Mechanism of excitation of type J receptors.
The type J receptors are stimulated during pulmonary congestion produced by occluding the aorta or left a-v junction which causes the left atrial pressure to rise with consequent rise in pulmonary artery pressure. Such acute congestion can be maintained only for brief periods (1-2 min). Longer lasting congestion leading eventually to pulmonary oedema is produced by injecting alloxan into the right atrium or right ventricle. A marked rise in pulmonary artery pressure follows the injection and after a lag there follows intense excitation of the type J receptors. It was concluded that this excitation was due to a rise in pulmonary capillary pressure and increase in permeability of the capillary membrane. Recent experiments have revealed that a considerable increase in activity can also be produced by injecting plastic microemboli (diameter 50 minus-plus 10 micrometers, i.v.). This increase occurs a few minutes after the rise in pulmonary artery pressure and is not due to a direct action of the microemboli on the endings nor can it be due to increased capillary permeability. Here, there can be no doubt that the increase in activity is a consequence of the rise in pulmonary artery pressure leading to a rise in pulmonary capillary pressure. This causes increase in interstitial volume leading to excitation of the endings. It was postulated that the endings were located in collagen tissue which acts like a sponge. Recently electronmicroscopic evidence has been obtained showing the presence of non-medullated sensory fibres in this collagen tissue but the precise structure of the endings (presumably type J) and their physical relation to the collagen tissue still remains to be established.
D000818:Animals; D001794:Blood Pressure; D002628:Chemoreceptor Cells / Q000502:physiology; D011650:Pulmonary Alveoli / Q000294:innervation*; D011651:Pulmonary Artery; D011655:Pulmonary Embolism / Q000503:physiopathology; D051381:Rats; D011984:Sensory Receptor Cells / Q000502:physiology*