Related Experiment Videos
[Effect of histamine on electrical properties in canine tracheal epithelium]
Insights
Histamine stimulates airway mucosa ion transport, increasing short-circuit current (Isc) via submucosal H1-receptors. This process involves prostaglandin synthesis, affecting chloride secretion and sodium absorption.
Area of Science:
- Respiratory Physiology
- Ion Transport Mechanisms
- Epithelial Biology
Context:
- Airway mucosa plays a crucial role in maintaining respiratory health.
- Histamine is a key mediator in allergic and inflammatory responses.
- Understanding ion transport is vital for respiratory disease research.
Purpose:
- To investigate the effects of histamine on ion transport in canine tracheal epithelium.
- To elucidate the specific receptors and signaling pathways involved in histamine's action.
- To characterize the impact of histamine on electrical properties of the airway mucosa.
Summary:
- Histamine applied to the submucosal side of canine tracheal epithelium significantly increased short-circuit current (Isc) in a dose-dependent manner.
- The histamine-induced Isc increase was partially blocked by amiloride, furosemide, and diphenylamine carboxylate, and fully by pyrilamine (an H1 antagonist), but not cimetidine (an H2 antagonist).
- Inhibition by indomethacin and mepacrine, but not H-7, suggests involvement of prostaglandin synthesis in mediating histamine's effects on chloride secretion and sodium absorption.
Impact:
- These findings highlight the role of submucosal H1-receptors in regulating airway ion and water transport.
- The study provides insights into the cellular mechanisms underlying histamine-mediated effects in the airways.
- This research contributes to understanding the pathophysiology of respiratory conditions involving histamine.
Abstract:
To characterize the action of histamine on ion transport across the airway mucosa, we measured the electrical properties of cultured tracheal epithelium from dogs by Ussing's short-circuited technique in vitro. The addition of histamine to the submucosal side increased short-circuit current (Isc), whereas mucosal addition of histamine had no effect. The histamine-induced increase in Isc was dose-dependent with the maximal increase from the baseline value and EC50 being 4.4 +/- 0.5 microA/cm2 and 10(-6) M, respectively. We also tested the effects of pharmacological blocking agents on the histamine-induced Isc increase. The effect of histamine on Isc was partially inhibited by pretreatment of cells with amiloride, furosemide and diphenylamine carboxylate. Furthermore, the effect of histamine was inhibited by pyrilamine, but not by cimetidine. To determine the contributions of several intracellular second messenger systems to the histamine-induced increase in Isc, we studied the change of Isc by pretreatment of cells with indomethacin, mepacrine and H-7. The increase in Isc produced by histamine was inhibited by indomethacin and mepacrine but not H-7. These results suggest that histamine stimulates both Cl secretion and Na absorption and may affect the subsequent movement of water across the airway epithelium through the activation of submucosal H1-receptor probably involving prostaglandin synthesis.