| Abstrakt: |
The hydrolysis of β-naphthyl acetate by plasma and by skin extracts has been investigated. In both cases the specimens from normal and atopic subjects yielded similar kinetic data. These results do not support the hypothesis of an abnormality in the enzyme acetylcholinesterase in the atopic. The atopic state is often described as one in which the subject displays an inbalance in the autonomic nervous system (Russell & Last, 1955; Mali, 1971). In general it appears that the sympathetic tone is reduced and that the parasympathetic tone is increased. This impression has been embodied in an elegant theory (Szentivanyi, 1968) in which it is suggested that the β-adrenergic receptors are in some way deficient. The β-receptors have been identified as the membrane-bound enzyme adenyl cyclase; this catalyses the production of Sutherland's ‘second messenger’, cyclic AMP, which in turn activates a cascade of intracellular enzymes (Sutherland & Robinson, 1966). Despite the convincing nature of Szentivanyi's arguments, his original model does not seem to fit the situation in atopic dermatitis, since kinetic studies of these enzymes have revealed no difference between normal and atopic skin (Mier & Urselmann, 1970; Holla et al., 1972; Mier & van den Hurk, 1972). It has already been pointed out, however, that the data presented by Szentivanyi will fit a number of other models equally well (Cotton, 1970; Cotton, 1972). In view of our inability to demonstrate any impairment of the β-adrenergic response, we have consequently turned our attention to the alternative possibility; that is, the existence of a defect which leads to the overstimulation of the parasympathetic aspect of the autonomic balance. The most plausible defect of this nature would seem to be an impairment of the enzyme acetylcholinesterase, resulting in a delayed clearance of acetylcholine from the tissue. Such a concept is wholly compatible with reports that atopic subjects show anomalous responses to this compound; examples include excessive vasodilatation (Ramsey, 1969) and an exaggerated sweat response (Warndorff, 1970). Although an acetylcholinesterase deficiency was regarded as ‘theoretically possible’ by Russell & Last (1955), and has been touched upon by a number of subsequent authors, no quantitative kinetic study of this enzyme in atopic subjects has been reported. In this and the following publication we wish to describe the results of two such investigations. The first of these utilized the synthetic substrate β-naphthyl acetate; this approach offers a simple, rapid and sensitive technique, the validity of which has already been established by model studies in the guinea-pig (Cotton & van den Hurk, 1972). [ABSTRACT FROM AUTHOR] |
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