pH Related Potassium Movements in Rabbit Atrium

Author(s):  
Diana L. Kunze ◽  
John M. Russell
Keyword(s):  
1978 ◽  
Vol 28 ◽  
pp. 93
Author(s):  
Shigeyuki Ando ◽  
Junji Toyama ◽  
Kazuo Yamada

1988 ◽  
Vol 24 (2-3) ◽  
pp. 287-302 ◽  
Author(s):  
J.S. Pasnani ◽  
K.G. Hemavathi ◽  
O.D. Gulati ◽  
A.P. Rajani
Keyword(s):  

Nature ◽  
1965 ◽  
Vol 205 (4973) ◽  
pp. 808-809 ◽  
Author(s):  
NOBORU TODA ◽  
THEODORE C. WEST

1981 ◽  
Vol 240 (4) ◽  
pp. H576-H583 ◽  
Author(s):  
D. M. Bers ◽  
K. D. Philipson ◽  
G. A. Langer

Striking correlations are found between cardiac contractility and Ca2+ binding to isolated cardiac sarcolemma in rabbit, neonatal rat, and frog ventricular tissue. Deviations from this correlation are seen in the adult rat ventricle and rabbit atrium. The observation of this correlation in the three former tissues and under various ionic conditions suggests that this correlation is not coincidental and that Ca2+ bound to the cardiac sarcolemma is of major importance in the control of myocardial contractility. The data are consistent with a functional Ca2+-induced Ca2+ release system in the sarcoplasmic reticulum (SR) of all the tissues (which is controlled by Ca2+ entry from sarcolemmal sites), with the adult rat ventricular and rabbit atrial SR Ca2+ release being much more sensitive to CA2+. It is suggested that the frog, neonatal rat, and rabbit ventricles depend more directly on the entry of Ca2+ from sarcolemmal sites for the control of tension development, whereas the adult rat ventricle and rabbit atrium depend to a greater extent on CA2+ released from the SR.


Author(s):  
Maurits A. Allessie ◽  
Felix I. M. Bonke ◽  
Francien J. G. Schopman
Keyword(s):  

1991 ◽  
Vol 260 (5) ◽  
pp. H1737-H1742 ◽  
Author(s):  
Y. Gotoh ◽  
Y. Imaizumi ◽  
M. Watanabe ◽  
E. F. Shibata ◽  
R. B. Clark ◽  
...  

The 1,4-dihydropyridine (DHP) Ca2+ antagonists and agonists can inhibit a time- and voltage-dependent, but intracellular Ca(2+)-independent transient outward K+ current (It), in myocytes from rabbit atrium. In the presence of 0.3 mM CdCl2, DHPs decreased the peak It slightly and markedly accelerated its apparent rate of inactivation. When the inhibition of It was measured from integrated It records, the 50% inhibitory concentrations (IC50) of nicardipine and BAY K 8644 were 630 nM and 7 microM, respectively, and the IC50 of nicardipine for inhibition of the Ca2+ current (ICa) was only approximately fourfold lower (160 nM). The inhibition of It by nicardipine was not affected by changing holding potential from -55 to -100 mV; in contrast, the inhibitory effect on ICa was significantly reduced by this hyperpolarization. We conclude that the DHP Ca2+ antagonist nicardipine blocks It at similar doses to those that block ICa and that nicardipine blocks this K+ current by mechanism different from that for ICa inhibition. This inhibitory effect on It is shared by other DHP compounds; the rank order for potency of It inhibition is nicardipine greater than benidipine greater than nisoldipine greater than BAY K 8644 greater than nitrendipine greater than nifedipine.


2008 ◽  
Vol 9 (3) ◽  
pp. 125-132 ◽  
Author(s):  
Roman Laszlo ◽  
Christian Eick ◽  
Norman Rueb ◽  
Slawomir Weretka ◽  
Hans-Joerg Weig ◽  
...  

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