The central role of the neuroendocrine system in modulating these proinflammatory responses has been strongly suggested by recent studies. The received results testify to ability of propranolol to increase adhesion and modulation of apoptosis and PMN free oxygen radicals production. The drugs' effect on PMN free oxygen radicals production, apoptosis and adhesion may constitute an additional mechanism of their activity. These data characterise the potential mechanism to explain effects immunomodulatory agents (neuroendocrine mediators) and beta-adrenergic modulation of pathway and therapy for inflammation, cardiovascular diseases and bronchial asthma; beta-adrenergic receptors are functionally coupled to signalling cascades in human neutrophils.