Hypoxanthine uptake at the fetal side of human placenta proceeds through a nucleobase-preferring carrier and a non-saturable process

Ramírez, Myriam; Acevedo, C.G.; Rojas, Susana; Bravo, Iván

doi:10.1016/s0143-4004(97)80067-7

“…Preparation viability was assessed by measuring lactic dehydrogenase activity in the perfusate of the isolated perfused cotyledon as described by Penfold et al (1981) and Acevedo et al (1995). In addition, we measured PO 2 in both arterial and venous effluents (Ramirez et al, 1997). The viability of this preparation during the perfusion period was also reflected by the stability of the fetal artery perfusion pressure, fetal perfusate flow rates and volume, which are considered control parameters for defining the viability of the tissue and the quality of the placenta (Hsieh et al, 1992;Malek et al, 1995).…”

Section: Placental Preparationmentioning

confidence: 99%

“…After a stabilization period in which the cotyledon was perfused with the Ringer-Krebs solution for at least 40 min, cellular uptake of 2-deoxy-D-[ 3 H]glucose (2-[ 3 H]DG) was measured in relation to an extracellular tracer ([ 14 C]sucrose) using a rapid, single-circulation paired-tracer technique as previously described (Acevedo et al, 1995;Ramirez et al, 1997). A 200 Al bolus containing a mixture of 2-deoxy D-[ 3 H]glucose (4 ACi) and [ 14 C]sucrose (1 ACi) was intra-arterially injected, which was followed by the immediate sequential collection of 8 samples of the venous perfusate at 5 s intervals.…”

Section: D-glucose Uptake In the Placental Cotyledonmentioning

confidence: 99%

Insulin and nitric oxide stimulates glucose transport in human placenta

Acevedo¹,

Márquez²,

Rojas³

et al. 2005

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“…Preparation viability was assessed by measuring lactic dehydrogenase activity in the perfusate of the isolated perfused cotyledon as described by Penfold et al (1981) and Acevedo et al (1995). In addition, we measured POµ in both arterial and venous effluents (Ram úrez et al 1997). The viability of this preparation during the perfusion period was reflected by the stability of the fetal artery perfusion pressure, fetal perfusate flow rates, and volume, which are considered as control parameters for defining the viability of the tissue and the quality of the placenta (Hsieh et al 1992;Malek et al 1995).…”

mentioning

confidence: 99%

“…After a stabilization period, in which the cotyledon was perfused with the Ringer-Krebs solution for at least 30 min, cellular uptake of ¬_[ÅH]arginine was measured in relation to an extracellular tracer ([ 14 C]sucrose) using a rapid, single-circulation paired-tracer technique, as already described (Acevedo et al 1995;Ram úrez et al 1997). A 200 ìl bolus containing a mixture of ¬_ [ÅH]arginine (4 ìCi; 0·1 ìÒ) and [ 14 C]sucrose (1 ìCi) was intra-arterially injected and was followed by the immediate sequential collection of six samples from the venous perfusate at 1 min intervals.…”

mentioning

confidence: 99%

L-Arginine Transport at the Fetal Side of Human Placenta: Effect of Aspirin in Pregnancy

ACEVEDO¹,

ROJAS²,

BRAVO³

1999

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summary ¬_Arginine transport by the fetal side of human placenta was investigated through the characterization of ¬_ [ÅH]arginine uptake in isolated perfused cotyledon. Competitive inhibition experiments suggest the presence of at least two transport systems: a Na¤-independent, pHinsensitive system inhibitable by cationic amino acids, similar to system y¤, and a Na¤-dependent system which recognizes both cationic and neutral amino acids only in the presence of Na¤, i.e. a B°, + -like system. The kinetic analysis of ¬-arginine uptake in the presence of Na¤ revealed that the process is mediated by saturable components: a high-affinity system (Km = 167 ± 18·0 ìÒ; Vmax = 0·174 ± 0·012 ìmol min¢) and a low-affinity carrier (Km = 980 ± 112 ìÒ; Vmax = 1·60 ± 0·12 ìmol min¢). In the absence of Na¤, ¬_arginine uptake was fitted by one model with a Michaelis-Menten constant of 200 ± 24·8 ìÒ. These results suggest that the high-affinity component corresponds to the Na¤-independent system y¤, whilst the low-affinity system may represent the activity of the Na¤-dependent B°, + transporter. Kinetic studies in placentae taken from aspirin-treated pregnancies showed that ¬_arginine is transported with a significantly higher affinity (Km = 42·5 ± 5·7 ìÒ), but with a lower capacity (Vmax = 0·064 ± 0·003 ìmol min¢) than in the non-treated group. The latter finding suggests that aspirin would facilitate the uptake of the NO precursor only at very low arginine concentrations.

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“…After a stabilization period, in which the cotyledon was perfused with the Ringer-Krebs solution for at least 30 min, cellular uptake of ¬_[ÅH]arginine was measured in relation to an extracellular tracer ([ 14 C]sucrose) using a rapid, single-circulation paired-tracer technique, as already described (Acevedo et al 1995;Ram úrez et al 1997). A 200 ìl bolus containing a mixture of ¬_ [ÅH]arginine (4 ìCi; 0·1 ìÒ) and […”

mentioning

confidence: 99%

L‐Arginine Transport at the Fetal Side of Human Placenta: Effect of Aspirin in Pregnancy

Acevedo¹,

Rojas²,

Bravo³

1999

Experimental Physiology

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summary ¬_Arginine transport by the fetal side of human placenta was investigated through the characterization of ¬_ [ÅH]arginine uptake in isolated perfused cotyledon. Competitive inhibition experiments suggest the presence of at least two transport systems: a Na¤-independent, pHinsensitive system inhibitable by cationic amino acids, similar to system y¤, and a Na¤-dependent system which recognizes both cationic and neutral amino acids only in the presence of Na¤, i.e. a B°, + -like system. The kinetic analysis of ¬-arginine uptake in the presence of Na¤ revealed that the process is mediated by saturable components: a high-affinity system (Km = 167 ± 18·0 ìÒ; Vmax = 0·174 ± 0·012 ìmol min¢) and a low-affinity carrier (Km = 980 ± 112 ìÒ; Vmax = 1·60 ± 0·12 ìmol min¢). In the absence of Na¤, ¬_arginine uptake was fitted by one model with a Michaelis-Menten constant of 200 ± 24·8 ìÒ. These results suggest that the high-affinity component corresponds to the Na¤-independent system y¤, whilst the low-affinity system may represent the activity of the Na¤-dependent B°, + transporter. Kinetic studies in placentae taken from aspirin-treated pregnancies showed that ¬_arginine is transported with a significantly higher affinity (Km = 42·5 ± 5·7 ìÒ), but with a lower capacity (Vmax = 0·064 ± 0·003 ìmol min¢) than in the non-treated group. The latter finding suggests that aspirin would facilitate the uptake of the NO precursor only at very low arginine concentrations.

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Hypoxanthine uptake at the fetal side of human placenta proceeds through a nucleobase-preferring carrier and a non-saturable process

Cited by 4 publications

References 21 publications

Insulin and nitric oxide stimulates glucose transport in human placenta

Insulin and nitric oxide stimulates glucose transport in human placenta

L-Arginine Transport at the Fetal Side of Human Placenta: Effect of Aspirin in Pregnancy

L‐Arginine Transport at the Fetal Side of Human Placenta: Effect of Aspirin in Pregnancy

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