Systemic effects resulting from carotid body stimulation-invited article.

The carotid body is stimulated by a number of blood-borne stimuli, ranging from increasing intensities of hypoxia, hypercapnia or acidosis to less studied stimuli, including hyperthermia, hyperosmolarity and hyperkalaemia. Although there exists heterogeneity in type I cell structure and function, there is no evidence to demonstrate that individual afferent fibres of the carotid sinus nerve subserve separate stimulus modalities. Thus, afferent information appears graded only for intensity (although this may be time-dependent) and not stimulus type. The response to carotid body stimulation, therefore, is to produce a graded, stereotypic response that can broadly be defined as the primary respiratory and cardiovascular reflexes of hyperventilation, bradycardia and peripheral vasoconstriction, originating directly as a consequence of increased afferent traffic in the carotid sinus nerve leading to augmented discharge in phrenic and intercostals nerves and altered activity in sympathetic and parasympathetic efferents. Where ventilation is not controlled, the secondary cardiovascular responses of tachycardia and peripheral vasodilation arise subsequent to the hyperventilation as a result of increased respiratory drive in the brainstem and increased activity of slowly adapting pulmonary stretch receptors in the airways. A role for the carotid body in mediating the hyperpnea of exercise, the aetiology of certain cardiovascular diseases, including sleep-apnoea derived hypertension and heart failure is supported by evidence but these complex situations generate reflex responses that can be mediated via a number of sensory and effector systems and the precise role of the carotid body is yet to be defined.