help button home button Biophys. J.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

Biophysical Journal 48: 919-930 (1985)
© 1985 the Biophysical Society

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Lebrun, P
Right arrow Articles by Atwater, I
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Lebrun, P
Right arrow Articles by Atwater, I

Effects of the calcium channel agonist, BAY K 8644, on electrical activity in mouse pancreatic B-cells.

P Lebrun and I Atwater

ABSTRACT

We studied the effects of the dihydropyridine derivative BAY K 8644 on the membrane potential of B-cells in mouse pancreatic islets. BAY K 8644, in a dose-dependent manner, decreased the spike frequency but increased the duration of the spikes elicited by glucose with or without quinine or tetraethylammonium (TEA). These effects were antagonized by cobalt and nifedipine but not by tetrodotoxin. The interval between spikes was proportionate to the duration of the spikes and the ratio of the interval to the spike duration was constant at all concentrations of BAY K 8644 tested. Peak inward current, estimated from the derivative of the action potential recorded in the presence of TEA, was increased by BAY K 8644 and decreased by nifedipine. BAY K 8644 elicited spike activity when the membrane was moderately depolarized by either 5.6 mM glucose or 15 mM K+, but did not change the membrane potential of the resting hyperpolarized B-cell. These results suggest that BAY K 8644 acts on the open Ca2+-channels. The threshold occurs at a membrane potential of -50 mV. Also, the modifications of the shape of the spikes appear to reflect specific changes in Ca2+ entry. We propose the existence of a Ca2+-induced Ca2+-channel inactivation process in the pancreatic B-cell.




This article has been cited by other articles:


Home page
Biophys. JHome page
M. Zhang, P. Goforth, R. Bertram, A. Sherman, and L. Satin
The Ca2+ Dynamics of Isolated Mouse {beta}-Cells and Islets: Implications for Mathematical Models
Biophys. J., May 1, 2003; 84(5): 2852 - 2870.
[Abstract] [Full Text] [PDF]


Home page
J. Pharmacol. Exp. Ther.Home page
R. Ouedraogo, Q.-A. Nguyen, M.-H. Antoine, C. Kane, M.J. Dunne, L. Pochet, B. Masereel, and P. Lebrun
Insulinotropic Effect of New Glibenclamide Isosteres
J. Pharmacol. Exp. Ther., May 1, 1999; 289(2): 625 - 631.
[Abstract] [Full Text]


Home page
Mol. Endocrinol.Home page
H. Safayhi, H. Haase, U. Kramer, A. Bihlmayer, M. Roenfeldt, H. P.T. Ammon, M. Froschmayr, T. N. Cassidy, I. Morano, M. K. Ahlijanian, et al.
L-Type Calcium Channels in Insulin-Secreting Cells: Biochemical Characterization and Phosphorylation in RINm5F Cells
Mol. Endocrinol., May 1, 1997; 11(5): 619 - 629.
[Abstract] [Full Text]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1985 by the Biophysical Society.