We demonstrated that hyperosmolar solutions stimulated both mucin and ly-sozyme secretion, suggesting that either there is co-regulation of secretion or that both mucous and serous cells respond in the same way to the hyperosmolar agents. This is supported by the observation that the rate of mucin secretion was approximately two times that of lysozyme secretion without stimulation and under all conditions of stimulation.
Mannitol appeared to induce mucin secretion to a greater extent than saline solution with similar osmo-larity, although this was not statistically significant. This is consistent with a report that increased mucin secretion in the cat trachea was greater after incubation with sucrose solution than with hypertonic saline solution at a similar osmolarity. The tracheal epithelium is more permeable to chloride ion than to mannitol, leading to a more rapid equilibration of osmolarity about the epithelium and across the air side of the cell; therefore, the local gradient in osmolarity around the epithelium is probably less with saline solution exposure than with mannitol. canadian healthcare mall
To understand the mechanism of hyperosmolar solution-induced airway secretion, we examined the effects of secretagogue inhibitors. In the rat trachea, hyperosmolar solutions can induce plasma exudation through neurogenic inflammation. Cholinergic antagonists and tachykinins can both cause vasodilatation, plasma exudation, and mucus secretion. Hyperosmolarity can also induce leukotriene and prostaglandin production, and these arachidonic acid metabolites can directly stimulate mucin secretion; however, neither atropine nor NDGA decreased saline solution-induced mucin secretion in this study.