TRPV1 and neuropeptide receptor immunoreactivity and expression in the rat lung and brainstem after lung ischemia-reperfusion injury.

BACKGROUND:Activation of capsaicin-sensitive sensory nerves and TRPV1 present on them can ameliorate the ischemia-reperfusion injury in vital organs by evoking the release of neuropeptides including calcitonin gene-related peptide (CGRP) and substance P. However, the underlying changes in TRPV1 and neuropeptide receptor expressions, including calcitonin receptor-like receptor (CRLR) and neurokinin 1 receptor (NK1R), after lung ischemia-reperfusion injury (LIRI) remain uncharacterized. METHODS:Thirty-two male Sprague-Dawley rats were randomly and equally divided into sham (sham thoracotomy) and ischemia-reperfusion (occlusion of the left pulmonary hilus for 1 h followed by reperfusion for 4 h) groups. Blood gas levels were measured and histopathologic examination was performed. Left lung lobes and brainstem tissue samples were harvested for use in quantitative real-time PCR, Western blot, and immunohistochemistry to measure TRPV1, CRLR, and NK1R transcript and protein levels. Additionally, CGRP and substance P protein levels were quantified in the lungs using enzyme-linked immunosorbent assay. RESULTS:LIRI exacerbated blood gas exchange and increased the pulmonary tissue injury score. Furthermore, LIRI increased CGRP levels in the lung, TRPV1-immunoreactivity (ir) in the bronchiolar epithelium and smooth muscle of the pulmonary artery, and the intensity of neuronal CRLR-ir and NK1R-ir in the commissural nucleus of the solitary tract. Similarly, LIRI significantly elevated both transcription and translation of TRPV1 in the lungs and CRLR and NK1R in the brainstem. CONCLUSIONS:Both transcription and translation of TRPV1 in the lungs and CRLR and NK1R in the brainstem of rats can be upregulated by LIRI in a rapid manner (within 5 h).

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