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

Inhibition by external Cd2+ of Na/Ca exchange and L-type Ca channel in rabbit ventricular myocytes

1997 ◽  
Vol 272 (5) ◽  
pp. H2164-H2172 ◽  
Author(s):  
I. A. Hobai ◽  
J. A. Bates ◽  
F. C. Howarth ◽  
A. J. Levi
Keyword(s):  
Ion Channels ◽  
Dissociation Constant ◽  
Ventricular Myocytes ◽  
Hill Coefficient ◽  
Ca Channel ◽  
Channel Current ◽  
Rabbit Ventricular Myocytes ◽  
Dissociation Constant Kd ◽  
Ca Channel Current ◽  
Exchange Activity

We investigated the effect of external Cd2+ on the Na/Ca exchange and the L-type Ca channel current (ICa,L) in whole cell patch-clamped rabbit ventricular myocytes at 36 degrees C. After the interfering ion channels and the Na/K pump were blocked, the exchange current was measured as the membrane current that was inhibited by 5 mM nickel. External Cd2+ inhibited Na/Ca exchange with a dissociation constant (KD) of 320.6 +/- 12.4 microM and a Hill coefficient of 1.5 +/- 0.09 (n = 13 cells) and ICa,L with a KD of 2.14 +/- 0.15 microM and a Hill coefficient of 0.74 +/- 0.03 (n = 11 cells). We observed some overlap in the Cd2+ concentration that blocked each mechanism. Cd2+ (100-500 microM) is used commonly to block ICa,L completely. However, 100 microM Cd2+ also inhibits 20% of the Na/Ca exchange activity, whereas 500 microM Cd2+ inhibits 60%.

Neuraminidase selectively enhances transient Ca2+ current in cardiac myocytes

1989 ◽  
Vol 256 (6) ◽  
pp. C1267-C1272 ◽  
Author(s):  
H. F. Yee ◽  
J. N. Weiss ◽  
G. A. Langer
Keyword(s):  
Sialic Acid ◽  
Ventricular Myocytes ◽  
Calcium Content ◽  
Selective Inhibition ◽  
Myocardial Cell ◽  
Ca Channel ◽  
Neuraminidase Treatment ◽  
Membrane Function ◽  
Channel Current ◽  
Current Exposure

Sialic acid, an anionic sugar moiety found peripherally on membrane glycoconjugates, is specifically hydrolyzed from the cell surface by neuraminidase. Because neuraminidase has previously been demonstrated to augment myocardial cell calcium content, the effects of neuraminidase on Ca channel function were studied on voltage-clamped guinea pig ventricular myocytes. In 25-50% of cells, neuraminidase treatment (0.12 U/ml for 20 min) enhanced current through the transient (T) Ca channel by 304 +/- 35% without significantly altering the magnitude of the long-lasting (L) Ca channel current. Exposure to neuraminidase did not affect the voltage dependence of activation or inactivation, nor did it affect the selective inhibition of the T-channel current by amiloride or the L-channel current by nifedipine. After neuraminidase treatment, the T-channel current inactivated more rapidly (time constant decreasing from 8.9 +/- 0.9 to 7.7 +/- 0.6 ms), whereas there was no change in the rate of inactivation of the L-channel current. Neuraminidase treatment removed approximately 20% of the total cellular sialic acid. These results indicate that neuraminidase treatment selectively modulates the function of the T Ca channel in ventricular myocytes, possibly through removal of sarcolemmal sialic acid, suggesting that glycosylation of membrane macromolecules may influence membrane function.

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.

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 Inactivation of calcium channel current in the calf cardiac Purkinje fiber. Evidence for voltage- and calcium-mediated mechanisms.

1984 ◽  
Vol 84 (5) ◽  
pp. 705-726 ◽  
Author(s):  
R S Kass ◽  
M C Sanguinetti
Keyword(s):  
Charge Carrier ◽  
Divalent Cations ◽  
Purkinje Fiber ◽  
Ca Channel ◽  
Channel Current ◽  
Zero Current ◽  
Dependent Inactivation ◽  
Voltage Dependent ◽  
Ca Channel Current ◽  
Dependent Mechanism

We have studied the influence of divalent cations on Ca channel current in the calf cardiac Purkinje fiber to determine whether this current inactivates by voltage- or Ca-mediated mechanisms, or by a combination of the two. We measured the reversal (or zero current) potential of the current when Ba, Sr, or Ca were the permeant divalent cations and determined that depletion of charge carrier does not account for time-dependent relaxation of Ca channel current in these preparations. Inactivation of Ca channel current persists when Ba or Sr replaces Ca as the permeant divalent cation, but the voltage dependence of the rate of inactivation is markedly changed. This effect cannot be explained by changes in external surface charge. Instead, we interpret the results as evidence that inactivation is both voltage and Ca dependent. Inactivation of Sr or Ba currents reflects a voltage-dependent process. When Ca is the divalent charge carrier, an additional effect is observed: the rate of inactivation is increased as Ca enters during depolarizing pulses, perhaps because of an additional Ca-dependent mechanism.

scholarly journals Modulation of voltage-dependent Ca channel current by arachidonic acid and other long-chain fatty acids in rabbit intestinal smooth muscle.

1992 ◽  
Vol 100 (1) ◽  
pp. 27-44 ◽  
Author(s):  
T Shimada ◽  
A P Somlyo
Keyword(s):  
Fatty Acids ◽  
Arachidonic Acid ◽  
Smooth Muscle ◽  
Ca Channel ◽  
Long Chain Fatty Acids ◽  
Channel Current ◽  
Kinase C ◽  
Voltage Dependent ◽  
Ca Channel Current ◽  
Long Chain

The effects of arachidonic acid (AA) and other long-chain fatty acids on voltage-dependent Ca channel current (ICa) were investigated, with the whole cell patch clamp method, in longitudinal smooth muscle cells of rabbit ileum. 10-30 microM AA caused a gradual depression of ICa. The inhibitory effect of AA was not prevented by indomethacin (10 microM) (an inhibitor of cyclooxygenase) or nordihydroguaiaretic acid (10 microM) (an inhibitor of lipoxygenase). 1-(5-Isoquinolinesulfonyl)-2-methylpiperazine (H7; 25-50 microM) or staurosporine (2 microM) (inhibitors of protein kinase C) did not block the AA-induced inhibition of ICa, and application of phorbol ester (a protein kinase C activator) (phorbol-12,13-dibutyrate, 0.2 microM) did not mimic the AA action. Some other cis-unsaturated fatty acids (palmitoleic, linoleic, and oleic acids) were also found to depress ICa, while a trans-unsaturated fatty acid (linolelaidic acid) and saturated fatty acids (capric, lauric, myristic, and palmitic acids) had no inhibitory effects on ICa. Myristic acid consistently increased the amplitude of ICa at negative membrane potentials. The present results suggest the possible role of AA, and perhaps other fatty acids, in the physiological and/or pathological modulation of ICa in smooth muscle.

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