Respiratory inputs to central cardiovascular neurons
Precise coordination of respiration and circulation is essential to obtain optimal delivery of oxygen and removal of carbon dioxide and to ensure normal homeostasis. One way that this coordination occurs is through connections between respiratory and sympathetic neurons in the brain stem and spinal cord. We know that these connections exist because sympathetic nerve activity often has a pronounced respiratory modulation. Respiratory modulation of sympathetic nerve activity was first noted by Adrian et a/. 1 in 1932. In the subsequent 60 years, much was discovered about the relationship between central inspiratory activity and sympathetic nerve activity. It is now clear that respiratory modulation of sympathetic nerve activity is a result of connections between central respiratory neurons and central cardiovascular neurons. It is not due simply to phasic changes in baroreceptor activation that might occur because of ventilation-induced changes in hemodynamics. This information has frequently been obtained by comparing the phasic discharges recorded from the phrenic nerve in paralyzed, ventilated, and often vagotomized animals in order to remove sources of external inputs to central autonomic neurons. Experiments of this type have shown, first, that respiratory rhythmicity, as measured by synchronization with phrenic nerve discharge, is present in animals that are ventilated at a rate different from phrenic nerve discharge.2·3 This means that changes in the activity of sensory afferent nerves are not the sole cause of the coupling between respiration and sympathetic nerve activity. Second, not all sympathetic nerves have the same type of respiratory rhythmicity. This means that different central sympathetic pathways must receive inputs from different components of the central respiratory rhythm generating network or at least that the proportion of such inputs received is variable.
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