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The following HTML text is provided to enhance online readability. Many aspects of typography translate only awkwardly to HTML. Please use the page image as the authoritative form to ensure accuracy. inhibitory actions. In this context, it should be remembered that a2-adrenergic receptors are intermediate arteriolar smooth muscle constriction. Therefore, this class of receptors is capable of being part of an excitatory signal-transduction process ( 36 ); furthermore, the signaling system induced by nerve injury may not be identical to that occurring in neurons normally. Does the idea of a change in cellular phenotype by the enhanced production of membrane receptors possibly apply to other situations? A similar process could operate in other versions of sympathetically related pain. It could also relate to Raynaud’s disease, another pathological process which, in part, appears to represent overreaction to sympathetic mediators and could possibly result from an increased expression of adrenergic receptors ( 37 ). Furthermore, enhanced reactions to adrenergic mediators by the vasculature have also been postulated for certain forms of hypertension ( 38 , 39 ). To conclude, the concept of increased expression of molecular receptors as a mechanism of disease, and in particular of pathological pain, deserves serious consideration and further exploration. I thank Ms. S. Derr for her assistance. Preparation of this paper was aided by grants NS 10321 and NS 14899 of the National Institute of Neurological Disorders and Stroke. 1. Mitchell, W. ( 1872 ) Injuries of Nerves and Their Consequences ( Lippincott , Philadelphia ). 2. Leriche, R. ( 1916 ) Presse Méd. 24 , 178–180 . 3. Evans, J. A. ( 1946 ) Surg. Clin. North Am. 26 , 435–448 . 4. Merskey, H. & Bogduk, N. 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