Upper respiratory tract infection has frequently been shown to precipitate or exacerbate the asthmatic condition and to increase airway reactivity to bronchospastic agents. The hypothesis first proposed by Szentivanyi suggested a beta-adrenoceptor deficiency in the pulmonary system in bronchial asthma leading to an alteration in the autonomic control of the airways in favour of excessive alpha-adrenergic and cholinergic bronchoconstrictor influence. Experimental exposure of isolated leukocytes and airway smooth muscle of laboratory animals and man with respiratory pathogens, e.g. influenzae virus, rhinovirus and Haemophilus influenzae has caused impaired pharmacological modulatory responses to isoprenaline, histamine (H2) and PGE, resulting in increased cellular release of inflammatory mediators and enhanced muscle contraction. Szentivanyi\'s hypothesis may now be extended to include impairment due to respiratory infection of other hormonal mechanisms responsible for bronchodilatation; i.e. histamine H2-receptor, PGE receptor and possibly non-adrenergic of "purinergic" receptor stimulation. Thus, the hypothesis of "pharmacological abnormality in bronchial asthma and the role of respiratory pathogens\' has been discussed using experimental evidence.