor stimulation and with the renal
denervation device affirms the importance of the sympathetic nervous system in
hypertension pathogenesis, and perhaps suggests a wider role for anti-
adrenergic antihypertensives, such as the
imidazoline drug class (
moxonidine,
rilmenidine) which act within the CNS to inhibit central sympathetic outflow, although the lack of large-scale outcome trials with this
drug class remains a very material deficiency.