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Cyclic ADP-ribose Induces Ca2+ Release from Caffeine-insensitive Ca2+ Pools in Canine Salivary Gland Cells

Department of Removable Prosthodontics

K. Morita

Department of Pharmacology, Hiroshima University School of Dentistry, Kasumi 1-2-3, Minami-ku, Hiroshima 734-8553, Japan

S. Kitayama

Department of Pharmacology, Hiroshima University School of Dentistry, Kasumi 1-2-3, Minami-ku, Hiroshima 734-8553, Japan

Y. Imai

Department of Pharmacology, Hiroshima University School of Dentistry, Kasumi 1-2-3, Minami-ku, Hiroshima 734-8553, Japan

K. Itadani

Department of Removable Prosthodontics

Y. Akagawa

Department of Removable Prosthodontics

T. Dohi

Department of Pharmacology, Hiroshima University School of Dentistry, Kasumi 1-2-3, Minami-ku, Hiroshima 734-8553, Japan

Cyclic ADP-ribose (cADPR), a novel putative messenger of the ryanodine receptor, was examined regarding its ability to mobilize Ca2+ from intracellular Ca2+ stores in isolated cells of parotid and submandibular glands of the dog. cADPR induced a rapid and transient Ca2+ release in the digitonin-permeabilized cells of salivary glands. cADPR-induced Ca²⁺ release was inhibited by ryanodine receptor antagonists ruthenium red, ryanodine, benzocaine, and imperatoxin inhibitor but not by the inositol 1,4,5-trisphosphate (IP ₃)-receptor antagonist heparin. Thapsigargin, at a concentration of 3 to 30 µM, inhibited IP₃-induced Ca2+ release, while higher concentrations were required to inhibit cADPR-induced Ca²⁺ release. Cross-potentiation was observed between cADPR and ryanodine or SrCl2, suggesting that cADPR sensitizes the Ca2+-induced Ca2+ release mechanism. Cyclic AMP plays a stimulatory role on cADPR- and IP3-induced Ca²⁺ release in digitonin-permeabilized cells. Calmodulin also potentiated cADPR-induced Ca2+ release, but inhibited IP₃-induced Ca²⁺ release. Acetylcholine and ryanodine caused the rise in intracellular free Ca2+ concentration ([Ca²⁺]_i) in intact submandibular and parotid cells. Caffeine did not produce any increase in Ca²⁺ release or [Ca ²⁺]_i rise in any preparation. ADP-ribosyl cyclase activity was found in the centrifuged particulate fractions of the salivary glands. These results suggest that cADPR serves as an endogenous modulator of Ca ²⁺ release from Ca2+ pools through a caffeine-insensitive ryanodine receptor channel, which are different from IP₃-sensitive pools in canine salivary gland cells. This system is positively regulated by cyclic AMP and calmodulin.

Key Words: cyclic ADP-ribose • parotid gland • submandibular gland • calcium • caffeine.

Journal of Dental Research, Vol. 77, No. 10, 1807-1816 (1998)
DOI: 10.1177/00220345980770100801


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