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Am J Physiol Cell Physiol 273: C1526-C1532, 1997;
0363-6143/97 $5.00
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Vol. 273, Issue 5, C1526-C1532, November 1997

Hormone-induced rise in cytosolic Ca2+ in axolotl hepatocytes: properties of the Ca2+ influx channel

Thomas Lenz and Jochen W. Kleineke

Abteilung Klinische Biochemie, Zentrum Innere Medizin, University of Göttingen, 37075 Göttingen, Germany

Calcium entry in nonexcitable cells occurs through Ca2+-selective channels activated secondarily to store depletion and/or through receptor- or second messenger-operated channels. In amphibian liver, hormones that stimulate the production of adenosine 3',5'-cyclic monophosphate (cAMP) also regulate the opening of an ion gate in the plasma membrane, which allows a noncapacitative inflow of Ca2+. To characterize this Ca2+ channel, we studied the effects of inhibitors of voltage-dependent Ca2+ channels and of nonselective cation channels on 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP)-dependent Ca2+ entry in single axolotl hepatocytes. Ca2+ entry provoked by 8-BrcAMP in the presence of physiological Ca2+ followed first-order kinetics (apparent Michaelis constant = 43 µM at the cell surface). Maximal values of cytosolic Ca2+ (increment ~300%) were reached within 15 s, and the effect was transient (half time of 56 s). We report a strong inhibition of cAMP-dependent Ca2+ entry by nifedipine [half-maximal inhibitory concentration (IC50) = 0.8 µM], by verapamil (IC50 = 22 µM), and by SK&F-96365 (IC50 = 1.8 µM). Depolarizing concentrations of K+ were without effect. Gadolinium and the anti-inflammatory compound niflumate, both inhibitors of nonselective cation channels, suppressed Ca2+ influx. This "profile" indicates a novel mechanism of Ca2+ entry in nonexcitable cells.

adenosine 3',5'-cyclic monophosphate; second messenger-operated calcium channel; calcium channel pharmacology; SK&F-96365; fenamates


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