Little more than twenty years ago studies on the paraventricular nucleus (PVN) in the hypothalamus were confined to its relationship with the pituitary. Then some elegant studies by several neuroanatomists alerted us to the numerous extrahypothalamic projections and especially those to the spinal cord. Subsequently studies have established that PVN neurones project to key cardiovascular control regions, notably the rostral ventrolateral medulla (RVLM) where they synapse with spinally projecting vasomotor neurones. A separate population of PVN neurones projects directly to innervate spinal sympathetic neurones involved in cardiovascular control, whilst a third group branch to innervate both RVLM and spinal cord neurones. These PVN neurones are topographically arranged and separate populations contain arginine vasopressin, oxytocin and glutamate although the latter is possibly also a co-transmitter with the peptides. Perhaps the most clearly documented function of the PVN is its role in blood volume regulation and unsurprisingly this seems to be a pivotol influence of the extrahypothalamic projecting neurones. Two key organs the heart and kidney are involved in blood volume regulation and sympathetic control of these allows fast and moment by moment adjustments. Haemorrhage reflexly leads to increases in sympathetic activity particularly to the kidney. This response depends on the activation of RVLM-spinal vasomotor neurones but the effect is lessened by pharmacological block of PVN-vasopressin synapses both in the RVLM and in the spinal cord. It has also been recently shown that the PVN-enhancement of renal sympathetic activity is negatively regulated by sympathetic neurone releasing nitric oxide which excites nearby glycine inhibitory interneurones which depress activity. An expansion of blood volume has been shown in a number of species to reflexly increase heart rate via sympathetic nerves and this effect is primarily an action of volume receptors at the vein atrial junctions in the heart. Stimulation of these volume receptors also leads to an inhibition of renal sympathetic nerve activity. Thus the reflex response to an increase in plasma volume consists of a distinctive unique pattern of sympathetic activity to maintain fluid balance. This reflex appears to be dependent on neurones in the PVN. Thus neurones in the PVN show early gene activation on stimulation of the cardiac receptors and a similar differential pattern of cardiac excitation and renal inhibition can be elicited by activating PVN neurones. Cardiac afferents selectively cause a PVN-GABA neurone induced inhibition within the PVN of PVN-spinal neurones projecting to renal sympathetic neurones. Furthermore there is a population of PVN-spinal neurones that selectively increase heart rate by the release of oxytocin a peptide pathway that has no action on the renal sympathetic outflow. Therefore we can envisage a reflex inhibition of renal sympathetic/glutamate neurones in PVN and an excitation of cardiac sympathetic oxytocin neurones to elicit the atrial receptor response. This role in volume regulation is a good example of how the CNS generates unique non-uniform patterns of sympathetic activity. Furthermore it suggests that such responses depend on specific functional and anatomical connections of the afferent input.