Sympathetic cardiovascular afferents may mediate the reflex excitation of sympathetic outflow and inhibition of vagal efferent activity observed in congestive heart failure.
Proposes an alternative hypothesis that sympathetic cardiovascular afferents, rather than just baroreceptor mechanisms, mediate the reflex excitation of sympathetic outflow in congestive heart failure.
Congestive heart failure is usually accompanied by cardiovascular signs of an increased sympathetic and a decreased parasympathetic efferent activity. A current hypothesis for these autonomic changes holds the baroreceptor mechanisms mainly responsible for this complex neural reflex pattern together with a decreased responsiveness of cardiac vagal afferent ffibers. An alternative hypothesis is proposed here. Afferent sympathetic fibers with sensory endings in the atria and in the pulmonary veins are progressively excited by volume load. In cats with a chronic spinal section at C8, breathing spontaneously, an infusion of saline induces a reflex tachycardia through a sympatho-sympathetic neural circuit. In chronic dogs with intact cardiovascular innervation, the stimulation of aortic or cardiac sympathetic afferent fibers elicits an excitatory sympathetic reflex leading to hypertension and tachycardia; in addition, the sensitivity of baroreflexes is markedly reduced. Therefore, in congestive heart failure, especially in the absence of hypotension, the reflex excitation of the sympathetic outflow and the inhibition of the vagal efferent activity directed to the heart could be due to reflex mechanisms mediated by sympathetic cardiovascular afferents.
Malliani et al. (Sun,) conducted a review in Congestive heart failure. Sympathetic cardiovascular afferents may mediate the reflex excitation of sympathetic outflow and inhibition of vagal efferent activity observed in congestive heart failure.