Pulmonary stretch receptor and vagal sensory nerve fiber (PSR)

Pulmonary stretch receptors (PSRs) are specialized mechanoreceptors located within the airway smooth muscle and lung parenchyma that sense lung inflation and transmit signals to the brain via vagal sensory nerve fibers [1.1.5, 1.4.2]. These receptors are primarily responsible for the Hering-Breuer reflex, which prevents over-inflation of the lungs by inhibiting inspiration and prolonging expiration [1.1.1, 1.1.5]. The molecular basis of mechanotransduction in PSRs is largely attributed to the Piezo2 ion channel, which is essential for sensing lung volume and maintaining normal breathing patterns [1.2.1, 1.2.2]. Vagal sensory fibers also include rapidly adapting receptors (RARs) and C-fibers, which express various receptors such as P2X3, TRPV1, and TRPA1 that respond to chemical irritants and inflammatory mediators [1.1.2, 1.3.1]. In clinical practice, this system is targeted by antitussive agents like benzonatate, which acts as a local anesthetic on the stretch receptors to suppress the cough reflex [1.3.2, 1.4.1]. Additionally, novel therapies like gefapixant target P2X3 receptors on vagal afferents to treat chronic refractory cough [1.3.1, 1.3.2]. Dysregulation of these sensory pathways is implicated in the pathophysiology of asthma, COPD, and idiopathic pulmonary fibrosis, where hypersensitivity of the fibers leads to excessive coughing and dyspnea [1.1.2, 1.3.2]. Understanding the interaction between these receptors and the autonomic nervous system is crucial for developing targeted treatments for respiratory distress and chronic airway diseases [1.1.2, 1.3.2].

Other names

Slowly adapting pulmonary stretch receptorSARRapidly adapting pulmonary stretch receptorRARHering-Breuer receptorVagal afferent fiberBronchopulmonary stretch receptorLung mechanoreceptor

Inhibition of mechanosensitive ion channels (e.g., Piezo2), blockade of voltage-gated sodium channels on sensory neurons, and antagonism of purinergic P2X3 receptors on vagal afferents.