<b>α1-Adrenoceptors relate Ca</b>^<b>2+</b><b> modulation and protein secretions in rat lacrimal </b><b>gland </b>

Abstract

Noradrenaline (NA) is a catecholamine with multiple roles including as a hormone and a neurotransmitter. Cellular secretory activities are enhanced by adrenergic stimuli as well as by cholinergic stimuli. The present study aimed to determine which adrenoceptors play a role in controlling intracellular calcium ion ([Ca 2+ ] i ) level in acinar cells of rat lacrimal glands. Expression of mRNA for adrenoceptor subtypes in the acinar cells was assessed using RT-PCR. ] i increase. The peroxidase activity was quantified as a measure of mucin secretion. Ca 2+ -dependent exocytotic secretion of peroxidase was detected in rat lacrimal glands. The RT-PCR results showed that MUC1, MUC4, MUC5AC, MUC5B, and MUC16 were expressed in acinar cells. These findings indicated that NA activates α1-adrenoceptors, which were found to be the main receptors in Ca 2+ -related cell homeostasis and protein (including mucin) secretion in lacrimal glands.The lacrimal gland is the main contributor to the aqueous component of the preocular tear film, which contains water, electrolytes, proteins, peroxidase, mucins, and lactoferrin. The lacrimal gland is composed of several cell types, including myoepithelial cells, ductal cells, goblet cells, and acinar cells, which are the major cell type constituting 80% of the gland. Acinar cells are highly polarized and joined by tight junctions at the luminal membrane, creating distinct basolateral and apical membranes (12). Goblet cells are a source of mucus in tears and secrete different types of mucins onto the ocular surface, especially in the conjunctiva. Although the number of goblet cells increases in the nasolacrimal duct, as the diameter of the nasolacrimal duct lumen is narrower than that of the lacrimal sac. Regulation of lacrimal gland fluid secretions is under neural control; activation of the sensory nerves in the cornea and conjunctiva initiates an afferent pathway leading to the central nervous system, which subsequently activates an efferent pathway that stimulates parasympathetic and sympathetic nerves, and ultimately, the lacrimal gland (32). The appropriate amount and composition of lacrimal gland fluid are crucial for a healthy, intact ocular surface (14). Sympathetic nerves release the catecholamine noradrenaline (NA). Catecholamines bind to adreno-

Effect of Intramuscular Medetomidine Administration on Tear Flow in Rats

“…As another possible mechanism, alteration of metabolism at the lacrimal gland cellular level through the α 2 -adrenoceptor has been proposed to decrease tear production [32]. At present, although the existence or function of α 1 -adrenoceptor in the lacrimal gland in rats or mice has been reported, there have been no reports regarding the α 2 -adrenoceptor in the lacrimal glands of any species [55,56]. Furthermore, it was also suggested that increased antinociception modulated by α 2 -adrenoceptor decreases reflex tear secretion [32].…”

Alpha-Adrenergic Agonists Stimulate Fluid Secretion in Lacrimal Gland Ducts

“…Because α-adrenergic stimulation is generally linked to Ca 2+ signaling, the effect of phenylephrine on [Ca 2+ ] i and ductal fluid secretion was investigated. 23 Although phenylephrine stimulation resulted in a small but statistically significant elevation of [Ca 2+ ] i , no statistically significant difference could be demonstrated in the fluid secretion between the Ca 2+ -chelator BAPTA-AMtreated and nontreated ducts.…”

3-Iodothyronamine, a trace amine-associated receptor agonist, regulates intracellular Ca2+ increases via CaMK II through Epac2 in rat cerebral arterioles

“…However, in the present study, isoproterenol failed to induce an increase in [Ca 2+ ] i in cerebral arteriole smooth muscle cells (data not shown). We previously reported that isoproterenol failed to induce an increase in [Ca 2+ ] i in lacrimal gland acinar cells, whereas noradrenaline mainly stimulated α1-adrenoceptors that induced an increase in [Ca 2+ ] i , which subsequently stimulated protein secretion in these cells (Satoh et al 1997;Ikeda-Kurosawa et al 2015).…”