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C C Petersen

Publications and source records attributed to C C Petersen.

28 records · Page 2Linked to original sources
PubMed1994

Single-channel recordings of volume-sensitive Cl- channels in human intestinal epithelial cells.

Under the double-patch configuration, stepwise closing unitary events could be observed in the on-cell patch upon applications of large positive potentials only when inactivating whole-cell Cl- currents were simultaneously observed in cultured human epithelial cells (Intestine 407) after osmotic swelling. Under the cell-attached configuration, the single channel events exhibited similar time- and voltage-dependent inactivation upon large depolarizations. The inactivation time course became shorter with increasing positive command pulses. The unitary slope conductance was around 63 pS at +140 mV and 46 pS at +100 mV exhibiting outward rectification.

Chloride Channels↗
PubMed1993

The role of endoplasmic reticulum calcium pumps during cytosolic calcium spiking in pancreatic acinar cells.

Many cell types show repetitive short lasting cytosolic calcium spikes with long interspike periods when stimulated with submaximal concentrations of agonists linked to the phosphoinositide signaling pathway. In pancreatic acinar cells these spikes have been shown to be evoked by constant levels of inositol trisphosphate through a mechanism of calcium-induced calcium release and do not depend acutely on the presence of external calcium. However, the processes involved in the interspike period have remained unclear. Here we report that the endoplasmic reticulum Ca(2+)-ATPase play a significant role, not only in resequestering calcium after a spike, but also in regulating the long interspike period. Decreasing the activity of the endoplasmic reticulum calcium pumps leads to shorter interspike intervals and thus higher spiking frequencies, while the duration of each spike increases. The endoplasmic reticulum Ca(2+)-ATPases are able to entirely suppress a response that can subsequently be evoked by partial inhibition of the pumps. This suggests that during the interspike period there is a considerable amount of calcium released from intracellular stores, which is rapidly buffered by the endoplasmic reticulum calcium pumps and the cytosolic calcium-binding proteins. A calcium spike will be initiated by calcium-induced calcium release only when the buffering is saturated.

Animals↗
PubMed1992

Intracellular effects of aluminium on receptor-activated cytoplasmic Ca2+ signals in pancreatic acinar cells.

The hypothesis that intracellular aluminium may interfere with cytoplasmic Ca2+ signals evoked by the activation of receptors linked to inositol lipid hydrolysis has been tested. Single mouse pancreatic acinar cells were used, because there is much information in this system on the mechanism by which acetylcholine (ACh) evokes cytoplasmic Ca2+ oscillations (spiking) and these spikes can be monitored in internally perfused cells by measuring the Ca(2+)-dependent chloride current. ACh normally evokes repetitive Ca2+ spikes, but when aluminium (1 microM-1 mM) is present in the internal perfusion solution the responses are reduced or absent. When aluminium is acutely infused into the internal perfusion solution the ACh-evoked Ca2+ signals quickly disappear. Aluminium also inhibits Ca2+ signals evoked by the Ca2+ releasing agent caffeine. Preliminary results suggest that silicic acid may protect against the toxic effects of aluminium. Silicic acid and citrate, in the absence of added Al3+, have the effect of enhancing the ACh-evoked Ca2+ signals. This could be due to binding of traces of Al3+ in the solutions. We conclude that aluminium can disrupt receptor-activated cytosolic Ca2+ signals when present inside cells.

Aluminum↗
PubMed1991

Inositol triphosphate produces different patterns of cytoplasmic Ca2+ spiking depending on its concentration.

In single mouse pancreatic acinar cells the effects of intracellular infusion of inositol 1,4,5-trisphosphate (InsP3) or the non-metabolizable InsP3 analogue inositol 1,4,5-triphosphorothioate (InsPS3) have been investigated using a wide range of concentrations. Different types of cytosolic Ca2+ fluctuation patterns (monitored as Ca(2+)-dependent Cl- current in patch-clamp whole-cell recording experiments) could be generated by InsP3 or InsPS3, dependent on concentration, resembling those previously shown to be evoked by varying degrees of receptor activation in these cells. Low InsPS3 concentrations evoked repetitive local Ca2+ spikes whereas at relatively high concentrations repetitive Ca2+ waves were produced. In the presence of intracellular citrate a much lower messenger level was sufficient to generate waves. The InsP3 concentration determines whether the cytosolic Ca2+ signals are local or global.

Animals↗
PubMed1991

Receptor-activated cytoplasmic Ca2+ spikes in communicating clusters of pancreatic acinar cells.

The transmission of receptor-generated cytoplasmic Ca2+ signals between communicating pancreatic acinar cells has been investigated by comparing patch-clamp recordings of Ca(2+)-dependent Cl- current in internally perfused single cells and small multi-cell clusters. Acetylcholine (50 nM) generates shortlasting repetitive spikes of Ca(2+)-dependent current and these spikes are not transmitted to neighbouring cells. Cholecystokinin octapeptide (5 pM) also generates repetitive spikes, but a significant proportion of these trigger longer and larger pulses of Ca(2+)-dependent current and these waves can easily spread from cell to cell. In pancreatic acinar units it is therefore possible to observe both local Ca2+ signals confined to the cell of its origin as well as Ca2+ signals that spread through communicating junctions to all cells in the unit.

Acetylcholine↗
PubMed1991

Different patterns of receptor-activated cytoplasmic Ca2+ oscillations in single pancreatic acinar cells: dependence on receptor type, agonist concentration and intracellular Ca2+ buffering.

Agonist-specific cytosolic Ca2+ oscillation patterns can be observed in individual cells and these have been explained by the co-existence of separate oscillatory mechanisms. In pancreatic acinar cells activation of muscarinic receptors typically evokes sinusoidal oscillations whereas stimulation of cholecystokinin (CCK) receptors evokes transient oscillations consisting of Ca2+ waves with long intervals between them. We have monitored changes in the cytosolic Ca2+ concentration ([Ca2+]i) by measuring Ca2(+)-activated Cl- currents in single internally perfused mouse pancreatic acinar cells. With minimal intracellular Ca2+ buffering we found that low concentrations of both ACh (50 nM) and CCK (10 pM) evoked repetitive short-lasting Ca2+ spikes of the same duration and frequency, but the probability of a spike being followed by a longer and larger Ca2+ wave was low for ACh and high for CCK. The probability that the receptor-evoked shortlasting Ca2+ spikes would initiate more substantial Ca2+ waves was dramatically increased by intracellular perfusion with solutions containing high concentrations of the mobile low affinity Ca2+ buffers citrate (10-40 mM) or ATP (10-20 mM). The different Ca2+ oscillation patterns normally induced by ACh and CCK would therefore appear not to be caused by separate mechanisms. We propose that specific receptor-controlled modulation of Ca2+ signal spreading, either by regulation of Ca2+ uptake into organelles and/or cellular Ca2+ extrusion, or by changing the sensitivity of the Ca2(+)-induced Ca2+ release mechanism, can be mimicked experimentally by different degrees of cytosolic Ca2+ buffering and can account for the various cytosolic Ca2+ spike patterns.

Acetylcholine↗
PubMed1985

Hormonal activation of single K+ channels via internal messenger in isolated pancreatic acinar cells.

The mechanism underlying hormonal activation of potassium channels was investigated in pig pancreatic acinar cells by patch-clamp single-channel and whole-cell current recordings. It was shown directly that a peptide hormone belonging to the cholecystokinin-gastrin family, CCK5, can activate single voltage-sensitive potassium channels which can be blocked by tetraethylammonium. The single-channel currents were recorded from electrically isolated cell-attached membrane patches to which the hormone had no access and the activation must therefore involve an intracellular messenger. The hormonal response requires external Ca2+ in the isolated membrane-patch area indicating that calcium gating is not directly linked to hormone-receptor interaction.

Animals↗
PubMed1982

Simulation of alternative designs of a cardiovascular risk reduction program for the U.S. Air Force.

A screening and intervention program, soon to be implemented by the U.S. Air Force, will screen personnel for cardiovascular risk and treat those at highest risk. Design alternatives were analyzed relating to the organization and method of delivery of this health service program. A simulation model was devised to aid the analysis. It includes the effect of turnover of personnel, the effect of treatment on the therapy group, and the effect of aging on blood pressure and cholesterol level. The model determines how the overall incidence of cardiovascular disease in the U.S. Air Force may be expected to change each year through a 20-year period under each of several design policies. Results are given to justify the choice of several design options, and the scope of future improvements in the simulation are outlined. It appears possible to achieve a reduction of one-third in the calculated risk of cardiovascular disease, and this more than justifies the risk reduction program, based on a cost-effectiveness study performed earlier. All design decisions have not been made but will await the result of a demonstration implementation. The demonstration will produce more accurate data on initial distribution of risk factors and effect of therapy, which in turn will permit a sharpening of the analyses presented here.

Adolescent↗
PubMedDate not supplied

Receptor-activated cytoplasmic Ca2+ oscillations in pancreatic acinar cells: generation and spreading of Ca2+ signals.

Receptor-activated cytoplasmic Ca2+ oscillations have been investigated using both single cell microfluorometry and voltage-clamp recording of Ca(2+)-dependent Cl- current in single internally perfused acinar cells. In these cells there is direct experimental evidence showing that the ACh-evoked [Ca2+]i fluctuations are due to an inositol trisphosphate-induced small steady Ca2+ release which in turn evokes repetitive Ca2+ spikes via a caffeine-sensitive Ca(2+)-induced Ca2+ release process. There is indirect evidence suggesting that receptor-activation in addition to generating the Ca2+ releasing messenger, inositol trisphosphate, also produces another regulator involved in the control of Ca2+ signal spreading. Intracellular inositol trisphosphate or Ca2+ infusion produce short duration repetitive spikes confined to the cytoplasmic area close to the plasma membrane, but these signals can be made to progress throughout the cell by addition of caffeine or by receptor activation.

Animals↗