Abstract
Pulmonary rapidly-adapting-receptors (RARs) are sensory nerve endings whose afferent fibers can be recorded in the vagus nerve. RARs may play a role in reflex bronchoconstriction as seen in anaphylaxis. They can be stimulated by chemical mediators of anaphylaxis, such as prostaglandin F 2 α (PGF 2 α ). PGF 2 α aerosol was administered to saline and bovine serum albumin (BSA)-treated guinea pigs while recording the activity of RARs. PGF 2 α (250 μg/ml) given for 7–13 minutes increased both tracheal pressure and nerve activity over that produced by saline exposure in untreated guinea pigs. PGF 2 α administered for three minutes (5–100 μg/ml) increased RAR nerve activity in a dose-related manner in the first five minutes of the experiment only in the BSA treated guinea pigs. Since changes in tracheal pressure did not show a significant dose-response relationship, the RARs responding to PGF 2 α seemed to be stimulated by a direct mechanism. No correlation was shown between tracheal pressure and RAR nerve activity during PGF 2 α treatment. Whereas, a significant correlation was found between tracheal pressure and RAR nerve activity during histamine aerosol treatment (r=0.985). Histamine aerosol (1 to 1000 μg/ml, 3 min.) increased intratracheal pressure for 3 out of 4 doses. RAR nerve activity increased significantly only at the highest dose. Therefore, a possible direct effect of PGF 2 α upon RARs exists while the effect of histamine seems dependent upon changes in airway pressure in the guinea pig.
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