Effect of respiratory tract viral infection on murine airway β‐adrenoceptor function, distribution and density

Peter J. Henry, Paul J. Rigby, John S. Mackenzie, Roy G. Goldie

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The effects of a respiratory tract viral infection on β‐adrenoceptor density, distribution and function were investigated in murine airways. Following intranasal inoculation of CBA/CaH mice with influenza A/PR‐8/34 virus, the virus proliferated rapidly in trachea (peak titres 2 days post‐inoculation) and lung (peak titres 4–6 days post‐inoculation). Respiratory tract viral infection was associated with a significant increase in lung weight (88% higher than control mice at day 6 post‐inoculation) that was related temporally to the development of peripheral lung inflammation and consolidation. Analysis of specific binding of [125I]‐cyanopindolol to β‐adrenoceptors revealed that on days 2, 4 and 8 post‐inoculation with virus, mouse isolated tracheal sections contained, on average, 40% more β‐adrenoceptors than tracheal sections from time matched control mice. Subsequent quantitative autoradiographic studies demonstrated that this increase in total tracheal β‐adrenoceptors was due primarily to a 90% increase in the density of β‐adrenoceptors in the tracheal epithelium in virus‐infected mice. In contrast, virus‐infection had no significant effect on the density of β‐adrenoceptors in tracheal airway smooth muscle, although within 2 days of inoculation with virus, mouse tracheal smooth muscle segments were approximately 2 fold less sensitive to the β‐adrenoceptor agonist, noradrenaline (mean pD2 = 6.57 ± 0.04, n = 24) and to the adenylyl cyclase‐activator forskolin (mean pD2 = 6.78 ± 0.04, n = 12) compared to segments from control mice (mean pD2 = 6.84 ± 0.06 for noradrenaline; mean pD2 = 7.03 ± 0.07 for forskolin). Similar values were obtained 8 days post‐inoculation. At day 2, but not day 8 post‐inoculation with virus, relaxation responses to theophylline were also marginally attenuated compared with controls. Mouse isolated tracheal segments obtained 2 days after virus inoculation and segments from time‐matched control mice were equisensitive to the spasmogenic actions of the muscarinic cholinoceptor agonist, carbachol. However, tracheal segments from mice inoculated with virus were less responsive to carbachol on day 4 (mean pD2 = 6.45 ± 0.04, n = 8) and day 8 (mean pD2 = 6.45 ± 0.02, n = 12) compared to control preparations (day 4, mean pD2 = 6.73 ± 0.06, n = 8; day 8, mean pD2 = 6.65 ± 0.04, n = 12, P < 0.05). In contrast, endothelin‐1‐induced contractions of tracheal smooth muscle were not affected by virus‐infection. These data demonstrate that respiratory tract viral infection can produce significant tissue‐selective changes in airway β‐adrenoceptor density as well as small reductions in airway smooth muscle muscarinic cholinoceptor and β‐adrenoceptor function. 1991 British Pharmacological Society

Original languageEnglish
Pages (from-to)914-921
Number of pages8
JournalBritish Journal of Pharmacology
Issue number4
Publication statusPublished - 1 Jan 1991


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