Cholinergic-adrenergic balance: Part 1. Relationship between central and peripheral sensitivities

Eight healthy volunteers were studied under double-blind conditions after acute challenge with the peripheral beta 2-agonist reproterol, either alone or combined with the peripheral indirect cholinomimetic neostigmine. Their responses were also studied after administration of the centrally active indirect cholinomimetic physostigmine. The beta-adrenergic rise in heart rate was cholinergically suppressed. The beta-adrenergic rise of plasma cyclic adenosine monophosphate (cAMP) was not cholinergically modulated, while that of plasma glucose tended to be cholinergically suppressed. Physostigmine induced an anergic-anhedonic syndrome accompanied by physiological, metabolic, and neuroendocrine stress phenomena. The beta-adrenergic and cholinergic sensitivities, respectively, of the various parameters investigated tended to be nonsignificantly intercorrelated. Only a limited portion of the variance was explained by drug effects. Sensitivity to neostigmine was completely unrelated to sensitivity to physostigmine. Thus, cholinergic sensitivity seems not to be decisive for the fine tuning of the highly complex regulatory systems studied and peripheral sensitivity not to be representative for the central one, at least if unselective drugs like neostigmine and physostigmine are used.