Introduction 14 25 1 Patterns of natural activity in sympathetic vasoconstrictor pathways 3 17 26 8 10 19 32 5 12 29 6 7 2+ + + 4 29 14 14 35 13 14 33 34 13 14 Transmission of vasoconstrictor signals through sympathetic ganglia 21 22 30 2+ + 27 28 Changes in vasoconstrictor outflow after spinal cord injury 1A 31 Fig. 1 A B  1B 15 Changes in connectivity in paravertebral ganglia after destruction of preganglionic neurones 16 23 16 Autonomic dysreflexia 20 36 36 36 Changes in vascular reactivity after spinal cord injury 9 24 2 Fig. 2 A B A B A B  11 18 11 38 2 3(2) 37 3(3) Fig. 3 Diagram showing sites of lesions used to study long term effects on neurovascular transmission in arterial vessels of rats. (1) Transection of thoracic spinal cord without damage to preganglionic neurones. (2) Transection of paravertebral chain to remove preganglionic inputs (decentralization). (3) Transection of postganglionic nerves to denervate artery. Segments of artery were removed from the animals after 2–8 weeks and contractile responses to stimulation of perivascular sympathetic nerves were recorded during exposure to adrenoceptor antagonists and other drugs. that selectively interfere with neurovascular mechanisms  Overall, the data so far suggest that blood vessels in spinalized animals would constrict more powerfully to even short bursts of sympathetic activity evoked reflexly below the lesion. As well as being consistent with the complaints of many spinally-injured people about cold feet and legs, and the common difficulties in healing pressure sores, this modified vascular reactivity could contribute strongly to the development of autonomic dysreflexia in humans. Conclusions Despite many years of investigation, we still know remarkably little about the way in which neurally-released transmitters, including NE, lead to constriction of vascular smooth muscle. It is now clear that, as for many autonomically-innervated tissues, the mechanisms are not the same as those activated by exogenous transmitters. The work discussed here emphasizes the diversity of mechanisms that underlie the neural control of arterial vessels in different vascular beds and the plasticity of both innervation and effector tissues after lesions to the nervous system. Marked changes can occur even when both pre- and postganglionic components of the sympathetic innervation are undamaged. While the findings in experimental animals need to be confirmed in spinally injured people, they may help us to devise better ways to improve their rehabilitation and long-term maintenance. In addition, we may need to revise our thinking about the role of sympathetic activity in the regulation of the cellular processes involved in neurovascular transmission, even in intact individuals.