Abstract
γ-Aminobutyric acid (GABA) is an important inhibitory neurotransmitter in the mammalian central nervous system and it is also found in peripheral tissues including the lung. Recent experiments have shown that GABA affects the contractile properties of airway smooth muscle. Therefore, to determine whether GABA affects the contractile properties of tracheal smooth muscle, we studied guinea pig trachea under isometric conditions in vitro in both normal and OA-sensitized guinea pigs. The following results were obtained.
1) In normal guinea pig tracheal ring, GABA and its related substances, baclofen and muscimol, had no effect on the resting tension, but reversibly depressed contractions induced by electrical field stimulation (EFS) in a dose-dependent fashion.
2) In OA-sensitized guinea pig tracheal ring, GABA and baclofen reversibly depressed the contractions induced by EFS, but to a lesser degree than in normal tracheal ring.
3) In OA-sensitized guinea pig tracheal ring, muscimol reversibly depressed contractions induced by EFS as in the normal group.
4) GABA inhibited tracheal contraction induced by EFS but had no effect on the contractile response to acetylcholine.
In conclusion, our study suggests that prejunctional GABAB receptors attenuate neuronally induced cholinergic contraction of airway smooth muscle, and that there may be a dysfunction of these prejunctional receptors in asthmatic, OA-sensitized guinea pig.
