The Sympathetic Nervous System in Chronic Heart Failure and Its Response to Vasodilator Therapy

Abstract

When the pumping action of the heart fails, one response of the body is an increase in the firing rate of the sympathetic fibers. The main peripheral sensors that trigger this reflex adjustment are the arterial baroreceptors. Other sensors may contribute, such as mechanoreceptors at the venoatrial junctions, which, when stretched, enhance the sympathetic outflow to the sinus node, although sympathetic outflow to the kidneys is reduced. The increase in sympathetic tone may, on the one hand, improve the patient’s circulatory function: for instance, released noradrenaline may shift the depressed myocardial length-active tension curve back toward normal; vasoconstriction may mobilize blood and maintain arterial pressure generation. On the other hand, the vascular effects of the sympathetic nervous system may be detrimental, in that they may increase ventricular filling pressure unduly and reduce cardiac output; in such cases, drugs that directly or indirectly antagonize the noradrenaline-induced vasoconstriction (α-adrenoceptor blocking agents and vasodilators sensu stricto, respectively) will be helpful.