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Biomedical subjects

S G Schultz

Publications and source records attributed to S G Schultz.

126 records · Page 7Linked to original sources
PubMed1967

Effect of inhibitors on alanine transport in isolated rabbit ileum.

The effects of metabolic inhibitors and ouabain on alanine transport across rabbit ileum, in vitro, have been investigated. Net transport of alanine and Na across short-circuited segments of ileum is virtually abolished by cyanide, 2,4-dinitrophenol, iodoacetate, and ouabain. However, these inhibitors do not markedly depress alanine influx from the mucosal solution, across the brush border, into the intestinal epithelium, and they do not significantly affect the Na dependence of this entry process. The results of this investigation indicate that: (a) the Na dependence of alanine influx does not reflect a mechanism in which the sole function of Na is to link metabolic energy directly to the influx process; and (b) the inhibition of net alanine transport across intestine is, in part, the result of an increased rate coefficient for alanine efflux out of the cell across the brush border. Although these findings do not exclude a direct link between metabolic energy and alanine efflux, the increased efflux may be the result of the increased intracellular Na concentration in the presence of these inhibitors. The results of these studies are qualitatively consistent with a model for alanine transport across the brush border which does not include a direct link to metabolic energy.

Alanine↗
PubMed1967

Alanine and sodium fluxes across mucosal border of rabbit ileum.

Unidirectional influxes of L-alanine and Na from the mucosal solution into the epithelium of in vitro rabbit ileum have been determined. In the presence of 140 mM Na, alanine influx is approximately 2.2 micromoles/hr cm(2), but is inhibited if the NaCl in the mucosal solution is replaced by choline Cl, Tris-Cl, mannitol, LiCl, or KCl. Although alanine influx is strongly dependent upon Na in the mucosal solution, it is uninfluenced by marked reduction of intracellular Na pools. In addition, alanine influx is unaffected by intracellular alanine concentration. Na influx is markedly inhibited by the presence of Li. Evidence is presented that Na transport across the mucosal border cannot be attributed to simple diffusion even though the net flux across this surface is in the direction of the electrochemical potential difference.

Alanine↗
PubMed1967

Kinetic relations of the Na-amino acid interaction at the mucosal border of intestine.

The relation between unidirectional influxes of Na and amino acids across the mucosal border of rabbit ileum was studied under a variety of conditions. At constant Na concentration in the mucosal bathing solution, amino acid influx followed Michaelis-Menten kinetics permitting determination of maximal influx and the apparent Michaelis constant, K(t). Reduction in Na concentration, using choline as substitute cation, caused an increase in K(t) for alanine but had no effect on maximal alanine influx. The reciprocal of K(t) was a linear function of Na concentration. Similar results were obtained for valine and leucine and these amino acids competitively inhibited alanine influx both in the presence and in the absence of Na. These results lead to a model for the transport system which involves combination of Na and amino acid with a single carrier or site leading to penetration of both solutes. The model predicts that alanine should cause an increase in Na influx and the ratio of this extra Na flux to alanine flux should vary with Na concentration. The observed relation agreed closely with predicted values for Na concentrations from 5 to 140 mM. These results support the hypothesis that interactions between Na and amino acid transport depend in part on a common entry mechanism at the mucosal border of the intestine.

Alanine↗
PubMed1967

Cation transport in Escherichia coli. VII. Potassium requirement for phosphate uptake.

When Escherichia coli K-12 is grown in media containing limiting amounts of K, growth continues normally until all the extracellular K has been consumed. Thereafter the rates of growth, glucose consumption, and oxygen consumption decrease progressively, and the cell contents of K and P fall. These changes, referred to as K limitation, are all reversed by the addition of K. By specifically altering the ionic composition of the cells it was shown that these metabolic disturbances are not due to changes in the cell content of K or Na, but are directly related to the absence of K from the extracellular medium. The cell pool of inorganic P and the uptake of PO(4) from the medium are low in K-limited cells and are immediately stimulated by the addition of K, suggesting that the primary effect of K limitation is to inhibit PO(4) uptake. All the metabolic effects of K limitation can be attributed to inhibition of PO(4) uptake. The requirement of extracellular K for PO(4) uptake may be due to a coupling between the uptake of K and PO(4).

Escherichia coli↗
PubMed1966

Effect of sugars on transport of alanine in intestine.

The eflect of glucose and galactose on transport of alanine by rabbit ileum has been investigated. Transmural transport and cellular ac cumulation of the amino acid were in hibited by the sugars, but alanine in flux across the mucosal border of the cells was unaltered.

Alanine↗
PubMed1966

Cation transport in Escherichia coli. VI. K exchange.

K influx and net K flux have been measured in suspensions of chloramphenicol-arrested Escherichia coli. The rate of K exchange in the steady state was independent of the K concentration of the medium over a 200-fold range. Under a number of experimental conditions the rate of exchange may be considerably increased or decreased without changing the cellular K content. These results show that under these conditions changes in K influx are associated with equal changes in K efflux, and suggest that the latter process is, at least in part, both carrier-mediated and tightly coupled to the influx process.

Biological Transport↗
PubMed1966

Amino acid and sugar transport in rabbit ileum.

L-Alanine and 3-O-methyl-D-glucose accumulation by mucosal strips from rabbit ileum has been investigated with particular emphasis on the interaction between Na and these transport processes. L-Alanine is rapidly accumulated by mucosal tissue and intracellular concentrations of approximately 50 mM are reached within 30 min when extracellular L-alanine concentration is 5 mM. Evidence is presented that intracellular alanine exists in an unbound, osmotically active form and that accumulation is an active transport process. In the absence of extracellular Na, the final ratio of intracellular to extracellular L-alanine does not differ significantly from unity and the rate of net uptake is markedly inhibited. Amino acid accumulation is also inhibited by 5 x 10(-5)M ouabain. 3-O-methyl-D-glucose accumulation by this preparation is similarly affected by ouabain and by incubation in a Na-free medium. The effects of amino acid accumulation, of ouabain, and of incubation in a Na-free medium on cell water content and intracellular Na and K concentrations have also been investigated. These results are discussed with reference to the two hypotheses which have been suggested to explain the interaction between Na and intestinal nonelectrolyte transport.

Alanine↗
PubMedDate not supplied

The role of paracellular pathways in isotonic fluid transport.

Paracellular pathways across "leaky" epithelia are the major route for transepithelial ionic diffusion. The permselective properties of these pathways suggest that they offer a watery environment through which ions diffuse in their hydrated forms. There is also suggestive evidence that, at least in some tissues, paracellular pathways provide a significant route for transepithelial water flow in response to an osmotic pressure difference; however, this has not as yet been definitively established. The effect of junctional complexes that are permeable to ions and water on the predictions of the standing-osmotic gradient model for isotonic water absorption is considered.

Animals↗