Abstract
β-adrenergic receptor (β-AR) stimulation increases cardiac L-type Ca2+ channel (CaCh) currents via cAMP-dependent phosphorylation. We report here that the affinity and maximum response of CaCh to isoproterenol (Iso), in mouse ventricular myocytes were significantly higher when Ba2+ was used as the charge carrier (I Ba) instead of Ca2+ (I Ca). The EC50 and maximum increase of peak currents were 43.7 ± 7.9 nM and 1.8 ± 0.1-fold for I Ca and 23.3 ± 4.7 nM and 2.4 ± 0.1-fold for I Ba. When cells were dialyzed with the faster Ca2+ chelator, BAPTA, both sensitivity and maximum response of I Ca to Iso were significantly augmented compared to cells with EGTA (EC50 of 23.1 ± 5.2 nM and maximal increase of 2.2 ± 0.1-fold). Response of I Ca to forskolin was also significantly increased when cells were dialyzed with BAPTA or when currents were measured in Ba2+. In contrast, depletion of the sarcoplasmic reticulum (SR) Ca2+ stores by ryanodine did not alter sensitivity of I Ca to Iso or forskolin. These results suggest that the Ca2+ entering through CaCh regulates cAMP-dependent phosphorylation, and such negative feedback may play a significant role in cellular Ca2+ homeostasis and contraction in cardiac cells during β-AR stimulation.
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Received: 10 December 1997 / Received after revision: 19 January 1998 / Accepted: 21 January 1998
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Sako, H., Sperelakis, N. & Yatani, A. Ca2+ entry through cardiac L-type Ca2+ channels modulates β-adrenergic stimulation in mouse ventricular myocytes. Pflügers Arch 435, 749–752 (1998). https://doi.org/10.1007/s004240050579
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DOI: https://doi.org/10.1007/s004240050579