Is augmented central respiratory–sympathetic coupling involved in the generation of hypertension?

Abstract Respiratory modulation of autonomic neural activity, with consequent phasic alteration of cardiac and vascular function, has been observed in many species including humans and is considered an index of cardiovascular health. Whilst many factors contribute to this modulation, including for example baroreceptor reflex feedback, it is accepted that a significant component is derived from an interaction within the central nervous system. Functional links between the brainstem circuitry generating the respiratory rhythm and neurons responsible for generate sympathetic and parasympathetic activity to the cardiovascular system have long been hypothesized, although the detailed understanding of these interactions is incomplete. There are several proposed physiological functions for these interactions including the matching of ventilation to cardiac output and tissue blood flow. However, recent observations suggest that altered central respiratory coupling may play a role in the development of hypertension and in the maintenance of elevated levels of sympathetic vasomotor activity in disease. The focus of this review article is to discuss these observations and place them within the context of current understanding of the neural substrates that might be responsible for respiratory–sympathetic coupling.