Am J Physiol Cell Physiol Journal of Applied Physiology
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Am J Physiol Cell Physiol 276: C1282-C1287, 1999;
0363-6143/99 $5.00
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Vol. 276, Issue 6, C1282-C1287, June 1999

Isoproterenol potentiates alpha -adrenergic and muscarinic receptor-mediated Ca2+ response in rat parotid cells

Akihiko Tanimura, Akihiro Nezu, Yosuke Tojyo, and Yoshito Matsumoto

Department of Dental Pharmacology, School of Dentistry, Health Sciences University of Hokkaido, Ishikari-Tobetsu, Hokkaido 061-0293, Japan

The effects of the cAMP pathway on the Ca2+ response elicited by phospholipase C-coupled receptor stimulations were studied in rat parotid cells. Although 1 µM isoproterenol (Iso) itself had no effect on the cytosolic Ca2+ concentration, the pretreatment with Iso potentiated Ca2+ responses evoked by phenylephrine. The potentiating effect of Iso was attributed to a shifting of the concentration-response curves of phenylephrine to the left and an increase in the maximal response. Half-maximal potentiation occurred at 3 nM Iso. Iso also potentiated the Ca2+ response elicited by carbachol. The potentiating effect of Iso was mimicked by forskolin (10 µM) and dibutyryl adenosine 3',5'-cyclic monophosphate (2 mM) and was blocked by 10 µM H-89. Iso potentiated the phenylephrine-induced Ca2+ response in the absence of extracellular Ca2+, but Iso did not increase the inositol trisphosphate (IP3) production induced by phenylephrine. These results suggest that the potentiation of the Ca2+ response can be attributed to a sensitization of IP3 receptors by cAMP-dependent protein kinase.

beta -adrenergic receptor; adenosine 3',5'-cyclic monophosphate; calcium release; potentiation


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