Changes in subsarcolemmal sodium concentration measured by Na-Ca exchanger activity during Na-pump inhibition and β-adrenergic stimulation in guinea-pig ventricular myocytes

1997 ◽  
Vol 435 (1) ◽  
pp. 112-118 ◽  
Author(s):  
M. J. Main ◽  
C. J. Grantham ◽  
M. B. Cannell
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Sodium Concentration ◽  
Adrenergic Stimulation ◽  
Na Pump

β-Adrenergic stimulation does not activate Na+/Ca2+ exchange current in guinea pig, mouse, and rat ventricular myocytes

2006 ◽  
Vol 290 (2) ◽  
pp. C601-C608 ◽  
Author(s):  
Xue Lin ◽  
Hikari Jo ◽  
Yutaka Sakakibara ◽  
Keiichi Tambara ◽  
Bongju Kim ◽  
...  
Keyword(s):  
Adenylate Cyclase ◽  
Guinea Pig ◽  
Maximum Concentration ◽  
Ventricular Myocytes ◽  
Reversal Potential ◽  
Exchange Current ◽  
Half Maximum ◽  
Adrenergic Stimulation ◽  
Rat Ventricular Myocytes ◽  
Ventricular Cells

The effect of β-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 β-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 β-adrenergic stimulation does not have significant effects on INCX in guinea pig, mouse, or rat ventricular myocytes.

Effects of sustained β-adrenergic stimulation on ionic currents of cultured adult guinea pig cardiomyocytes

2002 ◽  
Vol 282 (3) ◽  
pp. H880-H889 ◽  
Author(s):  
Li-Ming Zhang ◽  
Zhiguo Wang ◽  
Stanley Nattel
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Ionic Current ◽  
Ionic Currents ◽  
Delayed Rectifier ◽  
Adrenergic Stimulation ◽  
Cardiac Ion Channels ◽  
Current Voltage ◽  
Relationship Of ◽  
The Impact

Short-term stimulation of β-receptors is known to affect cardiac ion channels; however, the impact of longer-term stimulation on intrinsic channel function is poorly understood. To evaluate this, cultured guinea pig ventricular myocytes were exposed to isoproterenol (10 nM), vehicle, or isoproterenol plus propranolol (1 μM) for 48 h. Sustained exposure to isoproterenol decreased the density of the inward rectifier ( I K1), slow delayed rectifier ( I Ks), and L-type Ca2+( I Ca L) currents, effects that were fully prevented by propranolol. Changes in K+ currents were prevented by the β1-selective antagonist CGP-20712A, unaffected by the β2-antagonist ICI-118,551, and mimicked by the membrane-permeable cAMP analog 8-bromo-cAMP. Isoproterenol did not alter the current-voltage relationship of the K+currents but increased the density of T-type Ca2+ current ( I Ca T) and thereby increased the proportion of the total Ca2+ current at more negative potentials. We conclude that sustained exposure to isoproterenol reduces I K1, I Ks, and I Ca L density and increases the density of I Ca T. The direct ionic current remodeling effects of sustained β-adrenoceptor stimulation resemble changes reported with heart failure and may be important in arrhythmogenic ionic remodeling.

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