Kotliarova A. Ca2+-transport systems of the exorbital lacrimal gland secretory cells of the rat

IP3Rs of exorbital lacrimal gland cells were effectively inhibited by 2-APB and activated by IP3. Signaling pathways activated by P2Y-receptors in the lacrimal gland secretory cells were partially mediated by IP3Rs activation. RyRs of lacrimal gland secretory cells were activated by ryanodine and modulated by Ca2+ cations. Simultaneous activation of RyRs and IP3Rs in these cells caused Ca2+ release from the same store. Mitochondrial Ca2+-uniporter of lacrimal gland secretory cells was inhibited by ruthenium red. Effects of ryanodine and ruthenium red on the Ca2+ content in cells was statistically significantly non-additive. In addition to the endoplasmic reticulum RyRs activation, ryanodine inhibited the Ca2+ transport to the mitochondrial matrix, which was insensitive to ruthenium red. Adding carbacholine to the polarographic chapter caused an intensification of respiration of the studied cells. Mitochondrial Ca2+-uniporter inhibition, which prevents the Ca2+ flow in the matrix caused the leveling of carbacholine-stimulating effect, and IP3Rs inhibition partially eliminated the effect of carbacholine. Effect of FCCP was independent of any Ca2+-uniporter and IP3Rs inhibition. It has an important general biological significance because it allows for the regulation of mitochondrial respiration by a direct positive correlation - in advance before there is a lack of ATP and triggers the inverse regulatory effects, homeostatic (not signaling) by their nature. In summary, IP3Rs, RyRs, store-operated Ca2+-entry, PMCA, SERCA, mitochondrial Ca2+-uniporter play an important role in Ca2+-homeostasis maintenance in the secretory cells of the rat exorbital lacrimal gland.