Abstract
Quantitation using tissue homogenates has demonstrated a decrease in pulmonary β-receptors in experimental asthma. However, techniques using disrupted tissue have not permitted precise identification of the pulmonary structures where such decreases occur. Experimental asthma (A) was produced in guinea pigs by the sc injection of ovalbumin then daily exposure to ovalbumin aerosol for 4–5 weeks. Animals initially developed dyspnea during the aerosol exposures, but showed a tolerence to increasing ovalbumin concentrations over time. Using 3H-dihydroalprenolol, β-receptors were radioautographically localized and quantitated in lung sections of saline control (C) (n=6) and (A) (n=9) guinea pigs. Scatchard analysis showed a single class of binding sites with a Bmax of 368±32(C) and 258±15(A) fmole/mg protein (p<.005). Binding was of high affinity Kd=0.89±.09(C), 0.77±0.07(A) nM (N.S.). A 25–30% decrease in β-receptor number in alveolar, bronchiolar and bronchial epithelium (E) and bronchiolar smooth muscle (SM) (p<.001) appeared to be responsible for the 30% decrease in total (A) lung β-receptors. No decreases were noted in bronchial, arterial or venous SM. Despite the decrease in β-receptors no significant differences were noted in tidal volume, dynamic compliance and airway resistance between (C) and (A) animals in response to antigen challange as determined by body plethysmography immediately prior to sacrifice. These data suggest that decreases in β-receptor number can occur without changes in pulmonary function and decreases in E rather than SM β-receptors account for the majority of the observed change.
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Gatto, C., Green, T. & Johnson, D. 1761 ANATOMIC DISTRIBUTION AND QUANTITATIVE CHANGES IN GUINEA PIG PULMONARY β-RECEPTORS IN EXPERIMENTAL ASTHMA. Pediatr Res 19, 404 (1985). https://doi.org/10.1203/00006450-198504000-01779
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DOI: https://doi.org/10.1203/00006450-198504000-01779