Mechanism of action of H2-antagonists on histamine-or dimaprit-stimulated H2-receptors of spontaneously beating guinea-pig atrium

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

1970 ◽  
Vol 245 (23) ◽  
pp. 6424-6435 ◽  
Author(s):  
S.I. Chung ◽  
R.I. Shrager ◽  
J.E. Folk


1967 ◽  
Vol 242 (11) ◽  
pp. 2615-2621 ◽  
Author(s):  
J.E. Folk ◽  
P.W. Cole ◽  
J.P. Mullooly


1975 ◽  
Vol 24 (11-12) ◽  
pp. 1215-1219 ◽  
Author(s):  
Ivone Bareicha ◽  
M.Rocha e Silva
Keyword(s):  


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.







2010 ◽  
Vol 62 (2) ◽  
pp. e23
Author(s):  
Brigitte G.P. Loenders ◽  
Jan Verrelst ◽  
Hua Rong Lu ◽  
Eddy Vlaminckx ◽  
Jutta Rohrbacher ◽  
...  


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