Ohshima Kazunobu, Shiba Yoshiki, Hirono Chikara, Sugita Makoto, Iwasa Yoshiko, Shintani Hideaki
Department of Operative Dentistry, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan.
Eur J Oral Sci. 2003 Oct;111(5):405-9. doi: 10.1034/j.1600-0722.2003.00061.x.
Carbachol (CCh) enlarges the luminal space in rat parotid intralobular ducts, but the mechanism of their enlargement remains obscure. We investigated the involvement of intracellular calcium ions in the enlargement of luminal space by monitoring the luminal space under optical sectioning in a confocal laser scanning microscope using sulforhodamine B. Carbachol increased the intracellular concentration of calcium ions ([Ca2+]i) and the inside diameter without any change in the outside diameter. Removal of extracellular calcium ions modulated CCh-induced changes in [Ca2+]i to transient, but did not markedly inhibit the CCh-induced increase in the inside diameter. Additional loading of BAPTA (1,2-bis (o-aminophenoxy-ethane-n,n,n',n'-tetraacetic acid) in the duct cells suppressed CCh-induced changes. Diphenylamine-2-carboxylate (DPC), but not cytochalasin D, calmodulin inhibitor or nitric oxide synthase inhibitor profoundly suppressed CCh-induced changes. These results suggest that CCh induces enlargement of the luminal space through the activation of DPC-sensitive channels by the release of calcium ions from the intracellular pool.
