Beta-adrenergic stimulation does not activate Na+/Ca2+ exchange current in guinea pig, mouse, and rat ventricular myocytes |
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Authors: | Lin Xue Jo Hikari Sakakibara Yutaka Tambara Keiichi Kim Bongju Komeda Masashi Matsuoka Satoshi |
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Institution: | Department of Cardiovascular Surgery, Graduate School of Medicine, Kyoto University, Shogoin, Sakyo-ku, Kyoto, Japan. |
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Abstract: | The effect of -adrenergic stimulation on cardiac Na+/Ca2+ exchange has been controversial. To clarify the effect, we measured Na+/Ca2+ exchange current (INCX) in voltage-clamped guinea pig, mouse, and rat ventricular cells. When INCX was defined as a 5 mM Ni2+-sensitive current in guinea pig ventricular myocytes, 1 µM isoproterenol apparently augmented INCX by 32%. However, this increase was probably due to contamination of the cAMP-dependent Cl current (CFTR-Cl current, ICFTR-Cl), because Ni2+ inhibited the activation of ICFTR-Cl by 1 µM isoproterenol with a half-maximum concentration of 0.5 mM under conditions where INCX was suppressed. Five or ten millimolar Ni2+ did not inhibit ICFTR-Cl activated by 10 µM forskolin, an activator of adenylate cyclase, suggesting that Ni2+ acted upstream of adenylate cyclase in the -adrenergic signaling pathway. Furthermore, in a low-extracellular Cl bath solution, 1 µM isoproterenol did not significantly alter the amplitude of Ni2+-sensitive INCX at +50 mV, which is close to the reversal potential of ICFTR-Cl. No change in INCX amplitude was induced by 10 µM forskolin. When INCX was activated by extracellular Ca2+, it was not significantly affected by 1 µM isoproterenol in guinea pig, mouse, or rat ventricular cells. We concluded that -adrenergic stimulation does not have significant effects on INCX in guinea pig, mouse, or rat ventricular myocytes. cystic fibrosis transmembrane conductance regulator; nickel ion |
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