Bile canalicular contraction and dilatation in primary culture of rat hepatocytes - possible involvement of two different types of plasma membrane Ca 2+ -Mg 2+ -ATPase and Ca 2+ -pump-ATPase

2001 ◽  
Vol 34 (2) ◽  
pp. 115-122 ◽  
Author(s):  
H. Yokomori ◽  
Masaya Oda ◽  
Yoshitaka Kamegaya ◽  
Mariko Ogi ◽  
Nobuhiro Tsukada ◽  
...  
1991 ◽  
Vol 261 (5) ◽  
pp. G803-G809 ◽  
Author(s):  
J. G. Fitz ◽  
S. D. Lidofsky ◽  
M. H. Xie ◽  
M. Cochran ◽  
B. F. Scharschmidt

Na(+)-coupled HCO3- transport has been demonstrated in the basolateral membrane of hepatocytes, but there is uncertainty regarding its stoichiometry or capacity compared with other mechanisms of H(+)-HCO3- transport. After preincubation in medium free of Na+, either in the presence or absence of HCO3(-)-CO2, rat hepatocytes in primary culture were reexposed to Na+ or HCO3(-)-CO2 alone or in combination. Transporter electrogenicity was assessed by measuring membrane potential difference (PD), and the relative capacities of Na(+)-coupled HCO3- transport, Cl(-)-HCO3- exchange, and Na(+)-H+ exchange were assessed by measuring the magnitude and rate of change of intracellular pH (pHi) using BCECF. In the absence of Na+, exposure to HCO3- alone had no consistent effect on PD or pHi. In the absence of HCO3-, reexposure to Na+ depolarized cells by 3 +/- 1 mV and caused an amiloride-inhibitable increase in pHi of 0.031 +/- 0.02 units/min. In the presence of HCO3-, reexposure to Na+ hyperpolarized cells by -14 +/- 5 mV and increased pHi at a rate of 0.133 +/- 0.11 units/min; both the hyperpolarization and alkalinization were inhibited by SITS but unaffected by amiloride. These changes in PD indicate that Na(+)-coupled HCO3- transport is electrogenic, consistent with coupling of more than one HCO3- to each Na+. Furthermore, SITS-inhibitable Na(+)-dependent alkalinization exceeds amiloride-inhibitable Na(+)-dependent alkalinization by an order of magnitude, suggesting that the transport capacity of Na(+)-coupled HCO3- transport exceeds that of Na(+)-H+ exchange.(ABSTRACT TRUNCATED AT 250 WORDS)


Diabetes ◽  
1991 ◽  
Vol 40 (4) ◽  
pp. 462-464 ◽  
Author(s):  
M. Miralpeix ◽  
J. F. Decaux ◽  
A. Kahn ◽  
R. Bartrons

1981 ◽  
Vol 256 (22) ◽  
pp. 11677-11683
Author(s):  
B. Grandchamp ◽  
D.M. Bissell ◽  
V. Licko ◽  
R. Schmid

1978 ◽  
Vol 40 (02) ◽  
pp. 212-218 ◽  
Author(s):  
P Massini ◽  
R Käser-Glanzmann ◽  
E F Lüscher

SummaryThe increase of the cytoplasmic Ca-concentration plays a central role in the initiation of platelet activation. Four kinds of movements of Ca-ions are presumed to occur during this process: a) Ca-ions liberated from membranes induce the rapid shape change, b) Vesicular organelles release Ca-ions into the cytoplasm which initiate the release reaction, c) The storage organelles called dense bodies, secrete their contents including Ca-ions to the outside during the release reaction, d) At the same time a rearrangement of the plasma membrane occurs, resulting in an increase in its permeability for Ca-ions as well as in an increase in the number of Ca-binding sites.Since most processes occurring during platelet activation are reversible, the platelet must be equipped with a mechanism which removes Ca-ions from the cytoplasm. A vesicular fraction obtained from homogenized platelets indeed accumulates Ca actively. This Ca- pump is stimulated by cyclic AMP and protein kinase; it may be involved in the recovery of platelets after activation.It becomes increasingly clear that the various manifestations of platelet activation are triggered by a rise in the cytoplasmic Ca2+-concentration. The evidence for this and possible mechanisms involved are discussed in some detail in the contributions by Detwiler et al. and by Gerrard and White to this symposium. In this article we shall discuss four different types of mobilization of Ca-ions which occur in the course of the activation of platelets. In addition, at least one transport step involved in the removal of Ca2+ must occur during relaxation of activated platelets.


1992 ◽  
Vol 10 (3) ◽  
pp. 205-215 ◽  
Author(s):  
Scott L. Nyberg ◽  
Russell A. Shatford ◽  
William D. Payne ◽  
Wei-Shou Hu ◽  
Frank B. Cerra

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