Paintal A S, Damodaran V N, Guz A
Acta Neurobiol Exp (Wars). 1973;33(1):15-9.
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.
J 型感受器在通过阻断主动脉或左房室连接导致肺充血时被激活，这会使左心房压力升高，进而导致肺动脉压力升高。这种急性充血只能维持短暂时间（1 - 2分钟）。通过向右心房或右心室注射四氧嘧啶可产生持续时间更长的充血，最终导致肺水肿。注射后肺动脉压力显著升高，经过一段时间延迟后，J 型感受器会受到强烈刺激。得出的结论是，这种刺激是由于肺毛细血管压力升高和毛细血管膜通透性增加所致。最近的实验表明，静脉注射塑料微栓子（直径50±10微米）也可使活动显著增加。这种增加在肺动脉压力升高几分钟后出现，并非由于微栓子对神经末梢的直接作用，也不是由于毛细血管通透性增加。在这里，毫无疑问，活动增加是肺动脉压力升高导致肺毛细血管压力升高的结果。这会导致间质容积增加，从而刺激神经末梢。据推测，神经末梢位于类似海绵的胶原组织中。最近获得的电子显微镜证据显示，在这种胶原组织中存在无髓感觉纤维，但神经末梢（可能是 J 型）的精确结构及其与胶原组织的物理关系仍有待确定。
