Abstract
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 E1 and E2, which relax the smooth muscle of bronchi and pulmonary blood vessels in many species, and F2α, which contracts it, may be implicated in normal regulation of airway and pulmonary vascular calibre3. PGF2α has been proposed as a causal factor in asthma4. The bronchoconstrictor effect of PGF2α is reduced by atropine, hence a reflex component may be involved5. Cough and airway irritation have been reported in clinical trials of PGE1 and PGE2 as bronchodilators in the treatment of asthma6,7. 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‘) receptors8,9 and afferent C-fibre endings10,11 in the lungs of anaesthetised dogs. When PGF2α 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.
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COLERIDGE, H., COLERIDGE, J., GINZEL, K. et al. Stimulation of ‘irritant’ receptors and afferent C-fibres in the lungs by prostaglandins. Nature 264, 451–453 (1976). https://doi.org/10.1038/264451a0
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DOI: https://doi.org/10.1038/264451a0
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