Regulation of Plasma Adenosine Levels in Normal Pregnancy

Yoneyama, Yoshio; Sawa, Rintaro; Suzuki, Shunji; Ishino, Hiroshi; Miura, Asako; Kuwabara, Yoshimitsu; Kuwajima, Toyohiko; Ito, Naoko; Kiyokawa, Yasuko; Otsubo, Yasuo; Araki, Tsutomu

doi:10.1159/000052995

Cited by 28 publications

(21 citation statements)

References 13 publications

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“…6,66 The elevated adenosine level may be explained by platelet activation (releasing ATP and ADP), increments in plasma activity of 5′-nucleotidases (CD73), or decreases in adenosine deaminase (ADA) activity during pregnancy. 66,67 Also, ATP may be hydrolyzed faster during pregnancy because the ATP hydrolyzing enzymes CD39 and alkaline phosphatase are highly expressed in the placenta. 12,68 These pregnancy adaptations suggest that extracellular ATP levels need to be regulated tightly during pregnancy.…”

Section: Atp and Adenosine During Normal Pregnancymentioning

confidence: 99%

Danger Signals From ATP and Adenosine in Pregnancy and Preeclampsia

et al. 2014

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Section: Atp and Adenosine During Normal Pregnancymentioning

confidence: 99%

Danger Signals From ATP and Adenosine in Pregnancy and Preeclampsia

et al. 2014

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“…Thus, one recently proposed option is that altered adenosine transport in gestational diabetes could result from the elevated NO detected in HUVEC [26,], supporting other results in this cell type [23] and in rat ENT1 [70]. Reduced adenosine transport due to reduced expression and/or activity of ENTs is a phenomenon that could have several physiological implications since a reduced ENTs activity could partially explain the elevated extracellular adenosine concentration detected in the culture medium of HUVEC from gestational diabetic (~2 µM) vs. normal (~50-500 nM) pregnancies [23,26,71] and the reported adenosine concentration in human umbilical vein blood from normal pregnancies (~500 nM) [72,73].…”

Section: Nucleoside Transportmentioning

confidence: 89%

“…Preeclampsia has been associated with altered maternal and foetal circulating levels of adenosine [72,73,[136][137][138][139]. Initially, it was shown in pregnancies with preeclampsia that the umbilical blood level of adenosine measured by cordocentesis was in the range of ∼600 nM [136].…”

Section: Nucleoside Transportmentioning

confidence: 99%

“…In preeclamptic pregnancies complicated with high resistance of umbilical vessels, the plasma adenosine concentration has been shown to increase up to ∼1800 nM [88]. In addition, circulating maternal blood levels of adenosine in preeclampsia (~700 nM) are higher compared with normal pregnancies (~450 nM) [72,73,138,139]. Interestingly, higher plasma levels of adenosine, owing to the altered metabolism of this nucleoside [72,139], seem to be associated with the severity of preeclampsia [73].…”

Section: Nucleoside Transportmentioning

confidence: 99%

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Equilibrative Nucleoside (ENTs) and Cationic Amino Acid (CATs) Transporters: Implications in Foetal Endothelial Dysfunction in Human Pregnancy Diseases

Casanello¹,

Escudero²,

Sobrevía

2007

CVP

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Gestational diabetes (GD, characterized by abnormal D-glucose metabolism), intrauterine growth restriction (IUGR, a disease associated with reduced oxygen delivery (hypoxia) to the foetus), and preeclampsia (PE, a pregnancy complication characterized by high blood pressure, proteinuria and increased vascular resistance), induce foetal endothelial dysfunction with implications in adult life and increase the risk of vascular diseases. Synthesis of nitric oxide (NO) and uptake of L-arginine (the NO synthase (NOS) substrate) and adenosine (a vasoactive endogenous nucleoside) by the umbilical vein endothelium is altered in pregnancies with GD, IUGR or PE. Mechanisms underlying these alterations include differential expression of equilibrative nucleoside transporters (ENTs), cationic amino acid transporters (CATs), and NOS. Modulation of ENTs, CATs, and NOS expression and activity in endothelium involves protein kinase C (PKC), mitogen-activated protein kinases p42 and p44 (p42/44(mapk)), calcium, and phosphatidyl inositol 3 kinase (PI3k), among others. Elevated extracellular D-glucose and hypoxia alter human endothelial function. However, information regarding the transcriptional modulation of ENTs, CATs, and NOS is limited. This review focuses on the effect of transcriptional and post-transcriptional regulatory mechanisms involved in the modulation of ENTs and CATs, and NOS expression and activity, and the consequences for foetal endothelial function in GD, IUGR and PE. The available information will contribute to a better understanding of the cell and molecular basis of the altered vascular endothelial function in these pregnancy diseases and will emphasize the key role of this type of epithelium in placental function and the normal foetal development and growth.

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“…En mujeres gestantes, se ha mostrado una elevada concentración plasmática de adenosina respecto a no embarazadas 42 , lo cual ha sido asociado a una elevación en el metabolismo de ATP y degradación de adenosina hasta inosina 43 . Así, el embarazo normal per se, es un estado de mayor metabolismo purinérgico.…”

Section: Purinas En La Pre-eclampsiaunclassified

Purinas y ácido úrico en pre-eclampsia: interacciones fisiopatológicas y proyecciones en investigación

et al. 2013

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Uric acid and purine plasma levels as plausible markers for placental dysfunction in pre-eclampsia E l ácido úrico, producto final del metabolismo de las purinas, es utilizado como marcador de daño renal y factor de riesgo de morbilidad materna y neonatal en embarazos con pre-eclampsia 1-3 . Así, las mujeres hipertensas e hiperuricémicas tienen mayor riesgo de parto pretermino, retardo de crecimiento intrauterino (RCIU) y pre-eclampsia de origen temprano (< 34 semanas), que aquellas mujeres con embarazos normales o mujeres pre-eclámpticas sin hiperuricemia 3,4 . Conjuntamente, una serie de estudios 5-7 sugieren que los embarazos con preeclampsia cursan con altos niveles de purinas (i.e., ATP, ADP, AMP, adenosina). Las causas o efectos de este aumento en el metabolismo de las purinas hasta ácido úrico no se conocen; sin embargo, dado que pre-eclampsia (principalmente de origen temprano) se asocia a un aumento en la liberación de restos celulares hacia la circulación materna, es posible que estos constituyan el principal sustrato para el metabolismo de las purinas, y finalmente formación de ácido úrico 8 . Por ello, el aumento de ácido úrico y purinas en embarazos con pre-eclampsia no sólo obedecería a la alteración de la función renal, sino que sería un marcador de disfunción placentaria. El objetivo de este trabajo es contribuir en el análisis del rol de las purinas y el ácido úrico en la fisiopatología de pre-eclampsia y con ello replantear su potencial rol predictivo en pre-eclampsia y enfermedades cardiovasculares. Es necesario indicar que este es un análisis de la literatura disponible en el cual nos permitimos especular sobre estas posibles conexiones.

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Regulation of Plasma Adenosine Levels in Normal Pregnancy

Cited by 28 publications

References 13 publications

Danger Signals From ATP and Adenosine in Pregnancy and Preeclampsia

Danger Signals From ATP and Adenosine in Pregnancy and Preeclampsia

Equilibrative Nucleoside (ENTs) and Cationic Amino Acid (CATs) Transporters: Implications in Foetal Endothelial Dysfunction in Human Pregnancy Diseases

Purinas y ácido úrico en pre-eclampsia: interacciones fisiopatológicas y proyecciones en investigación

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