The T-type Ca channel in guinea-pig ventricular myocytes is insensitive to isoproterenol

1988 ◽  
Vol 411 (6) ◽  
pp. 704-706 ◽  
Author(s):  
J. Tytgat ◽  
B. Nilius ◽  
J. Vereecke ◽  
E. Carmeliet
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Ca Channel

scholarly journals Properties of L-type calcium channel gating current in isolated guinea pig ventricular myocytes.

1991 ◽  
Vol 98 (2) ◽  
pp. 265-285 ◽  
Author(s):  
R W Hadley ◽  
W J Lederer
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Channel Gating ◽  
Charge Movement ◽  
Ca Channel ◽  
Dependent Manner ◽  
Gating Current ◽  
Ca Current ◽  
Channel Inactivation ◽  
Time Dependencies

Nonlinear capacitative current (charge movement) was compared to the Ca current (ICa) in single guinea pig ventricular myocytes. It was concluded that the charge movement seen with depolarizing test steps from -50 mV is dominated by L-type Ca channel gating current, because of the following observations. (a) Ca channel inactivation and the immobilization of the gating current had similar voltage and time dependencies. The degree of channel inactivation was directly proportional to the amount of charge immobilization, unlike what has been reported for Na channels. (b) The degree of Ca channel activation was closely correlated with the amount of charge moved at all test potentials between -40 and +60 mV. (c) D600 was found to reduce the gating current in a voltage- and use-dependent manner. D600 was also found to induce "extra" charge movement at negative potentials. (d) Nitrendipine reduced the gating current in a voltage-dependent manner (KD = 200 nM at -40 mV). However, nitrendipine did not increase charge movement at negative test potentials. Although contamination of the Ca channel gating current from other sources cannot be fully excluded, it was not evident in the data and would appear to be small. However, it was noted that the amount of Ca channel gating charge was quite large compared with the magnitude of the Ca current. Indeed, the gating current was found to be a significant contaminant (19 +/- 7%) of the Ca tail currents in these cells. In addition, it was found that Ca channel rundown did not diminish the gating current. These results suggest that Ca channels can be "inactivated" by means that do not affect the voltage sensor.

Inhibition by nickel of the L-type Ca channel in guinea pig ventricular myocytes and effect of internal cAMP

2000 ◽  
Vol 279 (2) ◽  
pp. H692-H701 ◽  
Author(s):  
Ion A. Hobai ◽  
Jules C. Hancox ◽  
Allan J. Levi
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Cardiac Cells ◽  
Significant Shift ◽  
Ca Channel ◽  
Free Solution ◽  
Pipette Solution ◽  
Voltage Dependent ◽  
A Site ◽  
Maximal Block

The characteristics of nickel (Ni) block of L-type Ca current ( I Ca,L) were studied in whole cell patch-clamped guinea pig cardiac myocytes at 37°C in the absence and presence of 100 μM cAMP in the pipette solution. Ni block of peak I Ca,L had a dissociation constant ( K d) of 0.33 ± 0.03 mM in the absence of cAMP, whereas in the presence of cAMP, the K d was 0.53 ± 0.05 mM ( P = 0.006). Ni blocked Ca entry via Ca channels (measured as I Ca,L integral over 50 ms) with similar kinetics ( K d of 0.35 ± 0.03 mM in cAMP-free solution and 0.30 ± 0.02 mM in solution with cAMP, P = not significant). Under both conditions, 5 mM Ni produced a maximal block that was complete for the first pulse after application. Ni block of I Ca,L was largely use independent. Ni (0.5 mM) induced a positive shift (4 to 6 mV) in the activation curve of I Ca,L. The block of I Ca,L by 0.5 mM Ni was independent of prepulse membrane potential (over the range of −120 to −40 mV). Ni (0.5 mM) also induced a significant shift in I Ca,Linactivation: by 6 mV negative in cAMP-free solution and by 4 mV positive in cells dialyzed with 100 μM cAMP. These data suggest that, in addition to blocking channel conductance by binding to a site in the channel pore, Ni may bind to a second site that influences the voltage-dependent gating of the L-type Ca channel. They also suggest that Ca channel phosphorylation causes a conformational change that alters some effects of Ni. The results may be relevant to excitation-contraction coupling studies, which have employed internal cAMP dialysis, and where Ni has been used to block I Ca,L and Ca entry into cardiac cells.

Cyclic GMP regulates the Ca-channel current in guinea pig ventricular myocytes

1989 ◽  
Vol 413 (6) ◽  
pp. 685-687 ◽  
Author(s):  
Renzo C. Levi ◽  
Giuseppe Alloatti ◽  
Rodolphe Fischmeister
Keyword(s):  
Guinea Pig ◽  
Cyclic Gmp ◽  
Ventricular Myocytes ◽  
Ca Channel ◽  
Channel Current ◽  
Ca Channel Current

Sodium-calcium exchange-mediated contractions in feline ventricular myocytes

1992 ◽  
Vol 263 (4) ◽  
pp. H1161-H1169 ◽  
Author(s):  
H. B. Nuss ◽  
S. R. Houser
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Ventricular Myocytes ◽  
Membrane Potentials ◽  
Exchange Mechanism ◽  
Ca Channel ◽  
Ca Current ◽  
Voltage Step ◽  
Reverse Mode ◽  
Sodium Calcium ◽  
Calcium Exchange

The hypothesis that Ca entry by the sarcolemmal Na-Ca exchange mechanism induces sarcoplasmic reticulum (SR) Ca release, loads the SR with Ca, and/or directly induces contractions by elevating cytosolic free Ca was tested in voltage-clamped feline ventricular myocytes. Intracellular Na concentration was increased by cellular dialysis to enhance Ca influx via "reverse-mode" Na-Ca exchange at positive membrane potentials, at which the "L-type" Ca current (ICa) should be small. Contractions were induced in the presence of Ca channel antagonists by depolarization to these potentials, suggesting that Ca influx via reverse-mode Na-Ca exchange was involved. These contractions had both phasic (SR related) and tonic components of shortening. They were smaller and began with more delay after depolarization than contractions which involved ICa. The magnitude of shortening was graded by the amount and duration of depolarization, suggesting that Ca influx via reverse-mode Na-Ca exchange has the capacity to induce and grade SR Ca release. Small slow contractions could be evoked in the presence of ryanodine (to impair SR function) and verapamil (to block ICa), supporting the idea that Ca influx via Na-Ca exchange is sufficient to directly activate the contractile proteins. Contractions induced by voltage steps to +10 mV, which were usually small when ICa was blocked, were potentiated if preceded by a voltage step to strongly positive potentials. This potentiation was inhibited by ryanodine, suggesting that Ca entry that occurs by Na-Ca exchange may be important for normal SR Ca loading.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Inhibition of Na-K pump current in guinea pig ventricular myocytes by dihydroouabain occurs at high- and low-affinity sites.

1989 ◽  
Vol 64 (6) ◽  
pp. 1063-1069 ◽  
Author(s):  
D J Mogul ◽  
H H Rasmussen ◽  
D H Singer ◽  
R E Ten Eick
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Pump Current
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