A redox cycling model for the action of beta-adrenoceptor agonists.

A cyclic redox mechanism for the action of beta-adrenoceptor agonists is proposed. It has the following features: a) beta-adrenoceptor agonists act by 'reductive activation' of the beta-adrenoceptor (R); b) the redox state of R is reciprocally coupled to the redox state of the guanine nucleotide binding protein (G); c) binding of GTP to G reverses the agonist-induced alteration of the redox states of R and G; d) according to a specific version of the model the activation process involves a disulfide-thiol interchange reaction which leads to a GTP-revertible cross-linking of R and G by a disulfide bond. The way in which desensitization events may interfere with the proposed redox cycle is discussed.