Abstract
Twenty years ago, John and Hazel Coleridge made a major advance in the field of patho-physiology of the lungs when they presented, at the Krogh Centenary symposium held in Srinager in 1974, evidence showing that the J receptors, which they called pulmonary C-fibres, were clearly stimulated by rise in left atrial pressure and that the degree of this stimulation was related to the degree of rise in pressure (Coleridge & Coleridge, 1977). This quantitative relation between the degree of resulting pulmonary congestion and stimulation of the receptors was a considerable advance over what had been observed qualitatively, earlier (Paintal, 1955; 1969). A few years later, another important advance was made when it was shown that increasing cardiac output by about two times stimulated the J receptors effectively enough to produce marked reflex effects, notably the J reflex, thereby strengthening the view that the J receptors must be clearly stimulated during moderate exercise in man (Anand & Paintal, 1980). Six years later another advance was made when the Coleridges’ and their collaborators demonstrated the relation between the degree of congestion of the lungs as seen from histological evidence to the activity of the J receptors (Roberts, Bhattachharaya, Shultz, Coleridge & Coleridge, 1986). In the same year evidence was presented to show that these receptors produced sensations of irritation in the throat of man, leading to the production of dry cough when they were stimulated by lobeline or high altitude pulmonary edema (Paintal, 1986a). A short while later Anand, Raj, Singh & Paintal (1989) provided preliminary evidence to show that increase in permeability of the pulmonary capillaries produced by phosgene gas in cats caused much greater stimulation of the J receptors by phenyl diguanide (PDG).