In the anaesthetized dog almitrine bismesylate (A) increases ventilation after i.v. injections of more than 100 ug X kg-1. This ventilatory stimulation is due to the specific agonistic action of A on the peripheral chemoreceptors. With lower doses of A no modification of ventilation is recorded even though PaO2 significantly increases. The mechanisms by which A induces pulmonary gas exchange improvement are not clearly demonstrated. A long lasting potentiation of local hypoxic pulmonary vasoconstriction was initially postulated but more recent experimental results recorded on animals with heterogeneously ventilated lungs do not support this hypothesis. However, a redistribution of pulmonary blood flow due to the transient vasoconstrictor effect of A cannot be excluded: it might divert the blood from the well perfused lung bases towards the less well perfused lung apex. Other authors have demonstrated that undetected small ventilatory changes might improve alveolar ventilation and raise PaO2. The almitrine bismesylate molecule is a successful example of pharmacochemical research applied to bronchopulmonary pathology. By using qualitative structure activity relationships it has been possible to choose from a series of triazine derivatives, this remarkable molecule, exerting a clear tropism for the pulmonary tract with a dual effect improving both ventilatory and gasometric parameters through peripheral chemoreceptor stimulation, and characterized by a rapid onset of action and a durable activity. In this respect, the di-allyl-amino-triazine moiety may be considered as an inducer of gasometric and ventilatory effects. The piperazine nucleus is mainly responsible for the ventilatory/gasometric dissociation and for the kinetics of these pulmonary actions. Finally, the bisparafluorobenzydryl component is a 'modulator' of intensity of gasometric effects.