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Published ahead of print on June 19, 2003, doi:10.1165/rcmb.2003-0097OC

Am. J. Respir. Cell Mol. Biol., Volume 30, Number 1, January 2004, 20-30

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Submitted on March 25, 2003
Revised on June 18, 2003

Quantification of neuroepithelial bodies and their innervation in Fawn-Hooded and Wistar rat lungs

Jeroen Van Genechten1, Inge Brouns1, Geoff Burnstock2, Jean-Pierre Timmermans1, and Dirk Adriaensen1*

1 Laboratory of Cell Biology and Histology, University of Antwerp, Antwerp, Belgium, 2 Autonomic Neuroscience Institute, Royal Free and University College Medical School, London, United Kingdom

* To whom correspondence should be addressed. E-mail: dadria{at}ruca.ua.ac.be.

The Fawn-Hooded rat (FHR), a model for primary pulmonary hypertension, shows an unexplained hypersensitivity to airway hypoxia. Since pulmonary neuroepithelial bodies (NEBs) appear to express a functional oxygen-sensing mechanism and an extensive sensory innervation, possible changes in this system should be taken into consideration. In the present study a comparative analysis of NEBs and their selective innervation was performed in FHRs and Wistar control rats. In both rat strains, the number of NEBs was estimated to be around 3,500, about 40% of which were innervated by vagal sensory calbindin D28k-immunoreactive (IR) nerve endings and about 50% by spinal sensory calcitonin gene-related peptide (CGRP)-IR nerve terminals. The number of intrinsic pulmonary nitrergic neurons and the percentage of pulmonary NEBs revealing a nitrergic innervation were highly significantly lower in FHRs. Both in FHRs and Wistar rats, a remarkable morphological interaction was observed between the intrinsic nitrergic and the CGRP-IR sensory population contacting NEBs. Our findings suggest a possible link between the hypersensitivity to airway hypoxia observed in FHRs and a reduced intrinsic pulmonary nitrergic innervation, possibly via the interaction with pulmonary NEBs and their spinal sensory CGRP-IR innervation.




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