scholarly journals β‐Adrenergic stimulation modulates Ca 2+ ‐ and voltage‐dependent inactivation of L‐type Ca 2+ channel currents in guinea‐pig ventricular myocytes

2002 ◽  
Vol 541 (3) ◽  
pp. 741-751 ◽  
Author(s):  
Ian Findlay
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Adrenergic Stimulation ◽  
Dependent Inactivation ◽  
Voltage Dependent ◽  
Channel Currents

Phospholamban deficiency alters inactivation kinetics of L-type Ca2+ channels in mouse ventricular myocytes

1997 ◽  
Vol 272 (2) ◽  
pp. H606-H612 ◽  
Author(s):  
H. Masaki ◽  
Y. Sato ◽  
W. Luo ◽  
E. G. Kranias ◽  
A. Yatani
Keyword(s):  
Ventricular Myocytes ◽  
Mammalian Species ◽  
Cardiac Cells ◽  
Inactivation Kinetics ◽  
Compensatory Mechanism ◽  
Channel Inactivation ◽  
Dependent Inactivation ◽  
Voltage Dependent ◽  
Channel Currents ◽  
Ca2 Channels

Entry of Ca2+ through voltage-dependent L-type Ca2+ channels is critical for contraction in cardiac cells. In recent studies, cells from phospholamban (PLB) knockout (PLB-KO) mouse hearts showed significantly increased basal contractility with enhanced sarcoplasmic reticulum (SR) Ca2+ uptake. To test whether these effects of PLB ablation were associated with alterations of L-type Ca2+ channel function, we compared the properties of Ca2+ channel currents (I(Ca)) in ventricular myocytes isolated from wild-type (WT) and PLB-KO mouse hearts. L-type Ca2+ channels from mouse myocytes exhibited voltage-dependent gating and sensitivity to dihydropyridine drugs, similar to other mammalian species, and these properties were not altered by PLB ablation. I(Ca) from both WT and PLB-KO cells revealed two (fast and slow) components of inactivation kinetics. However, the proportion of the faster component was significantly larger in PLB-KO cells. Ryanodine (10 microM) reduced the rate of inactivation of I(Ca) for both WT and PLB-KO cells, but the reduction was more prominent in PLB-KO cells compared with WT cells. In contrast, the inactivation in a Ba2+ solution could be fitted by a single exponential similar to the slower component in Ca2+, and this was not altered in PLB-KO cells. The increase in the fast Ca2+-dependent inactivation component in PLB-KO cells supports the hypothesis that Ca2+ released from the SR regulates Ca2+ channel inactivation by affecting the levels of Ca2+ near the channel and suggests that this may be an important compensatory mechanism in the hyperdynamic PLB-KO heart.

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

Rectification of muscarinic K+ current by magnesium ion in guinea pig atrial cells

1987 ◽  
Vol 253 (1) ◽  
pp. H210-H214
Author(s):  
M. Horie ◽  
H. Irisawa
Keyword(s):  
Guinea Pig ◽  
Action Potentials ◽  
Single Channel ◽  
Outward Current ◽  
Atrial Cells ◽  
Voltage Dependent ◽  
K Current ◽  
Single Channel Currents ◽  
Channel Currents ◽  
Low K

Rectifying properties of the acetylcholine (ACh)-sensitive K+ channels were studied using a patch-clamp method in single atrial cells prepared enzymatically from adult guinea pig hearts. In the presence of micromolar concentration of nonhydrolyzable guanosine 5'-triphosphate (GTP) analogue 5'-guanylylimidodiphosphate (GppNHp) and the absence of Mg2+ at the inner surface of patch membrane [( Mg2+]i), the channel activity recovered in inside-out patch condition. The single channel conductance became ohmic between -80 and +80 mV (symmetrical 150 mM K+ solutions). The rapid relaxation of outward single channel currents was disclosed on a depolarization. [Mg2+]i blocked the outward current through the channel dose- and voltage-dependently and also induced a dose-dependent increase in the channel activation. The apparent paradoxical role of [Mg2+]i is important for the cholinergic control in the heart; voltage-dependent Mg block ensures a low K+ conductance of cell membrane at the plateau of action potentials during the exposure to ACh, thereby slowing the heart rate without unfavorable shortening of the action potentials.

Sign in / Sign up

Export Citation Format

Share Document