1. The mechanisms that control release of Ca$^2+$ from the sarcoplasmic
reticulum (SR) of guinea-pig ventricular cells were studied by observing
intracellular calcium concentration (Ca$^2+$i transients) and
membrane currents in voltage-clamped guinea-pig ventricular myocytes
perfused internally with Fura-2. 2. Sarcolemmal Ca$^2+$ current
was identified through the use of tetrodotoxin (TTX) and Ca$^2+$
channel antagonists (verapamil) and agonists (Bay K 8644). 3. Changes
in Ca$^2+$i attributable to release of Ca$^2+$ from the
SR were identified through the use of ryanodine, which abolishes
the ability of the SR to release Ca$^2+$. Ryanodine-sensitive
increases in Ca$^2+$i could be elicited either by depolarization
or by repolarization (from depolarizing pulses to relatively positive
membrane potentials). 4. At appropriate voltages, it is the initial
fast change in Ca$^2+$i elicited by either depolarization or
repolarization that is abolished by ryanodine, and is defined here
as ryanodine sensitive. 5. The amplitude of the ryanodine-sensitive
Ca$^2+$i transient elicited by depolarization had a bell-shaped
dependence on membrane potential with a maximum of about 500 nM at
10 mV, and with the upper minimum between 60 and 70 mV. Verapamil-sensitive
current activated over approximately the same potential range as
the Ca$^2+$i transient, with a peak amplitude at 10 mV, and
a reversal potential of 65 mV. 6. When a holding potential of -68
mV and TTX (30 microM) were used, the most negative pulse potential
at which activation of an inward current occurred was -49 mV while
changes in Ca$^2+$i occurred at -43 mV. 7. Ryanodine-sensitive
increases in Ca$^2+$i elicited by repolarization (tail transients)
were maximal for repolarization to 0 mV. Smaller changes in Ca$^2+$i
than maximal were elicited by repolarization to both more positive
and more negative potentials than 0 mV. The peak amplitude of the
verapamil-sensitive tail currents elicited by repolarization increased
continuously as the membrane was repolarized to potentials more negative
than 60 mV. 8. Increasing depolarizing pulse duration beyond 10-20
ms did not increase the amplitude of the Ca$^2+$i transient,
but prolonged it. 9. The experimental results are compared to the
predictions of two theories on the mechanism of excitation-contraction
coupling: Ca$^2+$-induced release of Ca$^2+$ (CICR), as it
has been formulated from data in skinned cardiac cells, and a charge-coupled
release mechanism (CCRM), as it has been formulated to explain
excitation-contraction coupling in skeletal muscle. 10. Some of the
results are clearly not consistent with certain features of a charge-coupled
release mechanism.(ABSTRACT TRUNCATED AT 400 WORDS)
%0 Journal Article
%1 Beuc_1988_233
%A Beuckelmann, D. J.
%A Wier, W. G.
%D 1988
%J J. Physiol.
%K , 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, 2475607 3-Pyridinecarboxylic Action Animals, Calcium, Carrier Cells, Concentration, Cultured, Electrophysiology, Exchanger, Gov't, Guinea In Intracellular Mathematics, Membrane Membranes, Methyl Myocardium, Nickel, Non-U.S. Osmolar P.H.S., Pigs, Potentials, Proteins, Research Reticulum, Ryanodine, Sarcolemma, Sarcoplasmic Sodium-Calcium Support, Tetrodotoxin, U.S. Verapamil, Vitro, acid, ester,
%P 233--255
%T Mechanism of release of calcium from sarcoplasmic reticulum of guinea-pig
cardiac cells.
%V 405
%X 1. The mechanisms that control release of Ca$^2+$ from the sarcoplasmic
reticulum (SR) of guinea-pig ventricular cells were studied by observing
intracellular calcium concentration (Ca$^2+$i transients) and
membrane currents in voltage-clamped guinea-pig ventricular myocytes
perfused internally with Fura-2. 2. Sarcolemmal Ca$^2+$ current
was identified through the use of tetrodotoxin (TTX) and Ca$^2+$
channel antagonists (verapamil) and agonists (Bay K 8644). 3. Changes
in Ca$^2+$i attributable to release of Ca$^2+$ from the
SR were identified through the use of ryanodine, which abolishes
the ability of the SR to release Ca$^2+$. Ryanodine-sensitive
increases in Ca$^2+$i could be elicited either by depolarization
or by repolarization (from depolarizing pulses to relatively positive
membrane potentials). 4. At appropriate voltages, it is the initial
fast change in Ca$^2+$i elicited by either depolarization or
repolarization that is abolished by ryanodine, and is defined here
as ryanodine sensitive. 5. The amplitude of the ryanodine-sensitive
Ca$^2+$i transient elicited by depolarization had a bell-shaped
dependence on membrane potential with a maximum of about 500 nM at
10 mV, and with the upper minimum between 60 and 70 mV. Verapamil-sensitive
current activated over approximately the same potential range as
the Ca$^2+$i transient, with a peak amplitude at 10 mV, and
a reversal potential of 65 mV. 6. When a holding potential of -68
mV and TTX (30 microM) were used, the most negative pulse potential
at which activation of an inward current occurred was -49 mV while
changes in Ca$^2+$i occurred at -43 mV. 7. Ryanodine-sensitive
increases in Ca$^2+$i elicited by repolarization (tail transients)
were maximal for repolarization to 0 mV. Smaller changes in Ca$^2+$i
than maximal were elicited by repolarization to both more positive
and more negative potentials than 0 mV. The peak amplitude of the
verapamil-sensitive tail currents elicited by repolarization increased
continuously as the membrane was repolarized to potentials more negative
than 60 mV. 8. Increasing depolarizing pulse duration beyond 10-20
ms did not increase the amplitude of the Ca$^2+$i transient,
but prolonged it. 9. The experimental results are compared to the
predictions of two theories on the mechanism of excitation-contraction
coupling: Ca$^2+$-induced release of Ca$^2+$ (CICR), as it
has been formulated from data in skinned cardiac cells, and a charge-coupled
release mechanism (CCRM), as it has been formulated to explain
excitation-contraction coupling in skeletal muscle. 10. Some of the
results are clearly not consistent with certain features of a charge-coupled
release mechanism.(ABSTRACT TRUNCATED AT 400 WORDS)
@article{Beuc_1988_233,
abstract = {1. The mechanisms that control release of {C}a$^{2+}$ from the sarcoplasmic
reticulum (SR) of guinea-pig ventricular cells were studied by observing
intracellular calcium concentration ([{C}a$^{2+}$]i transients) and
membrane currents in voltage-clamped guinea-pig ventricular myocytes
perfused internally with Fura-2. 2. Sarcolemmal {C}a$^{2+}$ current
was identified through the use of tetrodotoxin ({TTX}) and {C}a$^{2+}$
channel antagonists (verapamil) and agonists (Bay K 8644). 3. Changes
in [{C}a$^{2+}$]i attributable to release of {C}a$^{2+}$ from the
SR were identified through the use of ryanodine, which abolishes
the ability of the SR to release {C}a$^{2+}$. Ryanodine-sensitive
increases in [{C}a$^{2+}$]i could be elicited either by depolarization
or by repolarization (from depolarizing pulses to relatively positive
membrane potentials). 4. At appropriate voltages, it is the initial
fast change in [{C}a$^{2+}$]i elicited by either depolarization or
repolarization that is abolished by ryanodine, and is defined here
as ryanodine sensitive. 5. The amplitude of the ryanodine-sensitive
[{C}a$^{2+}$]i transient elicited by depolarization had a bell-shaped
dependence on membrane potential with a maximum of about 500 nM at
10 mV, and with the upper minimum between 60 and 70 mV. Verapamil-sensitive
current activated over approximately the same potential range as
the [{C}a$^{2+}$]i transient, with a peak amplitude at 10 mV, and
a reversal potential of 65 mV. 6. When a holding potential of -68
mV and {TTX} (30 microM) were used, the most negative pulse potential
at which activation of an inward current occurred was -49 mV while
changes in [{C}a$^{2+}$]i occurred at -43 mV. 7. Ryanodine-sensitive
increases in [{C}a$^{2+}$]i elicited by repolarization (tail transients)
were maximal for repolarization to 0 mV. Smaller changes in [{C}a$^{2+}$]i
than maximal were elicited by repolarization to both more positive
and more negative potentials than 0 mV. The peak amplitude of the
verapamil-sensitive tail currents elicited by repolarization increased
continuously as the membrane was repolarized to potentials more negative
than 60 mV. 8. Increasing depolarizing pulse duration beyond 10-20
ms did not increase the amplitude of the [{C}a$^{2+}$]i transient,
but prolonged it. 9. The experimental results are compared to the
predictions of two theories on the mechanism of excitation-contraction
coupling: {C}a$^{2+}$-induced release of {C}a$^{2+}$ (CICR), as it
has been formulated from data in skinned cardiac cells, and a charge-coupled
release mechanism ({CCRM}), as it has been formulated to explain
excitation-contraction coupling in skeletal muscle. 10. Some of the
results are clearly not consistent with certain features of a charge-coupled
release mechanism.(ABSTRACT TRUNCATED AT 400 WORDS)},
added-at = {2009-06-03T11:20:58.000+0200},
author = {Beuckelmann, D. J. and Wier, W. G.},
biburl = {https://www.bibsonomy.org/bibtex/245a2b5b9e8d42ae50331728b939f89cf/hake},
description = {The whole bibliography file I use.},
interhash = {0289ff5c93c3f33a22e0fef19d653a27},
intrahash = {45a2b5b9e8d42ae50331728b939f89cf},
journal = {J. Physiol.},
key = 99,
keywords = {, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, 2475607 3-Pyridinecarboxylic Action Animals, Calcium, Carrier Cells, Concentration, Cultured, Electrophysiology, Exchanger, Gov't, Guinea In Intracellular Mathematics, Membrane Membranes, Methyl Myocardium, Nickel, Non-U.S. Osmolar P.H.S., Pigs, Potentials, Proteins, Research Reticulum, Ryanodine, Sarcolemma, Sarcoplasmic Sodium-Calcium Support, Tetrodotoxin, U.S. Verapamil, Vitro, acid, ester,},
month = Nov,
pages = {233--255},
pmid = {2475607},
timestamp = {2009-06-03T11:21:03.000+0200},
title = {Mechanism of release of calcium from sarcoplasmic reticulum of guinea-pig
cardiac cells.},
volume = 405,
year = 1988
}