Stimulation of ‘irritant’ receptors and afferent C-fibres in the lungs by prostaglandins

THE lungs are among the many organs that generate, release and destroy prostaglandins (PGs) 1 . It has been suggested that PCs act as ‘local hormones’ 2 , so that prostaglandins E 1 and E 2 , which relax the smooth muscle of bronchi and pulmonary blood vessels in many species, and F 2α , which contracts it, may be implicated in normal regulation of airway and pulmonary vascular calibre 3 . PGF 2α has been proposed as a causal factor in asthma 4 . The bronchoconstrictor effect of PGF 2α is reduced by atropine, hence a reflex component may be involved 5 . Cough and airway irritation have been reported in clinical trials of PGE 1 and PGE 2 as bronchodilators in the treatment of asthma 6,7 . Thus PGs may stimulate afferent nerve endings in the lungs, and there has been speculation as to which endings are involved. We have recorded impulse activity from rapidly-adapting pulmonary stretch (’irritant‘) receptors 8,9 and afferent C-fibre endings 10,11 in the lungs of anaesthetised dogs. When PGF 2α was injected into the right atrium, lung ‘irritant’ receptors were strongly stimulated. Injection of PGEs, by contrast, caused marked and prolonged stimulation of lung C-fibres.