Vasoactive intestinal polypeptide-augmented insulin release: actions on ionic fluxes and electrical activity of mouse islets

Diabetologia ◽  
1993 ◽  
Vol 36 (10) ◽  
pp. 920-925 ◽  
Author(s):  
M. A. Wahl ◽  
S. G. Straub ◽  
H. P. T. Ammon
Keyword(s):  
Electrical Activity ◽  
Insulin Release ◽  
Vasoactive Intestinal Polypeptide ◽  
Ionic Fluxes ◽  
Mouse Islets ◽  
Intestinal Polypeptide

Insulin release, cGMP, cAMP, and membrane potential in acetylcholine-stimulated islets.

1978 ◽  
Vol 235 (5) ◽  
pp. E493 ◽  
Author(s):  
E Gagerman ◽  
L A Idahl ◽  
H P Meissner ◽  
I B T�ljedal
Keyword(s):  
Membrane Potential ◽  
Cyclic Amp ◽  
Insulin Release ◽  
Cyclic Gmp ◽  
Spike Activity ◽  
Obvious Effect ◽  
Ionic Fluxes ◽  
Mouse Islets ◽  
Silent State ◽  
Esterase Inhibitor

Acetylcholine potentiated the glucose-induced insulin release from microdissected mouse islets of Langerhans but had no effect on basal insulin release. Significant potentiation was obtained with 0.1 micron acetylcholine in the presence of 10 micron eserine and with 1 micron or more acetylcholine in the absence of a choline esterase inhibitor. Carbamylcholine, too, potentiated insulin release. Potentiation was blocked by methylatropine, whereas methylatropine alone had no effect on insulin release. Acetylcholine or carbamylcholine (5-500 micron) had no obvious effect on cyclic GMP or cyclic AMP in the islets. In the presence of 11.1 mM D-glucose, the membrane potential of beta-cells oscillated slowly between a polarized silent state of -50 to -55 mV and a depolarized active state of -33 to -39 mV, at which a fast spike activity occurred. Acetylcholine made the potential stay at the plateau and induced a continuous spike activity pattern. Atropine inhibited the electrical effects of acetylcholine but not those of glucose alone. It is suggested that cholinergic potentiation of insulin release is mediated by changes of transmembrane ionic fluxes, probably without the intervention of cyclic GMP or cyclic AMP.

Dissociation by methylamine of insulin release from glucose-induced electrical activity in isolated mouse islets of Langerhans

Metabolism ◽  
1985 ◽  
Vol 34 (12) ◽  
pp. 1122-1127 ◽  
Author(s):  
P. Lebrun ◽  
I. Atwater ◽  
L.M. Rosario ◽  
A. Herchuelz ◽  
W.J. Malaisse
Keyword(s):  
Electrical Activity ◽  
Insulin Release ◽  
Islets Of Langerhans ◽  
Mouse Islets

Somatostatin inhibition of glucose-induced electrical activity in cultured rat islet cells

1977 ◽  
Vol 233 (5) ◽  
pp. C164-C171 ◽  
Author(s):  
Caroline S. Pace ◽  
Mary Murphy ◽  
Susan Conant ◽  
Paul E. Lacy
Keyword(s):  
Electrical Activity ◽  
Insulin Release ◽  
Spike Activity ◽  
Inhibitory Action ◽  
Islet Cells ◽  
Secretory Response ◽  
Adrenergic Blockade ◽  
Ionic Fluxes ◽  
Electrophysiological Studies ◽  
Stimulus Secretion Coupling

Electrophysiological studies of rat islet cells in monolayer culture were undertaken to determine the role of transmembranous ionic fluxes in the inhibitory action of somatostatin on insulin release. In the presence of somatotropin release inhibiting factor (SRIF) (2.5 nM), hyperpolarization occured with or without glucose (16.6 mM) in the medium. SRIF also inhibited the incidence of glucose-induced spike activity. The inhibitory action of SRIF occurred within 5 min and was readily reversible. An increase in extracellular K+ (5–13 mM) or Ca2+ (2.3–4.6 mM) prevented SRIF inhibition of glucose-induced electrical activity. The secretory response of cultured islets to glucose (16.6 mM) was completely inhibited by SRIF (2.5 nM). The presence of high [Ca2+]0 or [K+]0, enhanced insulin release in the presence of SRIF and glucose. Although phentolamine (5.0 μg/ml) did not block the inhibition of glucose-induced electrical responses by SRIF, it prevented the inhibitory action of epinephrine (0.2 μg/ml). It is concluded that the primary action of SRIF is to alter transmembranous cationic fluxes, as manifested by hyperpolarization and a decrease in the incidence of spike activity, which may prevent glucose from eliciting a normal secretory response. insulin secretion; epinephrine; alpha-adrenergic blockade; stimulus-secretion coupling Submitted on February 14, 1977

Intracellular electrical activity of muscularis mucosae of the dog stomach

1985 ◽  
Vol 249 (2) ◽  
pp. G256-G263 ◽  
Author(s):  
K. G. Morgan ◽  
F. Angel ◽  
P. F. Schmalz ◽  
J. H. Szurszewski
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Electrical Activity ◽  
Vasoactive Intestinal Polypeptide ◽  
Mechanical Activity ◽  
Field Stimulation ◽  
Muscularis Mucosae ◽  
Spike Potential ◽  
Stimulation Of ◽  
Intestinal Polypeptide

Mechanical and intracellular electrical activity was recorded simultaneously in vitro from smooth muscle of the muscularis mucosae of the canine antrum. The intracellularly recorded membrane potential averaged -51 +/- 1.4 mV (mean +/- SE). Spontaneous electrical activity consisted of spike-shaped potentials that were 20–40 mV in amplitude. The rate of rise of the spike potential was slow (less than 0.2 V/s) and the half-time duration was long (0.5-5.0 s). Phasic contractions were often but not always coupled with spike potentials. Ion substitution studies suggested that the spike potential had a greater dependence on Na+ than on Ca2+. Field stimulation of intramural nerves hyperpolarized the membrane potential and abolished spikes or reduced their amplitude and frequency. These changes were associated with a reduction in tone and phasic contractile activity. The response to stimulation of inhibitory nerves was mimicked by epinephrine, neurotensin, and vasoactive intestinal polypeptide. The resistance to adrenergic blocking agents ruled out the possibility of norepinephrine as the transmitter. The tetrodotoxin sensitivity of the response to neurotensin suggests that neurotensin acts indirectly through the inhibitory nerves. Mimicry between the action of applied vasoactive intestinal polypeptide (VIP) and field stimulation provides support for the hypothesis that VIP may be an inhibitory neurotransmitter. These studies indicate that smooth muscle in the canine gastric muscularis mucosae generates spontaneous electrical and mechanical activity and receives a noncholinergic, nonadrenergic inhibitory innervation.

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