Processes Maintaining Calcium Homeostasis in Acinar Cells of the Rat Submandibular Salivary Gland |
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Authors: | Fedirko N V Klevets M Yu Kruglikov I A Voitenko N V |
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Institution: | (1) Franko National University, L'vov, Ukraine;(2) National Academy of Sciences of Ukraine, Bogomolets Institute of Physiology, Kyiv, Ukraine |
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Abstract: | Using a Ca2+-sensitive fluorescent indicator, fura-2/AM, we recorded calcium transients in secretory cells of isolated acini of the rat submandibular salivary gland; these transients were induced by hyperpotassium-induced depolarization (after an increase in K+]
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up to 50 mM) of the plasma membrane of the above cells. Calcium transients were significantly suppressed by 50 M nifedipine. Addition of 10 M carbonyl cyanide m-chlorophenylhydrazone to the normal extracellular solution was accompanied by a rise in Ca2+]
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, whereas when hyperpotassium solution is used the effect was less expressed. Blockers of CA2+-ATPase in the cellular membrane and in the endoplasmic reticulum, eosin Y (5 M) and cyclopiazonic acid (CPA, 5 M), respectively, evoked a significant increase in Ca2+]
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and a decrease in the K+-depolarization-induced calcium transient. Extracellular application of caffeine (2, 10, or 30 mM) was accompanied by a concentration-dependent rise in Ca2+]
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. Therefore, potassium depolarization of the plasma membrane of acinar cells of the rat submandibular salivary gland activates both the voltage-dependent Ca2+ influx and Ca2+-induced Ca2+ release from the endoplasmic reticulum; the initial level of Ca2+]
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was restored at the joint involvement of Ca2+-ATPases in the plasma membrane and the membranes of the endoplasmic reticulum and mitochondria. |
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Keywords: | acinar secretory cells calcium transients voltage-operated Ca2+ channels Ca2+-ATPase Ca2+-induced Ca2+ release |
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