Differential corticosterone responses to stress in the lung in two strains of Flinders rats

Acute stress affects a variety of organs and cellular systems. These include the hypothalamic-pituitary-adrenal (HPA) axis, corticotropin-releasing factor (CRF), mast cells and nerves. Flinders-sensitive (FSL) rat strains have hypercholinergic responses and are more sensitive than Flinders-resistant rats (FRL) to anaphylaxis.

To investigate the effects of acute water avoidance stress (1 h) on FSL and FRL tracheal epithelial tissue.

We measured short circuit current (I(sc)) as a measure of tracheal response, and the effect of substance P (SP) on tracheal epithelium in Ussing chambers. Electron microscopy was performed to assess mast cell activation.

Both strains showed increased I(sc) responses to stress, inhibited by prior injection of the CRF receptor 1 and 2 antagonist, alpha-helical CRF-(9-41). No increases in conductance were seen. Stress responses were accompanied by electron microscopic morphologic evidence for mast cell degranulation, which was not completely inhibited by alpha-helical CRF-(9-41) pre-treatment. Stress primed the epithelium for an enhanced response to SP in FSL, but this again was not inhibited by alpha-helical CRF-(9-41). FRL had 2.5 times the corticosterone response of FSL.

Acute stress affects the tracheal epithelium, not accompanied by changes in ion permeability, but associated with mast cell degranulation. Because blunted HPA axis responses are associated with vulnerability to inflammation, this may partially explain the findings. These stress effects on the lung have a genetic basis associated with relative corticosterone responses, are complex and only in part mediated by CRF.