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Biomedical subjects

E K Matthews

Publications and source records attributed to E K Matthews.

At least 73 records · Page 4Linked to original sources
PubMed1972

Control of pancreatic amylase release in vitro: effects of ions, cyclic AMP, and colchicine.

1. The time course and concentration-response relationship of amylase release from pieces of guinea-pig pancreas in vitro in response to bethanechol and pancreozymin was determined.2. Removal of Ca(++) from the medium had no effect on basal amylase release but abolished the stimulating effect on release of bethanechol.3. Elevation of the concentration of Mg(++) in the medium increased basal amylase release and reduced the response to bethanechol.4. Elevation of the concentration of K(+) in the medium increased amylase release; this effect was blocked by a concentration of atropine which blocked also the response to bethanechol.5. Cyclic AMP, dibutyryl cyclic AMP and theophylline failed to stimulate amylase release. Pancreatic cyclic AMP concentrations were found not to be increased by bethanechol, pancreozymin or an elevated concentration of K(+) in the medium.6. Colchicine had no effect on basal amylase release or the response to bethanechol or pancreozymin.7. It is concluded that the coupling of stimulus to secretion involves ionic control but that neither cyclic AMP production nor microtubular mechanisms play a major role in controlling exocytosis in the pancreatic acinar cell. These findings are discussed in relation to the stimulus-secretion coupling processes in other cells.

Amylases↗
PubMed1972

Pancreatic acinar cells: measurement of membrane potential and miniature depolarization potentials.

1. Intracellular recordings of membrane potentials have been made in vitro from the exocrine acinar cells of the mouse pancreas using glass micro-electrodes.2. The mean membrane potential of the acinar cells was -41.2 mV. Spontaneous miniature depolarization potentials of 0.5-5.0 mV amplitude and occurring at random intervals were often observed superimposed upon the resting membrane potential. Atropine 2.8 x 10(-6)M decreased, and physostigmine 1.23 x 10(-5)M increased, the frequency and amplitude of the miniature potentials.3. Electrical stimulation of the pancreatic nerves depolarized the acinar cells. Acetyl beta-methylcholine 10(-6)M produced a sustained depolarization. Atropine 1.4 x 10(-6)M blocked the depolarization to both electrical stimulation and acetyl beta-methylcholine.4. Pancreozymin depolarized the exocrine acinar cells but secretin did not.5. These results suggest that the miniature depolarization potentials are of cholinergic origin and that depolarization of the pancreatic exocrine cells by nerve stimulation or pancreozymin may trigger secretion.

Animals↗
PubMed1970

Glucose-induced electrical activity in pancreatic islet cells.

1. Intracellular recording of the transmembrane potential in mouse pancreatic cells revealed a membrane potential of -20.1 +/- 0.8 mV for islet cells and -41.2 +/- 1.4 mV for acinar cells.2. The membrane potential of islet cells was glucose dependent and in the absence of glucose the cells hyperpolarized to -32.7 mV; with glucose 27.7 mM they depolarized to -16.1 mV.3. Above a threshold concentration of glucose (4 mM) small action potentials of amplitude 1-4 mV were induced in islet cells. The percentage of cells impaled exhibiting action potentials reached a maximum of 80% at 27.7 mM glucose.4. Mannose 16.6 mM was similar to glucose in its ability to induce action potential discharge in islet cells.5. 2,4-Dinitrophenol (0.25 mM) hyperpolarized islet cells and blocked electrical activity induced by glucose 11.1 mM.6. Adrenaline (1 muM) completely blocked glucose-induced electrical activity but without altering the membrane potential.7. The origin and functional significance of glucose-induced electrical activity in islet cells is discussed in relation to insulin secretion.

Action Potentials↗
PubMed1970

Electrical activity in pancreatic islet cells: effect of ions.

1. Intracellular micro-electrode recording techniques have been used to study the effects of varying the external ion concentration on the membrane potential and glucose-induced electrical activity in cells from mouse islets of Langerhans.2. Increasing [K](o) to 47 mM depolarized islet cells without inducing electrical activity. Normal action potentials were generated in response to glucose after removal of [K](o) for 60 min.3. Reduction of [Cl](o) to 12 mM did not affect the membrane potential and glucose still induced electrical activity.4. Reduction of [Na](o) to 26 mM increased the amplitude of action potentials; subsequently the cells depolarized.5. Removal of [Ca](o) caused cells, already firing action potentials intermittently in response to glucose, to change their pattern of discharge to one of continuous firing. The time constant of the action potentials was also increased. Depletion of calcium for 60 min before addition of glucose prevented the appearance of electrical activity.6. Increasing [Ca](o) threefold to 7.7 mM in the presence of glucose, 11.1 mM, increased action potential amplitude to 12 mV, but a tenfold increase of [Ca](o) to 25.6 mM completely blocked action potential discharge.7. Exposure of islet cells simultaneously to reduced [Na](o) (26 mM) and increased [Ca](o) (7.7 mM) increased the amplitude of glucose-induced action potentials to about 20 mV.8. Strontium, 2.56 mM, was an effective substitute for [Ca](o), 2.56 mM, and maintained a normal pattern of electrical activity in response to glucose.9. Increasing the magnesium concentration tenfold to 11.3 mM did not block electrical activity whereas manganese, 2 mM, blocked glucose-induced action potentials and depolarized islet cells.10. It was concluded that the action potential induced by glucose in islet beta-cells is due predominantly to calcium entry and that sodium ions tend to repress this calcium influx.

Action Potentials↗
PubMed1967

Membrane potential measurement in cells of the adrenal gland.

1. Recordings of transmembrane potentials have been made in vitro from the cells of the adrenal gland using glass micro-electrodes.2. There was only a small species variation in the mean membrane potential of the cortical cells of the rabbit, rat and kitten; 66.2, 70.5, and 71.4 mV respectively.3. The membrane potential of cortical cells was dependent upon the external potassium concentration, [K](o). Raising [K](o) above the normal concentration of 4.7 mM by addition of KCl decreased the membrane potential; lowering [K](o) from normal increased it. The decrease in membrane potential was still evident when chloride was replaced by sulphate. Increasing [K](o) 10-fold decreased the membrane potential of rabbit cortical cells by 44 mV and of kitten cortical cells by 50 mV.4. The mean membrane potential measured in medullary chromaffin cells was for the rabbit 24.2 mV, rat 20 mV, and kitten 31.7 mV. The potentials of medullary cells were much less affected by changes in [K](o) than were cortical cell potentials.5. Age had little influence upon either cortical or medullary membrane potentials of adrenal glands, at least in early life.

Journal Article↗
PubMed1967

Steroid production and membrane potential measurement in cells of the adrenal cortex.

1. The relation between corticosteroid production and the cellular membrane potential of adrenocortical cells has been investigated using a flow system for the incubation in vitro of adrenal glands from neonatal rabbits. Corticosteroid production by the adrenal cells was determined by a fluorescence method; membrane potentials were measured with glass micro-electrodes.2. Adrenocorticotrophic hormone (ACTH) increased corticosteroid production without altering the membrane potential of the adrenocortical cells. Conversely, a 5-fold increase in [K](o) did not increase corticosteroid production but decreased the cellular membrane potential. The increase in [K](o) did not impair the stimulation of corticosteroid production by ACTH.3. The log dose-response relation between the concentration of ACTH in the incubation medium and the amount of corticosteroid produced by the adrenal tissue was linear.4. No evidence was found of a direct relation between the production of corticosteroid by adrenocortical cells and the cellular membrane potential. Indeed, the output of steroid appeared to be relatively independent of the polarization of the cell membrane.

Journal Article↗