Abstract
Abstract: :
Purpose: Activation of cholinergic receptors stimulates glandular protein and fluid secretion. Activation of adrenergic receptors is known to induce protein secretion from isolated acinar cells and gland fragments. Our goal is to determine if α–adrenergic receptor activation with phenylepherine (PE) stimulates fluid secretion.Methods:Fluid samples were collected into calibrated microcapillaries from the distal duct of exorbital lacrimal glands in situ in anesthetized C57 mice. Fluid secretion was elicited by the addition of 10 µM carbachol (CARB) or 10 µM PE to the fluid bathing the gland in situ, and minute flows were measured via videomicroscopy. Cells were isolated from C57 exorbital lacrimal glands and allowed to rest for 24 hours on matrigel. Cells were then exposed to CARB or PE and the effects on cell volume and membrane currents were measured. Results: In intact glands, CARB elicited a prompt, reversible rise in tear flow. In contrast, exposure to PE had no observable effect on fluid flow. In isolated cells, CARB induced a ∼10% shrinkage, an effect consistent with the onset of fluid secretion. Cell volume was unaffected by PE exposure. CARB resulted in marked increases in outward and inward membrane currents consistent with activation of K+ and Cl– channels. PE caused a similar increase in outward (K+) current, while the rise in inward (Cl–) current was significantly smaller than with CARB. Conclusions: The reduced outward flux of chloride caused by PE is consistent with the undetectable shrinkage of the cells and the failure to detect PE induced fluid flow from the intact gland. These data suggest that there is differential neural control of the lacrimal gland. Cholinergic activation results in increased protein and fluid flow while sympathetic activation results in increased protein secretion but no detectable fluid flow.
Keywords: lacrimal gland • innervation: neural regulation • neurotransmitters/neurotransmitter systems