PubMed Health⌕ Search

Biomedical subjects

G Klemperer

Publications and source records attributed to G Klemperer.

8 recordsLinked to original sources
PubMed1988

Influence of serosal Cl on transport properties and cation activities in frog skin.

The effects of serosal substitution of isosmotic Na2SO4-Ringer solution for NaCl-Ringer solution were studied in the short-circuited frog skin (Rana pipiens, Northern variety). Despite prompt changes of transepithelial measurements, initial cellular effects were slight. After 30 to 45 min, however, the transcellular current had decreased and the cell electrical potential had depolarized, in association with decrease of the apical membrane fractional resistance and basolateral membrane conductance. Apical membrane slope conductance was unaffected. Similar effects were obtained with isolated epithelia. With the use of gluconate or NO3 in place of Cl, the effects on cellular current and conductance were minimal or insignificant, despite changes of the cell potential, fractional resistance, and basolateral conductance similar to those seen with sulfate. Following prolonged exposure to serosal SO4-Ringer, the extent of depolarization induced by raising the serosal K concentration decreased, indicating diminution of basolateral K conductance and the existence of other basolateral conductances. Equilibration in serosal gluconate-Ringer enhanced polarization on serosal restoration of Cl or removal of Na, again indicating a time-dependent change in the basolateral conductance pattern. Depolarization on removal of serosal Cl was not attributable to inhibition of the pump. Nor was it the result of decrease of the K equilibrium potential EK: exposure to serosal SO4-Ringer decreased cell K activity aKc from 104 +/- 6 to 58 +/- 4 mM (n = 5), but EK was reduced only slightly; exposure to serosal gluconate increased aKc and EK. Serosal sulfate lowered the cell Na activity aNac, but the electrochemical potential difference for Na across the apical surface was unaffected. The concurrent decrease of both aKc and aNac following serosal substitution of SO4 for Cl raises questions concerning mechanisms of osmoregulation.

Amiloride↗
PubMed1987

Basolateral membrane K permselectivity and regulation in bullfrog cornea epithelium.

In the isolated bullfrog cornea epithelium, under short-circuit conditions the regulation of the K permeability of the basolateral membrane was studied with conventional and K-selective microelectrodes in Cl-free Ringers. In Cl-free Ringers, the transcellular current is less than 1 microA/cm2, allowing estimation of the basolateral membrane electromotive force from measurements of the membrane voltage (Vsc). The apparent basolateral membrane K conductance was determined from measurements of the effects of single ion substitutions of K for Na on the Vsc. An increase of K from 2.5 to 25 mM on the stromal side depolarized the membrane voltage by 29 mV, whereas additional increases to 56 and 100 mM resulted in depolarizations consistent with a Nernstian prediction. In the range between 25 and 56 mM K, these decreases in membrane voltage were smaller after either decreasing the stromal-side pH from 8.1 to 7.2 or substitution of sulfate with gluconate. In contrast, preincubation with 0.1 mM ouabain did not change the membrane voltage depolarizations over any of the K ranges between 2.5 and 100 mM. Equivalent circuit analysis, based on the effects of nystatin on the electrical parameters, was used to validate the changes in the apparent basolateral membrane K conductance following increases in [K], substitution of SO4 with gluconate and Na:K pump inhibition. An increase in the [K] to 120 mM decreased the basolateral membrane resistance nearly three-fold, whereas gluconate substitution resulted in a 2.5-fold increase of the basolateral membrane resistance. This resistance increased an additional 2-fold after exposure to 5 mM Ba.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Cell sodium activity and sodium pump function in frog skin.

Cell Na activity, acNa, was measured in the short-circuited frog skin by simultaneous cell punctures from the apical surface with open-tip and Na-selective microelectrodes. Skins were bathed on the serosal surface with NaCl Ringer and, to reduce paracellular conductance, with NaNO3, Ringer on the apical surface. Under control conditions acNa averaged 8 +/- 2 mM (n = 9, SD). Apical addition of amiloride (20 microM) or Na replacement reduced acNa to 3 mM in 6-15 min. Sequential decreases in apical [Na] induced parallel reductions in acNa and cell current, Ic. On restoring Na after several minutes of exposure to apical Na-free solution Ic rose rapidly (approximately less than 30 sec) to a stable value while acNa increased exponentially, with a time constant of 1.8 +/- 0.7 min (n = 8). Analysis of the time course of acNa indicates that the pump Na flux is linearly related to acNa in the range 2-12 mM. These results indicate that acNa plays an important role in relating apical Na entry to basolateral active Na flux.

Animals↗
PubMed1986

Basolateral membrane potential and conductance in frog skin exposed to high serosal potassium.

In studies of apical membrane current-voltage relationships, in order to avoid laborious intracellular microelectrode techniques, tight epithelia are commonly exposed to high serosal K concentrations. This approach depends on the assumptions that high serosal K reduces the basolateral membrane resistance and potential to insignificantly low levels, so that transepithelial values can be attributed to the apical membrane. We have here examined the validity of these assumptions in frog skins (Rana pipiens pipiens). The skins were equilibrated in NaCl Ringer's solutions, with transepithelial voltage Vt clamped (except for brief perturbations delta Vt) at zero. The skins were impaled from the outer surface with 1.5 M KCl-filled microelectrodes (Rel greater than 30 M omega). The transepithelial (short-circuit) current It and conductance gt = -delta It/delta Vt, the outer membrane voltage Vo (apical reference) and voltage-divider ratio (Fo = delta Vo/delta Vt), and the microelectrode resistance Rel were recorded continuously. Intermittent brief apical exposure to 20 microM amiloride permitted estimation of cellular (c) and paracellular (p) currents and conductances. The basolateral (inner) membrane conductance was estimated by two independent means: either from values of gt and Fo before and after amiloride or as the ratio of changes (-delta Ic/delta Vi) induced by amiloride. On serosal substitution of Na by K, within about 10 min, Ic declined and gt increased markedly, mainly as a consequence of increase in gp. The basolateral membrane voltage Vi (= -Vo) was depolarized from 75 +/- 4 to 2 +/- 1 mV [mean +/- SEM (n = 6)], and was partially repolarized following amiloride to 5 +/- 2 mV.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Cell K activity in frog skin in the presence and absence of cell current.

Cell K activity, acK, was measured in the short-circuited frog skin by simultaneous cell punctures from the apical surface with open-tip and K-selective microelectrodes. Strict criteria for acceptance of impalements included constancy of the open-tip microelectrode resistance, agreement within 3% of the fractional apical voltage measured with open-tip and K-selective microelectrodes, and constancy of the differential voltage recorded between the open-tip and the K microelectrodes 30-60 sec after application of amiloride or substitution of apical Na. Skins were bathed on the serosal surface with NaCl Ringer and, to reduce paracellular Cl conductance and effects of amiloride on paracellular conductance, with NaNO3 Ringer on the apical surface. Under control conditions acK was nearly constant among skins (mean +/- SD = 92 +/- 8 mM, 14 skins) in spite of a wide range of cellular currents (5 to 70 microA/cm2). Cell current (and transcellular Na transport) was inhibited by either apical addition of amiloride or substitution of Na by other cations. Although in some experiments the expected small increase in acK after inhibition of cell current was observed, on the average the change was not significant (98 +/- 11 mM after amiloride, 101 +/- 12 mM after Na substitution), even 30 min after the inhibition of cell current. The membrane potential, which in the control state ranged from -42 to -77 mV, hyperpolarized after inhibition of cell current, initially to -109 +/- 5 mV, then depolarizing to a stable value (-88 +/- 5 mV) after 15-25 min. At this time K was above equilibrium (EK = 98 +/- 2 mV), indicating that the active pump mechanism is still operating after inhibition of transcellular Na transport. The measurement of acK permitted the calculation of the passive K current and pump current under control conditions, assuming a "constant current source" with almost all of the basolateral conductance attributable to K. We found a significant correlation between pump current and cell current with a slope of 0.31, indicating that about one-third of the cell current is carried by the pump, i.e., a pump stoichiometry of 3Na/2K.

Amiloride↗
PubMed1980

Suppression of gastric acid secretion by furosemide in isolated gastric mucosa of guinea pig.

The effect of furosemide on acid secretion and Cl- transport was studied in isolated fundic mucosa of the guinea pig. Furosemide (10(-3) M), applied to the serosal side produced an immediate effect on the short-circuit current (Isc), lowering it by 47 +/- 2%. Potential difference decreased by 29 +/- 3%, electrical conductance by 18 +/- 4%, acid secretion by 38 +/- 1%, and net flux of Cl- from serosal-to-mucosal side by 37%. Application of the drug to the mucosal side produced similar effects on acid secretion and on the electrical parameters. It is suggested that furosemide blocks the entrance of Cl-, by the Na+--Cl- cotransport mechanism, through the basolateral membrane of the secreting cell. The consequent reduction in electrogenic Cl- transport would cause Isc and acid secretion to decrease. A reduction of Cl- conductance of the apical membrane, upon mucosal application of the drug, would cause similar effects on acid secretion and Cl- transport.

Animals↗