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Plasma ADMA Concentrations (plasma + adma_concentration)

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Medical Sciences	100%

Selected Abstracts

Plasma Asymmetric Dimethylarginine, Symmetric Dimethylarginine, l -Arginine, and Nitrite/Nitrate Concentrations in Cats with Chronic Kidney Disease and Hypertension

JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 2 2008
R.E. Jepson
Background: Chronic kidney disease (CKD) and hypertension have been associated with decreased bioavailability of nitric oxide (NO) and endothelial dysfunction. Increased concentrations of the endothelial nitric oxide synthase (eNOS) inhibitor asymmetric dimethylarginine (ADMA) are implicated. Hypothesis: Plasma ADMA concentration is increased in cats with CKD and systemic hypertension corresponding to a decrease in total plasma nitrate/nitrite (NOx) availability. Decrease in systolic blood pressure (SBP) and proteinuria during treatment of hypertension with amlodipine besylate may be associated with increased NOx availability. Animals: Sixty-nine client-owned normotensive and hypertensive cats with variable azotemia. Methods: Plasma ADMA, symmetric dimethylarginine (SDMA), and l -arginine were measured simultaneously by hydrophilic-interaction liquid chromatography-electrospray tandem mass spectrometry in cats from 6 groups: normotensive nonazotemic (n = 10), normotensive mildly azotemic (n = 10), hypertensive mildly azotemic with hypertensive retinopathy (n = 20), hypertensive mildly azotemic without hypertensive retinopathy (n = 10), normotensive moderately azotemic cats (n = 10), and hypertensive nonazotemic cats (n = 9). Plasma NOx concentrations were measured. Results: A moderate correlation between plasma creatinine and ADMA (n = 69, r= .608, P < .001), SDMA (n = 69, r= .741, P < .001), and NOx concentrations (n = 69, r= .589, P < .001) was observed. There was no association among plasma ADMA, SDMA, and NOx concentrations and SBP. Conclusions and Clinical Importance: Plasma ADMA and SDMA concentrations are increased in cats with CKD and correlate with plasma creatinine concentration. This may imply the presence of endothelial dysfunction in cats with CKD. Plasma ADMA concentrations were not associated with systemic hypertension. Treatment of systemic hypertension with amlodipine besylate did not affect plasma ADMA or NOx concentrations. [source]

Plasma ADMA concentrations at birth and mechanical ventilation in preterm infants: A prospective pilot study

PEDIATRIC PULMONOLOGY, Issue 12 2008
Milan C. Richir MD
Abstract Rationale Nitric oxide (NO) produced in the lung is an important mediator of normal lung development, vascular smooth muscle relaxation, and ventilation perfusion matching. NO is synthesized from arginine by the action of NO-synthase (NOS). Asymmetric dimethylarginine (ADMA), an endogenous derivate of arginine, inhibits NOS and is thereby a determinant of NO synthesis. We compared ADMA and arginine levels in preterm infants requiring mechanical ventilation with preterm infants who did not require mechanical ventilation and determined the relation between ADMA and the length of mechanical ventilation in these infants. Methods Thirty preterm infants, mean (SD) gestational age 29.3 (1.7) weeks and birth weight 1,340 (350) gram, of the Neonatal Intensive Care Unit of the VU University Medical Center were included. ADMA and arginine were measured in umbilical cord blood and the length of mechanical ventilation (days) was registered. Results Gestational age and birth weight were significantly smaller in infants requiring mechanical ventilation, but were not significantly correlated with plasma ADMA concentration after birth. Plasma ADMA concentrations were significantly higher in infants who required mechanical ventilation than in infants who did not require mechanical ventilation (1.53,±,0.23 and 1.37,±,0.14 µmol/L, respectively; P,=,0.036). ADMA concentration was significantly related to length of mechanical ventilation (B,=,3.4; 95% CI: 1.1,5.6; P,=,0.006), also after adjustment for gestational age (B,=,2.3; 95% CI: 0.4,4.2; P,=,0.024). Conclusions Preterm infants who require mechanical ventilation have increased ADMA levels compared to non-ventilated preterm infants. ADMA levels at birth are related to the length of mechanical ventilation. An increased ADMA concentration could reduce NO synthesis, which could lead to insufficient gas exchange and, consequently, a longer period of mechanical ventilation. Pediatr. Pulmonol. 2008; 43:1161,1166. © 2008 Wiley-Liss, Inc. [source]

Asymmetric dimethylarginine (ADMA): the silent transition from an ,uraemic toxin' to a global cardiovascular risk molecule

EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 2 2005
D. Fliser
Abstract Endothelial dysfunction as a result of reduced bioavailability of nitric oxide (NO) plays a central role in the process of atherosclerotic vascular disease. In endothelial cells NO is synthesized from the amino acid l -arginine by the action of the NO synthase (NOS), which can be blocked by endogenous inhibitors such as asymmetric dimethylarginine (ADMA). Acute systemic administration of ADMA to healthy subjects significantly reduces NO generation, and causes an increase in systemic vascular resistance and blood pressure. Increased plasma ADMA levels as a result of reduced renal excretion have been associated with atherosclerotic complications in patients with terminal renal failure. However, a significant relationship between ADMA and traditional cardiovascular risk factors such as advanced age, high blood pressure and serum LDL-cholesterol, has been documented even in individuals without manifest renal dysfunction. As a consequence, the metabolism of ADMA by the enzyme dimethylarginine dimethylaminohydrolase (DDAH) has come into the focus of cardiovascular research. It has been proposed that dysregulation of DDAH with consecutive increase in plasma ADMA concentration and chronic NOS inhibition is a common pathophysiological pathway in numerous clinical conditions. Thus, ADMA has emerged as a potential mediator of atherosclerotic complications in patients with coronary heart disease, peripheral vascular disease, stroke, etc., being the culprit and not only an innocent biochemical marker of the atherosclerotic disease process. [source]