Myocardial amino acid transport by canine sarcolemma vesicles

1987 ◽  
Vol 252 (6) ◽  
pp. H1070-H1076
Author(s):  
L. H. Young ◽  
B. L. Zaret ◽  
E. J. Barrett
Keyword(s):  
Amino Acid ◽  
Sarcoplasmic Reticulum ◽  
Membrane Vesicles ◽  
Amino Acid Uptake ◽  
Ventricular Myocardium ◽  
Transport Systems ◽  
Acid Uptake ◽  
Leucine Uptake ◽  
Alanine Transport ◽  
Canine Ventricular Myocardium

The transport of L-alanine and L-leucine into membrane vesicles isolated from mature canine ventricular myocardium was studied. Transport was assessed in purified sarcolemma and in vesicles differentially enriched either for sarcolemma or sarcoplasmic reticulum to further localize these transport systems. An imposed inward gradient of a NaNO3 stimulated uptake of L-alanine but not L-leucine by these vesicles. Amino acid uptake by these vesicles occurred into an osmotically active space. The stimulatory effect of Na+ on alanine transport was most striking in the purified sarcolemma vesicles, where Na+-stimulated alanine flux was 45 +/- 14 pmol X mg-1 X min-1. Furthermore, Na+-dependent alanine transport activity appeared to copurify with Na+-K+-ATPase activity, which served as a marker for sarcolemma membrane when these activities were compared in the three different membrane preparations. Leucine transport by sarcolemma was not altered by an imposed Na+ gradient. However, leucine uptake was a saturable function of extravesicular leucine and was inhibited by valine. In contrast, in sarcoplasmic reticulum membrane vesicles leucine uptake increased proportionately with increasing media leucine and was unaffected by valine. Our results demonstrate the feasibility of directly studying the transport of naturally occurring amino acids in membrane vesicles from mammalian heart, and the presence of Na+-dependent alanine transport system and a Na+-independent leucine transporter in the sarcolemma but not in sarcoplasmic reticulum of canine ventricular myocardium.

Placental toxicology: tobacco smoke, abused drugs, multiple chemical interactions, and placental function

1991 ◽  
Vol 3 (4) ◽  
pp. 355 ◽  
Author(s):  
BV Sastry
Keyword(s):  
Amino Acid ◽  
Amino Acid Transport ◽  
Drugs Of Abuse ◽  
Amino Acid Uptake ◽  
Transport Systems ◽  
Acid Uptake ◽  
Acid Transport ◽  
Ach Release ◽  
Placental Blood ◽  
Abused Drugs

There are increasing numbers of reports on the tobacco smoking and ingestion of abused drugs (e.g. morphine, cocaine) by pregnant women and the effects of the substances on the developing fetus and newborn infant. The passage of drugs and chemicals from the mother to the fetus is influenced by the placental transport and metabolism of the substances. Further, these drugs and chemicals affect the nutrient transport systems in the placenta. The three major drugs of abuse-nicotine, morphine and cocaine-depress both active amino-acid uptake by human placental villi and transplacental amino-acid transport by reason of the drugs' influence on placental cholinergic and opiate systems. Part of this depression (10-16%) is not reversible. Nicotine blocks the cholinergic receptor and thus blocks acetylcholine (ACh)-facilitated amino-acid transport. Morphine stimulates opiate kappa receptors and depresses ACh release. Cocaine blocks Ca2+ influx and thus blocks ACh release. ACh causes dilation of blood vessels and maintains placental blood flow by the activation of endothelial muscarinic receptors. By interfering with ACh release and placental blood flow, the three drugs of abuse may depress the diffusion of amino acids and other nutrients from the trophoblast into the placental circulation. Three regulatory systems are delineated for amino-acid uptake by the placenta: placental ACh, phospholipid N-methyltransferase, and the gammaglutamyl cycle. These systems operate in concert with one another and are dependent on cellular formation of adenosine 5'-triphosphate (ATP). Placental hypoxia induced by carbon monoxide and other tobacco gases depresses the energy-dependent processes and thus the ATP levels of placental cells. Maternal tobacco smoking and drug abuse cause placental insufficiencies for amino-acid transport, which may partially explain the fetal intrauterine growth retardation caused by these substances. Part of the amino-acid deficits may be compensated for by the induction of new amino-acid transport systems. Specific receptors or drug-binding proteins for the three drugs of abuse are present in the placenta. A DNA adduct selective for maternal smoking has been demonstrated in the placenta. DNA adducts selective for cocaine, morphine and other environmental chemicals have yet to be demonstrated ins the placenta.

Amino acid uptake systems in Bacteroides ruminicola

1979 ◽  
Vol 25 (10) ◽  
pp. 1161-1168 ◽  
Author(s):  
Roselynn M. W. Stevenson
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Nitrogen Sources ◽  
Amino Acid Uptake ◽  
Defined Medium ◽  
High Rate ◽  
Transport Systems ◽  
Acid Uptake ◽  
Chemical Structures ◽  
Kinetic Inhibition

Uptake of amino acids by Bacteroides ruminicola was observed in cells grown in a complete defined medium, containing ammonia as the nitrogen source. A high rate of uptake occurred only in fresh medium, as an inhibitory substance, possibly acetate, apparently accumulated during growth. All amino acids except proline were taken up and incorporated into cold trichloroacetic acid precipitable material. Different patterns of incorporation and different responses to 2,4-dinitrophenol and potassium ferricyanide indicated multiple uptake systems were involved. Kinetic inhibition patterns suggested six distinct systems were present for amino acid uptake, with specificities related to the chemical structures of the amino acids. Thus, the failure of free amino acids to act as sole nitrogen sources for growth of B. ruminicola is not due to the absence of transport systems for these compounds.

Anionic amino acid uptake by microvillous membrane vesicles from human placenta

1989 ◽  
Vol 257 (5) ◽  
pp. C1005-C1011 ◽  
Author(s):  
A. J. Moe ◽  
C. H. Smith
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Glutamate Uptake ◽  
Membrane Vesicles ◽  
Amino Acid Uptake ◽  
Maternal Blood ◽  
Acid Uptake ◽  
Dependent Manner ◽  
Concentration Dependent Manner

The transport mechanisms for anionic amino acids in trophoblast microvillous (maternal facing) membrane were investigated by characterization of L-[3H]aspartate and L-[3H]glutamate uptake in membrane vesicles. Uptake of the anionic amino acids was by a single high-affinity Na+-dependent K+-stimulated cotransporter that is pH sensitive and electrogenic. A second Na+-dependent transporter could not be discriminated, and there was no observable Na+-independent uptake. An outwardly directed K+ gradient (100 mM KCl inside) resulted in a 5- to 10-fold stimulation in glutamate uptake in the presence of Na+. Intravesicular KCl had no effect on transporter affinity but increased transporter velocity in a concentration-dependent manner. Inhibition of Na+-K+-dependent uptake of L-aspartate and L-glutamate (20 mM, 30 s) by 2 mM unlabeled amino acids demonstrated stereoselectivity for L-glutamate but not for L-aspartate. The neutral amino acids (L-alanine, L-threonine, L-serine, L-cysteine, L-phenylalanine) were not effective inhibitors. These data are consistent with an anionic amino acid transporter in the microvillous membrane of the trophoblast, which has characteristics qualitatively similar to the X-AG system found in other epithelia. This system may mediate the concentrative placental uptake of anionic amino acids from maternal blood in utero.

Placental amino acid uptake. VI. Regulation by intracellular substrate

1982 ◽  
Vol 243 (1) ◽  
pp. C46-C51 ◽  
Author(s):  
R. B. Steel ◽  
C. H. Smith ◽  
L. K. Kelley
Keyword(s):  
Amino Acid ◽  
Placental Tissue ◽  
Membrane Vesicles ◽  
Amino Acid Uptake ◽  
Maternal Plasma ◽  
Acid Uptake ◽  
L System ◽  
Intracellular Amino Acids ◽  
Human Placental Tissue

Amino acid uptake by human placental tissue is regulated by intracellular amino acids. alpha-Aminoisobutyric acid (AIB) uptake was reduced at intracellular AIB concentrations of 0.8 mM. The magnitude of reduction increased sharply between 1 and 3 mM and reached a maximum of 45% at 5 mM. Suppression was specific to the "A" system. It occurred only when both the amino acid used for preloading and that used as an uptake substrate were active with that system. In the "L" system, facilitation apparently occurs, and in the "ASC" system there is no apparent effect. The system specificity as well as other evidence indicated that suppression is caused by substrate present intracellularly rather than by dilution of extracellular substrate. Suppression was independent of inhibitors of protein synthesis and was not seen in membrane vesicles prepared from preloaded tissue, indicating that intracellular substrate interacts directly with the carrier (transinhibition) rather than altering its synthesis or degradation. The A system transinhibition has the potential to regulate syncytial uptake in vivo and limit variation due to changes in maternal plasma amino acid concentration.

In vivo muscle amino acid transport involves two distinct processes

2004 ◽  
Vol 287 (1) ◽  
pp. E136-E141 ◽  
Author(s):  
Sharon Miller ◽  
David Chinkes ◽  
David A. MacLean ◽  
Dennis Gore ◽  
Robert R. Wolfe
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Amino Acid Transport ◽  
Interstitial Fluid ◽  
Muscle Blood Flow ◽  
Amino Acid Uptake ◽  
Transport Systems ◽  
Acid Uptake ◽  
Acid Transport ◽  
Rate Limiting

We have tested the hypothesis that transit through the interstitial fluid, rather than across cell membranes, is rate limiting for amino acid uptake from blood into muscle in human subjects. To quantify muscle transmembrane transport of naturally occurring amino acids, we developed a novel 4-pool model that distinguishes between the interstitial and intracellular fluid compartments. Transport kinetics of phenylalanine, leucine, lysine, and alanine were quantified using tracers labeled with stable isotopes. The results indicate that interstitial fluid is a functional compartment insofar as amino acid kinetics are concerned. In the case of leucine and alanine, transit between blood and interstitial fluid was potentially rate limiting for muscle amino acid uptake and release in the postabsorptive state. For example, in the case of leucine, the rate of transport between blood and interstitial fluid compared with the corresponding rate between interstitial fluid and muscle was 247 ± 36 vs. 610 ± 95 nmol·min−1·100 ml leg−1, respectively ( P < 0.05). Our results are consistent with the process of diffusion governing transit from blood to interstitial fluid without selectivity, and of specific amino acid transport systems with varying degrees of efficiency governing transit from interstitial fluid to muscle. These results imply that changes in factors that affect the transit of amino acids from blood through interstitial fluid, such as muscle blood flow or edema, could play a major role in controlling the rate of muscle amino acid uptake.

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