Screening of cardiotropic substances on a strip of frog myocardium

1985 ◽  
Vol 19 (12) ◽  
pp. 837-842
Author(s):  
N. V. Dmitrieva ◽  
E. I. Shtrasgeim ◽  
G. M. Kitaigorodskaya ◽  
S. S. Kosolapov ◽  
Sh. S. Gil'manov ◽  
...  
Keyword(s):  
Frog Myocardium

Hydrogen sulfide in regulation of frog myocardium contractility

2013 ◽  
Vol 7 (1) ◽  
pp. 52-57 ◽  
Author(s):  
N. N. Khaertdinov ◽  
D. R. Ahmetshina ◽  
A. L. Zefirov ◽  
G. F. Sitdikova
Keyword(s):  
Hydrogen Sulfide ◽  
Frog Myocardium

scholarly journals Location of Ryanodine and Dihydropyridine Receptors in Frog Myocardium

2003 ◽  
Vol 84 (2) ◽  
pp. 1079-1092 ◽  
Author(s):  
Pierre Tijskens ◽  
Gerhard Meissner ◽  
Clara Franzini-Armstrong
Keyword(s):  
Dihydropyridine Receptors ◽  
Frog Myocardium

scholarly journals A photoisomerizable muscarinic antagonist. Studies of binding and of conductance relaxations in frog heart.

1982 ◽  
Vol 79 (4) ◽  
pp. 657-678 ◽  
Author(s):  
J Nargeot ◽  
H A Lester ◽  
N J Birdsall ◽  
J Stockton ◽  
N H Wassermann ◽  
...  
Keyword(s):  
Time Course ◽  
Potassium Conductance ◽  
Resting Potential ◽  
Frog Heart ◽  
Activation Kinetics ◽  
Frog Myocardium ◽  
Data Yield ◽  
Xenon Flashlamp ◽  
The Right ◽  
Kinetics Of

These experiments employ the photoisomerizable compound, 3,3'-bis-[alpha-(trimethylammonium)methyl]azobenzene (Bis-Q), to study the response to muscarinic agents in frog myocardium. In homogenates from the heart, trans-Bis-Q blocks the binding of [3H]-N-methylscopolamine to muscarinic receptors. In voltage-clamped atrial trabeculae, trans-Bis-Q blocks the agonist-induced potassium conductance. The equilibrium dose-response curve for carbachol is shifted to the right, suggesting competitive blockade. Both the biochemical and electrophysiological data yield a dissociation constant of 4-5 microM for trans-Bis-Q; the cis configuration is severalfold less potent as a muscarinic blocker. Voltage-clamped preparations were exposed simultaneously to carbachol and Bis-Q and were subjected to appropriately filtered flashes (less than 1 ms duration) from a xenon flashlamp. Trans leads to cis and cis leads to trans photoisomerizations cause small (less than 20%) increases and decreases, respectively, in the agonist-induced current. The relaxation follows an S-shaped time course, including an initial delay or period of zero slope. The entire waveform is described by [1 - exp(-kt)]n. At 23 degrees C, k is approximately 3 s-1 and n is 2. Neither k nor n is affected when: (a) [Bis-Q] is varied between 5 and 100 microM; (b) [carbachol] is varied between 1 and 50 microM; (c) carbachol is replaced by other agonists (muscarine, acetylcholine, or acetyl-beta-methylcholine); or (d) the voltage is varied between the normal resting potential and a depolarization of 80 mV. However, in the range of 13-30 degrees C, k increases with temperature; the Q10 is between 2 and 2.5. In the same range, n does not change significantly. Like other investigators, we conclude that the activation kinetics of the muscarinic K+ conductance are not determined by ligand-receptor binding, but rather by a subsequent sequence of two (or more) steps with a high activation energy.

scholarly journals Birefringence signals in mammalian and frog myocardium. E-C coupling implications.

1983 ◽  
Vol 82 (1) ◽  
pp. 79-117 ◽  
Author(s):  
R E Weiss ◽  
M Morad
Keyword(s):  
Time Course ◽  
Frog Heart ◽  
Optical Signals ◽  
Mammalian Heart ◽  
Movement Artifact ◽  
Mammalian Myocardium ◽  
Frog Myocardium ◽  
Diffraction Patterns ◽  
Maximum Rate Of Rise ◽  
Frequency Temperature

Birefringence signals from mammalian and frog hearts were studied. The period between excitation and the onset of contraction in which optical signals were free of movement artifact was determined by changes in scattered incandescent light and changes in laser diffraction patterns. The birefringence signal preceding contraction was found to behave as a change in retardation and was not contaminated measurably by linear dichroic or isotropic absorption changes. There were two components of the birefringence signal in mammalian heart muscles but only one component in the frog heart. The first component of the birefringence signals in both mammalian and frog hearts had a time course coincident with the action potential upstroke. The second component in mammalian preparations was sensitive to inotropic interventions, such as variation of extracellular Ca2+, stimulation frequency, temperature, and epinephrine, in a manner that correlated with the maximum rate of rise of tension. Caffeine (2-10 mM) not only failed to generate a second component in the frog heart, but also suppressed the second component in the mammalian heart while potentiating twitch tension. The results suggest that the second component of the birefringence signal in the mammalian myocardium is related to Ca2+ release from the sarcoplasmic reticulum.

scholarly journals Effects of Temperature on Membrane Currents of the Frog Myocardium

1976 ◽  
Vol 52 (7) ◽  
pp. 389-392 ◽  
Author(s):  
Masayosi GOTO ◽  
Masahiko SAITO ◽  
Yoshimi IKEMOTO ◽  
Yasuo TSUDA
Keyword(s):  
Membrane Currents ◽  
Frog Myocardium ◽  
Effects Of Temperature

Effect of Sodium Ions on Calcium-Loaded Rat Heart Mitochondria and Frog Myocardium

2021 ◽  
Vol 57 (6) ◽  
pp. 1241-1250
Author(s):  
S. M. Korotkov ◽  
K. V. Sobol ◽  
I. V. Shemarova ◽  
V. P. Nesterov
Keyword(s):  
Rat Heart ◽  
Heart Mitochondria ◽  
Sodium Ions ◽  
Frog Myocardium ◽  
Rat Heart Mitochondria

Frog ventricle: participation of SR in excitation-contraction coupling

1989 ◽  
Vol 256 (5) ◽  
pp. H1432-H1439
Author(s):  
M. E. Anderson ◽  
I. J. Fox ◽  
C. R. Swayze ◽  
S. K. Donaldson
Keyword(s):  
Steady State ◽  
Sarcoplasmic Reticulum ◽  
Inhibitory Effects ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Resting Tension ◽  
Mammalian Myocardium ◽  
Frog Myocardium ◽  
Frog Ventricle ◽  
Important Site

Activation of the first beat (B1) following a 60-s pause is diminished in isometrically contracting frog ventricular strips, in contrast to the augmentation documented for sarcoplasmic reticulum (SR)-dependent mammalian myocardium. However, treatment of frog ventricular strips with ouabain, an indirect inhibitor of the sarcolemmal Na+-Ca2+ exchanger, selectively enhanced postpause beats suggesting that in the absence of ouabain significant extrusion of cellular Ca2+ occurred during the pause. Because resting tension did not increase during the pause in ouabain-treated strips, the nonextruded Ca2+ must have been sequestered into a compartment such as SR. Steady-state beats were not affected by ouabain; its actions appeared to be separate from its known positive inotropism. Caffeine, a direct SR stimulus, initially enhanced B1 and subsequently decreased activation of all beats, which was consistent with initial augmentation of SR Ca2+ release and subsequent depletion of SR Ca2+ stores. Ouabain both potentiated the stimulatory effects and blocked the inhibitory effects of caffeine, suggesting that ouabain increased Ca2+ stores in the same intracellular Ca2+ pool as that acted on by caffeine, the SR. Ryanodine, an inhibitor of SR in mammalian myocardium, did not affect activation of frog myocardium. SR may be an important site for activator Ca2+ cycling in frog myocardium under control conditions as well as after long diastolic intervals in the presence of ouabain.

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