Sympathetic vasoconstrictor neurons that had previously innervated blood vessels in hairy skin were made to reinnervate the vasculature of the hairless skin of the paw pad by suturing the central stump of the cut sural nerve to the distal stump of the cut tibial nerve. After allowing sufficient time for the reinnervation, electrical stimulation of the vasoconstrictor pathway in the lumbar sympathetic trunk produced a reduction of the blood flow that was significantly greater than in control animals. There was also a clear sign of a "denervation supersensitivity" of the blood vessels as evidenced by a significantly increased vasoconstriction that followed the systemic application of the alpha 1-adrenoceptor specific agonist phenylephrine. Neurogenic vasodilation evoked by antidromic excitation of small diameter primary afferent neurones was significantly impaired although myelinated and unmyelinated primary afferents had re-grown into the target tissue. Electrical stimulation of the intact tibial nerve (containing sympathetic vasoconstrictor axons and nociceptive primary afferent fibres) in control animals, always produced vasodilatation indicating that the neurogenic vasodilatation can override the sympathetic vasoconstrictor response. By contrast, electrical stimulation of cross-unioned nerves consistently produced a robust vasoconstriction. We conclude that sympathetic vasoconstrictor neurons have a high capacity to functionally reinnervate autonomic effector organs in the adult cat. Despite this functional recovery, the blood vessels exhibited stronger than normal responses to an alpha 1-adrenoceptor agonist. The impaired neurogenic vasodilatation mediated by small diameter afferents may be due to their poor ability to re-establish their efferent vasodilatory function. Alternatively it may be masked by the strong vasoconstriction.