Neuronal determinants of non‐uniform activation of sympathetic outflow to different vascular beds.

The non‐uniform distribution of cardiac output to different vascular beds, which varies according to the type of behaviour/response, is a fundamental feature of cardiovascular control. The vascular changes are in the main dependent on sympathetic nerve activity. Thus during arousal or defence‐like behaviour skeletal muscle beds vasodilate whist other vascular beds vasoconstrict and in sleep the opposite occurs. Similarly the pattern of non‐uniform changes in sympathetic activity is unique in homeostatic responses such as in combating changes in blood volume. Such responses require that each vascular bed is represented by neurones in the central nervous system. How then does the brain elicit a unique repetoire of sympathetic activity? Activation of both central nervous sites and of peripheral afferents can evoke identifiable patterns of sympathetic activity like those in sleep, defence, blood volume regulation etc suggesting there are command centres where the pattern is encoded into the motor outflow. Encoding may in part be expressed by chemical phenotype of brain pre‐sympathetic neurones. However recent studies of the response to stimulation of cardiac atrial receptors, to mimic blood volume expansion, indicate that it is the specific functional and anatomical connections of the afferent input from modality specific sources, that is a key factor. Essentially in the case of blood volume regulation it is the selective connections of the atrial afferent input with the local circuits of target specified pre‐sympathetic paraventricular neurones in the hypothalamus that determines the pattern of sympathetic changes. Supported by Wellcome Trust and British Heart Foundation.