Properties of the outward currents in frog atrial muscle

1971 ◽  
Vol 329 (4) ◽  
pp. 321-331 ◽  
Author(s):  
A. de Hemptinne
1985 ◽  
Vol 63 (9) ◽  
pp. 1065-1069 ◽  
Author(s):  
Julio L. Alvarez ◽  
Miguel Garcia ◽  
Francisco R. Dorticós ◽  
Jesús A. Morlans

The effects of MnCl2 on outward currents in frog atrial muscle were investigated under voltage-clamp conditions. MnCl2 (3 mmol/L), which completely abolished the slow inward current, produced a decrease in the outward background current (Ib) at potentials positive to −50 mV. The delayed outward current (Ix, time dependent) was not altered by Mn. "Isochronic activation curves" for Ix and decay of current tails at −40 mV remained unaffected after Mn. Effects on Ib probably reflect a decrease in [Formula: see text] related to the decrease in Ca influx as well as a reduction in the Na–Ca exchange current.


Data in Brief ◽  
2021 ◽  
Vol 34 ◽  
pp. 106668
Author(s):  
Alberto Montalbano ◽  
Cesare Sala ◽  
Chiara Abrardo ◽  
Nicoletta Murciano ◽  
Farhad Jahanfar ◽  
...  

1996 ◽  
Vol 270 (6) ◽  
pp. G932-G938 ◽  
Author(s):  
J. Jury ◽  
K. R. Boev ◽  
E. E. Daniel

Single smooth muscle cells from the opossum body circular muscle were isolated and whole cell currents were characterized by the whole cell patch-clamp technique. When the cells were held at -50 mV and depolarized to 70 mV in 20-mV increments, initial small inactivating inward currents were evoked (-30 to 30 mV) followed by larger sustained outward currents. Depolarization from a holding potential of -90 mV evoked an initial fast inactivating outward current sensitive to 4-aminopyridine but not to high levels of ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA). The outward currents reversed near K+ equilibrium potential and were abolished when KCl was replaced by CsCl in the pipette solution. The sustained outward current was inhibited by quinine and cesium. High EGTA in the pipette solution reduced but did not abolish the sustained outward currents, suggesting that both Ca(2+)-dependent and -independent currents were evoked. The nitric oxide (NO)-releasing agents Sin-1 and sodium nitroprusside increased outward K+ currents. High levels of EGTA in the pipette solution abolished the increase in outward current induced by Sin-1. The presence of cyclopiazonic acid, an inhibitor of the sarcoplasmic reticulum (SR) Ca2+ pump, blocked the effects of NO-releasing agents. We conclude that NO release activates K+ outward currents in opossum esophagus circular muscle, which may depend on Ca2+ release from the SR stores.


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