scholarly journals Bradykinin enhances membrane electrical activity of pancreatic beta cells in the presence of low glucose concentrations

2000 ◽  
Vol 33 (9) ◽  
pp. 1089-1092 ◽  
Author(s):  
A.S. Moura
Keyword(s):  
Electrical Activity ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Low Glucose

Contributions of modeling to understanding stimulus-secretion coupling in pancreatic beta-cells

1996 ◽  
Vol 271 (2) ◽  
pp. E362-E372 ◽  
Author(s):  
A. Sherman
Keyword(s):  
Electrical Activity ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Electrical Coupling ◽  
Calcium Handling ◽  
Isolated Cells ◽  
Ionic Fluxes ◽  
Pancreatic Islets Of Langerhans ◽  
Stimulus Secretion Coupling ◽  
Model Independent

Mechanisms of ionic control of insulin secretion in beta-cells of the pancreatic islets of Langerhans are reviewed. The focus is on aspects that have been treated by mathematical models, especially those related to bursting electrical activity. The study of these mechanisms is difficult because of the need to consider ionic fluxes, calcium handling, metabolism, and electrical coupling with other cells in the islet. The data come either from islets, where experimental maneuvers tend to have multiple effects, or from isolated cells, which have degraded electrical activity and secretory sensitivity. Modeling aids in the process by integrating data on individual components such as channels and calcium handling and testing hypotheses for coherence and quantitative plausibility. The study of a variety of models has led to some general mathematical results that have yielded qualitative model-independent insights.

scholarly journals A role for calcium release-activated current (CRAC) in cholinergic modulation of electrical activity in pancreatic beta-cells

1995 ◽  
Vol 68 (6) ◽  
pp. 2323-2332 ◽  
Author(s):  
R. Bertram ◽  
P. Smolen ◽  
A. Sherman ◽  
D. Mears ◽  
I. Atwater ◽  
...  
Keyword(s):  
Electrical Activity ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Calcium Release ◽  
Cholinergic Modulation

Effects of amino acids on membrane potential and 86Rb+ fluxes in pancreatic beta-cells

1981 ◽  
Vol 240 (3) ◽  
pp. E245-E252 ◽  
Author(s):  
J. C. Henquin ◽  
H. P. Meissner
Keyword(s):  
Amino Acids ◽  
Membrane Potential ◽  
Carboxylic Acid ◽  
Electrical Activity ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Intrinsic Property ◽  
Free Medium ◽  
Potassium Permeability ◽  
Mouse Islets

The membrane potential of beta-cells was studied with microelectrodes in mouse islets and their potassium permeability was evaluated by measuring 86Rb+ fluxes in rat islets. In the absence of glucose, L-leucine, its metabolite ketoisocaproate, and its nonmetabolized analogue 2-aminonorbornane-2-carboxylic acid (BCH) depolarized beta-cells and triggered bursts of electrical activity like glucose. The effect of leucine was weak, but was potentiated by a low concentration of glucose or by theophylline; the effect of ketoisocaproate was stronger and faster than that of an equimolar concentration of glucose. Arginine alone produced only a fast depolarization of beta-cells, insufficient to trigger electrical activity. Leucine and arginine potentiated the activity induced by glucose. In a glucose-free medium, alanine only slightly depolarized beta-cells, whereas isoleucine and phenylalanine had no effect. Leucine, ketoisocaproate, and BCH reversibly decreased 86Rb+ efflux from islets perifused in the absence of glucose and increased 86Rb+ uptake. By contrast, both in the absence or presence of glucose, arginine increased 86Rb+ efflux and decreased 86Rb+ uptake. It is proposed that leucine, ketoisocaproate, and BCH, as glucose, depolarize beta-cells by decreasing their potassium permeability, whereas arginine acts differently. The appearance of bursts of electrical activity with secretagogues unrelated to glucose suggests that they reflect an intrinsic property of the beta-cell membrane.

Membrane and intracellular effects of adenosine in mouse pancreatic beta-cells

1989 ◽  
Vol 257 (4) ◽  
pp. E473-E478 ◽  
Author(s):  
G. Bertrand ◽  
P. Petit ◽  
M. Bozem ◽  
J. C. Henquin
Keyword(s):  
Electrical Activity ◽  
Beta Cells ◽  
Insulin Release ◽  
Pancreatic Beta Cells ◽  
Cell Function ◽  
Islet Cells ◽  
Pancreatic Beta Cell ◽  
Nucleoside Transport ◽  
High Concentration ◽  
Pancreatic Beta Cell Function

Mouse islets were used to study the effects of adenosine and its stable analogue L-N6-phenylisopropyladenosine (L-PIA) on pancreatic beta-cell function. At a high concentration (500 microM), adenosine augmented glucose-induced electrical activity in beta-cells and potentiated insulin release. These effects were prevented by the inhibitor of nucleoside transport nitrobenzylthioguanosine. They probably result from the metabolism of adenosine by beta-cells. At a lower concentration (50 microM), adenosine caused a small and transient inhibition of glucose-induced electrical activity and insulin release. L-PIA (10 microM) slightly and transiently inhibited insulin release, 45Ca efflux and 86Rb efflux from islet cells, and decreased electrical activity in beta-cells. When adenylate cyclase was stimulated by forskolin in the presence of 15 mM glucose, insulin release was strongly augmented. Under these conditions, L-PIA and adenosine (with nitrobenzylthioguanosine) caused a sustained inhibition. No such inhibition was observed when insulin release was potentiated by dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP). These data are consistent with the existence of A1 purinergic receptors on mouse beta-cells. They could mainly serve to attenuate the amplification of insulin release brought about by agents acting via cAMP.

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