Presynaptic effect of muscle relaxants on the release of3H-norepinephrine controlled by endogenous acetylcholine in guinea pig atrium

1989 ◽  
Vol 76 (3) ◽  
pp. 169-180 ◽  
Author(s):  
F. F. Földes ◽  
O. Kobayashi ◽  
M. Kinjo ◽  
L. G. Harsing ◽  
H. Nagashima ◽  
...  

1990 ◽  
Vol 31 (1-2) ◽  
pp. 23-35 ◽  
Author(s):  
M. J. Krielaart ◽  
D. M. J. Veenstra ◽  
K. J. H. Buuren


1988 ◽  
Vol 255 (4) ◽  
pp. C479-C485 ◽  
Author(s):  
H. Nunez-Duran ◽  
L. Riboni ◽  
E. Ubaldo ◽  
E. Kabela ◽  
L. Barcenas-Ruiz

Mammalian cells specifically internalize some molecular species through receptor-mediated endocytosis (RME). We have used four different experimental protocols to investigate whether ouabain enters cardiac cells of guinea pig atrium through this pathway. First, by electron microscope morphometry we found that ouabain increased endocytic vesicles in atrial cells. Second, by scintillation counting we found that [3H]ouabain uptake by the tissue is decreased by three treatments that decrease RME, i.e., NH4Cl, trifluoperazine, and 16 mM [K+]0. Third, by radioautography at the electron microscope level, we checked that in preceding experiments [3H]ouabain was washed out of plasma membrane after 60-min rinse and interiorized into the cardiac cells. Fourth, isometric tension recordings showed that the positive inotropic effect of ouabain was diminished in the presence of inhibitors, whereas that of a hydrophobic analogue, ouabagenin, was not affected. These results suggest that ouabain enters cardiac cells through RME and also that an intracellular site may, at least in part, be responsible for its inotropic effect.



1969 ◽  
Vol 54 (4) ◽  
pp. 494-511 ◽  
Author(s):  
Gerald R. Little ◽  
William W. Sleator

A Krebs-Henseleit (KH) medium made hypertonic by adding nonpermeant molecules substantially increased the isometric peak tension at steady-state contractions below 3 per sec in guinea pig atrium at 27°C. Action potential durations were decreased. KH plus 100 mM raffinose or sucrose resulted in similar and nearly maximal changes which were essentially reversible upon return to normal KH. When one active contracting atrium was used to passively stretch a second atrium, the difference in Ca ion exchange (1 min exchange with the extracellular space) between active and stretched atria significantly increased at 1 per sec and at 2 per sec in going from normal to 100 mM hypertonic KH. The calculated mean Ca ion cellular exchange per beat per 100 g of cells (a) doubled in changing from normal to 100 mM hypertonic KH, and (b) decreased slightly in changing from contractions of 1 per sec to 2 per sec in normal KH. These data are consistent with the hypothesis (a) that Ca ion entry per beat from the extracellular space is proportional to membrane depolarized time with a constant medium and a steady-state condition, and the hypothesis (b) that 100 mM hypertonicity doubles the Ca ion entry rate during depolarization. These data enable rejection of the hypothesis that the peak tension is proportional to the Ca ion entry per beat from the extracellular space under steady-state conditions, and suggest that any additional Ca ion involved in the larger contractions at higher frequencies comes from an increase in Ca ion available from intracellular stores.



Abstracts ◽  
1977 ◽  
pp. 489
Author(s):  
A. G . Garcia ◽  
J. Gonzalez-Lopez ◽  
P. San-chez-Garcia ◽  
R. Pascual


1977 ◽  
Vol 233 (2) ◽  
pp. H203-H210
Author(s):  
R. B. Robinson ◽  
W. W. Sleator

The activation process in isolated electrically driven guinea pig atria was studied by means of simultaneous microelectrode and tension recording. Reducing external calcium from 2.5 to 1.25 mM prolonged the plateau but further reduction of calcium shortened it. Progressively increasing doses of the calcium antagonist D600 (up to 1.4 micrometer), however, monotonically decreased plateau duration. Either protocol monotonically decreased steady-state tension, but with markedly different effects on the restitution relation. Epinephrine, and to a lesser extent isoproterenol, restored plateau duration after exposure to either a calcium-free or D600-containing solution, but only the isoproterenol effect was propranolol sensitive. Addition of calcium chelators enhanced rather than prevented the effect of epinephrine on plateau duration in a calcium-free solution, extending the plateau duration to more than 3 times normal in some cases. These results are explained in terms of two opposing effects of a change in calcium concentration on plateau formation, one action being through the slow inward current and the second through a shift in a calcium dependence of the inward-rectifying, potassium conductance system.



2009 ◽  
Vol 458 (5) ◽  
pp. 837-849 ◽  
Author(s):  
Dimitar P. Zankov ◽  
Futoshi Toyoda ◽  
Mariko Omatsu-Kanbe ◽  
Hiroshi Matsuura ◽  
Minoru Horie


2016 ◽  
Vol 67 (4) ◽  
pp. 523-529 ◽  
Author(s):  
Denis V. Abramochkin ◽  
Viktoria M. Karimova ◽  
Tatiana S. Filatova ◽  
Andre Kamkin


1997 ◽  
Vol 321 (1) ◽  
pp. 27-31 ◽  
Author(s):  
Hiroaki Nishio ◽  
Yukiko Morimoto ◽  
Tomomi Nuibe ◽  
Akiko Fujii ◽  
Yoshihiro Nakata


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