scholarly journals Dual modulation of unitary L-type Ca2+ channel currents by [Ca2+]i in fura-2-loaded guinea-pig ventricular myocytes.

1994 ◽  
Vol 480 (3) ◽  
pp. 449-463 ◽  
Author(s):  
Y Hirano ◽  
M Hiraoka
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Fura 2 ◽  
Channel Currents

Regulation of contraction and relaxation by membrane potential in cardiac ventricular myocytes

2000 ◽  
Vol 278 (5) ◽  
pp. H1618-H1626 ◽  
Author(s):  
Gregory R. Ferrier ◽  
Isabel M. Redondo ◽  
Cindy A. Mason ◽  
Cindy Mapplebeck ◽  
Susan E. Howlett
Keyword(s):  
Membrane Potential ◽  
Sarcoplasmic Reticulum ◽  
Guinea Pig ◽  
Voltage Dependence ◽  
Ventricular Myocytes ◽  
Release Mechanism ◽  
Fura 2 ◽  
Regulation Of Contraction ◽  
Contraction And Relaxation ◽  
Sustained Responses

Control of contraction and relaxation by membrane potential was investigated in voltage-clamped guinea pig ventricular myocytes at 37°C. Depolarization initiated phasic contractions, followed by sustained contractions that relaxed with repolarization. Corresponding Ca2+ transients were observed with fura 2. Sustained responses were ryanodine sensitive and exhibited sigmoidal activation and deactivation relations, with half-maximal voltages near −46 mV, which is characteristic of the voltage-sensitive release mechanism (VSRM) for sarcoplasmic reticulum Ca2+. Inactivation was not detected. Sustained responses were insensitive to inactivation or block of L-type Ca2+ current ( I Ca-L). The voltage dependence of sustained responses was not affected by changes in intracellular or extracellular Na+ concentration. Furthermore, sustained responses were not inhibited by 2 mM Ni2+. Thus it is improbable that I Ca-L or Na+/Ca2+ exchange generated these sustained responses. However, rapid application of 200 μM tetracaine, which blocks the VSRM, strongly inhibited sustained contractions. Our study indicates that the VSRM includes both a phasic inactivating and a sustained noninactivating component. The sustained component contributes both to initiation and relaxation of contraction.

5-hydroxydecanoate inhibits ATP-sensitive K+ channel currents in guinea-pig single ventricular myocytes

1992 ◽  
Vol 220 (1) ◽  
pp. 35-41 ◽  
Author(s):  
Tatsuto Notsu ◽  
Kiyokazu Ohhashi ◽  
Isao Tanaka ◽  
Hiroshi Ishikawa ◽  
Takeshi Niho ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
K Channel ◽  
Single Ventricular Myocytes ◽  
Channel Currents

Voltage-dependent properties of macroscopic and elementary calcium channel currents in guinea pig ventricular myocytes

1986 ◽  
Vol 406 (5) ◽  
pp. 437-448 ◽  
Author(s):  
Terence F. McDonald ◽  
Adolfo Cavali� ◽  
Wolfgang Trautwein ◽  
Dieter Pelzer
Keyword(s):  
Guinea Pig ◽  
Calcium Channel ◽  
Ventricular Myocytes ◽  
Voltage Dependent ◽  
Channel Currents

Caffeine-induced Ca2+ release activates Ca2+ extrusion via Na+-Ca2+ exchanger in cardiac myocytes

1989 ◽  
Vol 257 (1) ◽  
pp. C147-C152 ◽  
Author(s):  
G. Callewaert ◽  
L. Cleemann ◽  
M. Morad
Keyword(s):  
Guinea Pig ◽  
Cardiac Myocytes ◽  
Time Course ◽  
Ventricular Myocytes ◽  
Whole Cell ◽  
Inward Current ◽  
Fura 2 ◽  
Transient Inward Current ◽  
Inward Currents

Rapid application of caffeine in fura-2-dialyzed and whole cell-clamped rat and guinea pig ventricular myocytes activated reversibly large intracellular Ca2+ transients that accompanied Na+-dependent transient inward currents. Such transient inward currents had the same time course as the intracellular Ca2+ transient and were suppressed by Ni2+ and removal of extracellular Na+. Because Ca2+ release signals were not altered by addition of Ni2+ or removal of Na+, we concluded that the rise in intracellular Ca2+ concentration was necessary for the activation of the transient inward current. Thus the caffeine-induced transient inward current represents efflux of Ca2+ via the Na+-Ca2+ exchanger.

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