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R Wondergem

Publications and source records attributed to R Wondergem.

26 records · Page 2Linked to original sources
PubMed1984

Transmembrane potential and intracellular potassium ion activity in fetal and maternal liver.

We have compared transmembrane potentials (Em) of maternal liver with Em of fetal liver, and as an initial step to account for differences in Em, we have measured intracellular potassium ion activities (aiK) in both tissues. Paired segments of maternal and fetal (day 17) mouse liver were suffused (15 ml/min) with Krebs' physiologic salt solution equilibrated with 95% 02-5% CO2 (pH 7.3-7.4) at 37 degrees C. To measure Em, cells were impaled with open-tip microelectrodes filled with 0.5 M KCl. Intracellular voltage recordings that were stable +/- 2 mV for at least 10 s were considered valid impalements. Maternal liver mean Em = -41 +/- 1 (SEM) mV, n = V 10 animals. In contrast, fetal liver mean Em = -23 +/- 1 (SEM) mV, n = 10 animals. In the same segments we measured aiK with potassium-selective liquid ion-exchanger microelectrodes. Maternal liver mean aik = 95 +/- 7 (SEM) mM and fetal liver mean aiK = 62 +/- 4 (SEM) mM. in addition, Em and aiK of fetal liver increased to values comparable to those of maternal liver during the first 8 days of neonatal life. The differences of Em and aik between fetal and maternal liver, and the changes in these values that occur in the neonate, may result from activity of a membrane Na-K exchange pump that increases with tissue development.

Animals↗
PubMed1983

Insulin depolarization of rat hepatocytes in primary monolayer culture.

Rat hepatocytes in primary monolayer culture demonstrated two stable states of transmembrane potential (Em). Low potentials ranging from -10 to -15 mV followed impalements with glass microelectrodes, and in some cells low potentials increased spontaneously or in response to a train of intermittent current (5 nA) to stable potentials of -50 mV, which were comparable to hepatocyte Em in vivo. Adding insulin at 20 mU/ml depolarized the stable higher Em 22.4 +/- 2.6 mV (n = 6) over an 11-min interval, and input resistance increased 21.4 +/- 4.7 M omega (n = 6) during the depolarization. The insulin effect was dose dependent, because adding insulin at 0.2 mU/ml depolarized the stable high Em 5.0 +/- 1.5 mV (n = 3) and increased input resistance 6.3 +/- 1.8 M omega (n = 3). In one experiment the Em repolarized 32 min after insulin was washed out. Adding metabolic inhibitors KCN (1 mM) and 2,4-dinitrophenol (10 and 1 mM) and increasing external potassium (60 mM, with external sodium reduced equivalently) also depolarized Em, but they did not increase input resistance. Thus insulin depolarized hepatocytes from a stable high Em, which is equivalent to the Em of liver in vivo, to a stable low Em, which occurs in hepatocytes in primary monolayer culture. This hormone action is consistent with changes in membrane ion conductance, and it further demonstrates that these cells can sustain two stable states of Em.

2,4-Dinitrophenol↗
PubMed1981

Transmembrane potential of rat hepatocytes in primary monolayer culture.

Transmembrane potentials of rat hepatocytes in primary monolayer culture on collagen gels were measured with glass microelectrodes. Potentials for cells in culture for 23-30 h comprised two populations. The mean +/- SD for a population of stable low potentials was -9.7 +/- 2.0 mV (n = 93). This was compared with -23.6 +/- 9.4 mV (n = 42), the mean value for stable potentials that followed spontaneous increases in the low potentials, 0.5-2.0 min after the impalement. The estimated input resistance increased during these spontaneous hyperpolarizations. In some cells, after 48 h in culture, the transmembrane potential oscillated rhythmically, with an amplitude of 25 mV and a period of 7 min. Suffusing the cells with 120 mM potassium chloride decreased the potential and eliminated the oscillations. The stable high potentials were considered more accurate estimates of the hepatocyte transmembrane potential, based on comparison with values for intact liver. Low potentials may have resulted from current leaking through an electrode shunt resistance, followed by an increase in potential as the membrane "sealed" the shunt pathway. However, these events may also reflect cells capable of two stable transmembrane potentials.

Animals↗
PubMed1980

Membrane potential measurements during rat liver regeneration.

Membrane potential was measured in perfused rat liver and was shown to increase from -33 +/- 1.0 mV in livers from normal rats to -50 +/- 1.1 mV in livers from rats 12 hr after partial hepatectomy. The hyperpolarization of the membrane in regenerating liver was no longer evident after perfusion with 1 mM ouabain for 5 min. Ouabain had a small (4 mV) depolarizing effect on membrane potential in normal liver. The potential measured in normal and regenerating liver decreased as a function of the external potassium concentration above 5 mM; however, the potential was more electronegative in regenerating liver compared to normal liver at all values of external potassium concentration, and the differences in potential between the two kinds of cells did not decrease at higher concentrations of external potassium. Thus, a plot of membrane potential vs external potassium concentration resulted in approximately parallel curves for the two different cell types. We conclude that hyperpolarization of the liver cell membrane is an early event during rat liver regeneration and results from an electrogenic Na-K pump.

Animals↗
PubMed1980

Transmembrane potential and amino acid transport in rat hepatocytes in primary monolayer culture.

Transmembrane potential (Em) and alpha-aminoisobutyric acid (AIB) transport were measured in primary monolayer cultures of rat hepatocytes obtained from unoperated control rats and from rats 12 hr following partial hepatectomy. Measurements were performed 20-24 hr after plating the cells. The capacity of both kinds of cells to concentrate AIB depended upon extracellular sodium: however, the steady-state accumulation in regenerating cells was twice that of control cells. Transmembrane potentials, recorded with glass microelectrodes, were -13 +/- 0.6 mV and -27 +/- 1.6 mV in control and regenerating cells, respectively. Ouabain (1 mM) depolarized regenerating cell to -18 +/- 1.0 mV, but it had no effect on control cells. The initial rates of 1 mM AIB transport into control and regenerating cells were 1.2 +/- 0.1 and 3.1 +/- 0.1 nanomoles/mg protein x 4 min, respectively. Ouabain (1 mM) reduced the initial rate of AIB transport into regenerating cells to 2.7 +/- 0.1 nanomoles/mg protein x 4 min, but it had no effect on AIB transport into control cells. Glucagon (10(-7) M) added to control cells 12 hr before measurements hyperpolarized Em to -31 +/- 1.3 mV and increased AIB transport rate to 3.1 nanomoles/mg protein x 4 min. The results suggest a relationship between increases in Em and increases in AIB transport in rat hepatocytes. An electrogenic Na-K pump may be involved in both of these events.

Aminoisobutyric Acids↗
PubMed1978

Serum somatomedin stimulation in thyroxine-treated hypophysectomized rats.

Somatomedin activity in rat serum was measured by sulfate incorporation into embryonic chick cartilage. Hypophysectomized male rats were treated daily for 21 days with 20 microgram/kg L-thyroxine (T4) and/or 25 microgram bovine (b) GH. Serum from rats given T4 alone or with bGH had somatomedin potencies of 0.88 and 0.83, respectively, comparable to normal serum (1.00) and significantly greater than serum from bGH-treated hypophysectomized rats (0.62). Hypophysectomized rats had no measurable somatomedin activity. T4 treatment resulted in a return to normal of the basal metabolic rate and serum T4 and T3 concentrations. Addition of T4 or T3 to serum from normal rats to produce concentrations comparable to those found in serum of hypophysectomized rats after T4 and/or bGH treatment did not alter the somatomedin activity. Higher concentrations of T4 (10(-7) M) or T3 (10(-8) or 10(-7) M) did, however, enhance the sulfation potency of normal serum. T4 (10(-9) M to 10(-6) M) or T3 (10(-10) M to 10(-7) M) added to serum-free medium provided minimal sulfation activity that represented only a fraction of the activity of serum. T4 may stimulate production of somatomedin in the absence of adequate bGH or may be metabolized to an active sulfation factor.

Animals↗