Abstract
We studied the effect of beta-adrenoceptor antagonist propranolol on the regulation of spontaneous apoptosis in neutrophils, priming of lipopolysaccharide-treated neutrophils, and expression of neutrophil adhesion factors. The influence of propranolol on apoptosis, adhesion, and generation of oxygen radicals by neutrophils was shown to be an additional mechanism of the action of beta-adrenoceptor antagonists. This pathophysiological mechanism probably mediates the effect of neuroendocrine transmitters and explains the role of adrenergic antagonists in the pathogenesis and therapy of inflammation, cardiovascular diseases, and bronchial asthma.
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