The link between sleep apnoea and systemic hypertension in humans is well documented. However, a direct causal association between the two diseases independent of comorbidities has been difficult to establish. Comorbidities clearly play an important role in this strong relationship; however, new findings also suggest that sleep apnoea is an independent risk factor for hypertension. This relationship appears to be at least in part a result of chronically elevated sympathetic activity, and therefore manifests as a neurally mediated hypertension. Although the mechanism(s) for this causal relationship of sleep apnoea to hypertension remains ill defined, a growing body of literature suggests that autonomic dysfunction, mediated by abnormal chemoreflex control of sympathetic activity, is a potential mechanism. Abnormal chemoreflex responses to both acute and chronic apnoea or hypoxia have been demonstrated. Hypothesized mechanisms by which chemoreflex dysfunction may contribute to chronically elevated sympathetic tone and ultimately hypertension are explored in this review. Thus, this review focuses on the current evidence linking chemoreflex function to obstructive sleep apnoea and systemic hypertension in humans and provides an analysis of these data and their implications.