Abstract
The effect of β-adrenergic stimulation on cardiac Na/Ca exchange current (INCX) has been controversial. Recently, 25–400% increase by isoproterenol of INCX was reported. To reexamine this effect, we measured 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 about 32%. However, this increase was probably due to contamination of the cAMP-dependent Cl− current (ICFTR), because Ni2+ inhibited the activation of ICFTR by 1 μM isoproterenol, with a half-maximum concentration of 0.5 mM under the conditions where INCX was suppressed. 5 or 10 mM Ni2+ did not inhibit ICFTR activated by 10 μM forskolin, an activator of adenylate cyclase, suggesting that Ni2+ acted upstream of adenylate cyclase in the β-adrenergic signaling pathway. Furthermore, in a low Cl− bath solution, 1 μM isoproterenol did not significantly alter the amplitude of Ni2+-sensitive INCX at +50 mV, which was close to the reversal potential of ICFTR. No change in INCX amplitude was induced by 10 μM forskolin. When INCX was activated by external Ca2+, it was not significantly affected by 1 μM isoproterenol in guinea-pig, mouse or rat ventricular cells. We concluded that β-adrenergic stimulation does not have significant effects on INCX in guinea-pig, mouse or rat ventricular myocytes. [J Physiol Sci. 2006;56 Suppl:S72]
