The effect of a chemical phosphatase on single calcium channels and the inactivation of whole-cell calcium current from isolated guinea-pig ventricular myocytes

1995 ◽  
Vol 430 (1) ◽  
pp. 68-80 ◽  
Author(s):  
T. J. A. Allen ◽  
R. A. Chapman
1990 ◽  
Vol 424 (1) ◽  
pp. 205-228 ◽  
Author(s):  
Y M Shuba ◽  
B Hesslinger ◽  
W Trautwein ◽  
T F McDonald ◽  
D Pelzer

1999 ◽  
Vol 342 (2) ◽  
pp. 269-273 ◽  
Author(s):  
Yi CUI ◽  
Antony GALIONE ◽  
Derek A. TERRAR

Actions of photoreleased cADP-ribose (cADPR), a novel regulator of calcium-induced calcium release (CICR) from ryanodine-sensitive stores, were investigated in cardiac myocytes. Photoreleased cADPR caused an increase in the magnitude of whole-cell calcium transients studied in mammalian cardiac ventricular myocytes (both guinea-pig and rat) using confocal microscopy). Approx. 15 s was required following photorelease of cADPR for the development of its maximal effect. Photoreleased cADPR also increased the frequency of calcium ‘sparks’, which are thought to be elementary events which make up the whole-cell calcium transient, and were studied in rat myocytes, but had little or no effect on spark characteristics (amplitude, rise time, decay time and distance to half amplitude). The potentiating effects of photoreleased cADPR on both whole-cell transients and the frequency of calcium sparks were prevented by cytosolic application of the antagonist 8-amino-cADPR (5 μM). These experiments, therefore, provide the first evidence in any cell type for an effect of cADPR on calcium sparks, and are the first to show the actions of photoreleased cADPR on whole-cell calcium transients in mammalian cells. The observations are consistent with the effects of cADPR in enhancing the calcium sensitivity of CICR from the sarcoplasmic reticulum in cardiac ventricular myocytes, leading to an increase in the probability of occurrence of calcium sparks and to an increase in whole-cell calcium transients. The slow time-course for development of the full effect on whole-cell calcium transients might be taken to indicate that the influence of cADPR on CICR may involve complex molecular interactions rather than a simple direct action of cADPR on the ryanodine-receptor channels.


1994 ◽  
Vol 1191 (1) ◽  
pp. 205-208 ◽  
Author(s):  
Alain Lacampagne ◽  
François Gannier ◽  
Jorge Argibay ◽  
Didier Garnier ◽  
Jean-Yves Le Guennec

1999 ◽  
Vol 276 (5) ◽  
pp. H1724-H1733 ◽  
Author(s):  
Toshitsugu Ogura ◽  
Lesya M. Shuba ◽  
Terence F. McDonald

Guinea pig ventricular myocytes in whole cell configuration were treated with tyrosine kinase (TK) inhibitors [genistein (Gst), tyrphostin A23 (T23), and tyrphostin A25 (T25)] and with inactive analogs [daidzein, genistin, and tyrphostin A1 (T1)] to measure effects on L-type Ca2+ current ( I Ca,L). Gst inhibited I Ca,L(IC50 = 47 μM) without affecting its time course or shifting the I Ca,L-voltage relationship. At the highest concentration of isoflavone tested (200 μM), I Ca,L was inhibited by 66 ± 7% (Gst), 22 ± 2% (daidzein), and 1 ± 3% (genistin). Inhibition of I Ca,L by the active tyrphostins was significantly larger than inhibition by T1; at 200 μM the inhibitions were 72 ± 6% (T23), 71 ± 6% (T25), and 27 ± 6% (T1). The phosphotyrosine phosphatase inhibitor orthovanadate (1 mM) had a small stimulatory effect (6 ± 2%) on basal I Ca,L and blocked the inhibition of I Ca,L by TK inhibitors. The data suggest a role for the TK-phosphotyrosine phosphatase system in the regulation of cardiac Ca2+ channels.


1999 ◽  
Vol 126 (7) ◽  
pp. 1531-1533 ◽  
Author(s):  
George P Thomas ◽  
Morris Karmazyn ◽  
Andrew C Zygmunt ◽  
Charles Antzelevitch ◽  
Njanoor Narayanan

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