Abstract
The phosphorylation hypothesis of smooth muscle contraction relates formation of cyclic AMP, resulting from beta-adrenergic stimulation, to inhibition of myosin light-chain phosphorylation and hence to bronchial relaxation. The hypothesis can therefore explain why beta-adrenergic blockade promotes bronchospasm in susceptible individuals. In the light of this molecular schema, various novel approaches to the use of beta-adrenergic blocking therapy for hypertension in the presence of asthma are discussed.
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