SummaryBromocriptine, a drug acting directly upon dopaminergic receptors, has been found to have a significant therapeutic action in a double-blind study of 20 patients with idiopathic Parkinsonism whE were already receiving conventional therapy, including levodopa. Neurological deficits improved by almost 20% in severely disabled patients; amelioration of mildly affected patients was about 10%. Adverse reactions were similar to those encountered with levodopa-they were all dose-dependent and reversible. These observations are discussed in relation to certain theoretical advantages which might be expected from a drug which acts directly on dopaminergic receptors.

The response of the β‐adrenoceptors of human lymphocytes to selective agonists and antagonists has been studied quantitatively by measuring changes in cyclic adenosine‐3′,5′‐monophosphate (cyclic AMP) levels. The receptor was activated by isoprenaline and by salbutamol, and blocked by propranolol but not by practolol. A similar pattern of response was obtained with fragments of human lung tissue. The mean value for pA2 for propranolol was 8.34 and for practolol was 3.95. These findings indicate that the lymphocyte β‐adrenoceptor is a β2‐receptor and support the validity of using lymphocytes to study β‐adrenoceptor function in bronchial asthma. It may also be of use in the evaluation of selective β2‐blocking drugs in man.

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A B S T R A C T 83-adrenoceptor function has been compared in lymphocytes of normal subjects, asthmatic patients taking large doses of f3-adrenergic bronchodilators, and comparable asthmatics treated exclusively with nonadrenergic medication. The effect of prolonged administration of 8-adrenoceptor agonists on receptor function in normal subjects has also been examined. ,8-receptor response in each situation was quantitated by changes in levels of cyclic AMP, measured by a protein-binding assay.Dose response curves to isoproterenol (10 nM-0.1 mM) have been constructed for each group. Maximal increase in cyclic AMP in lymphocytes from normal subjects (393.2+44.0%) and in asthmatics on nonadrenergic preparations (408.3±46.7%) was significantly greater (P<0.001) than in asthmatics taking large doses of,8f-sympathomimetics (67.5±24.2%).Depression of the cyclic AMP response appeared to correlate with the degree of exposure to 13-adrenergic agonists but not with the prevailing severity of the patient's asthma.Withdrawal of 13-adrenergic drugs was followed by a reversion of the cyclic AMP response to normal values, which suggests that the depression was drug-induced rather than an inherent feature of the disease.This interpretation was confirmed by the finding that prolonged exposure of normal subjects to high doses of a,13-adrenergic agonist caused a marked and significant (P < 0.001) reduction in the cyclic AMP response, very similar to that seen in asthmatics on large doses of adrenergic bronchodilators.A possible link between drug-induced changes in the cyclic AMP response and the rise in the United Kingdom asthma death rate in the 1960's is discussed.

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