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Am J Physiol Cell Physiol 277: C262-C270, 1999;
0363-6143/99 $5.00
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Vol. 277, Issue 2, C262-C270, August 1999

Nitric oxide acts independently of cGMP to modulate capacitative Ca2+ entry in mouse parotid acini

Eileen L. Watson1,2, Kerry L. Jacobson1, Jean C. Singh1, and Sabrina M. Ott1

Departments of 1 Oral Biology and 2 Pharmacology, University of Washington, Seattle, Washington 98195

Carbachol- and thapsigargin-induced changes in cGMP accumulation were highly dependent on extracellular Ca2+ in mouse parotid acini. Inhibition of nitric oxide synthase (NOS) and soluble guanylate cyclase (sGC) resulted in complete inhibition of agonist-induced cGMP levels. NOS inhibitors reduced agonist-induced Ca2+ release and capacitative Ca2+ entry, whereas the inhibition of sGC had no effect. The effects of NOS inhibition were not reversed by 8-bromo-cGMP. The NO donor GEA-3162 increased cGMP levels blocked by the inhibition of sGC. GEA-3162-induced increases in Ca2+ release from ryanodine-sensitive stores and enhanced capacitative Ca2+ entry, both of which were unaffected by inhibitors of sGC but reduced by NOS inhibitors. Results support a role for NO, independent of cGMP, in agonist-mediated Ca2+ release and Ca2+ entry. Data suggest that agonist-induced Ca2+ influx activates a Ca2+-dependent NOS, leading to the production of NO and the release of Ca2+ from ryanodine-sensitive stores, providing a feedback loop by which store-depleted Ca2+ channels are activated.

carbachol; thapsigargin; GEA-3162; nitric oxide synthase inhibitors; calcium ion release


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