Adenosine and Hemodialysis in Humans

Guieu, Régis; Brunet, Philippe; Sampol, J.; Bechis, Guy; Fenouillet, Emmanuel; Mège, Jean‐Louis; Capo, Christian; Vitte, Joana; Ibrahim, Zein Shaban; Carrega, Louis; Lerda, D.; Rochat, Hervé; Berland, Yvon; Dussol, Bertrand

doi:10.2310/6650.2001.34091

Cited by 15 publications

(31 citation statements)

References 62 publications

(94 reference statements)

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“…6,7 Venous blood (3 mL) was withdrawn under vacuum together with a stop solution in Vacutainer tubes (Becton Dickinson). This method allowed blood samples to be mixed rapidly with 4 mL of stop solution, which prevents adenosine degradation and uptake.…”

Section: Adenosine Plasma Levelsmentioning

confidence: 99%

“…6,7 Briefly, a modular system with a UV detector was used. Lyophilized samples were dissolved in 1 mL of phosphate buffer (pH 4) and eluted with a methanol gradient on a Merck LIChrospher C18 column.…”

Section: Adenosine Plasma Levelsmentioning

confidence: 99%

“…Patients with a negative head-up tilt test had baseline adenosine plasma levels that were in the same range as those reported in the venous blood of normal healthy volunteers. 6,8 (2) During syncope, adenosine levels increased by an average of 52% compared with baseline levels. The higher the adenosine plasma level, the earlier the symptoms appeared and the greater the slowing of heart rate.…”

Section: Saadjian Et Al Endogenous Adenosine In Vasovagal Syncopementioning

confidence: 99%

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Role of Endogenous Adenosine as a Modulator of Syncope Induced During Tilt Testing

et al. 2002

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Background-Previous reports that used head-up tilt testing and adenosine administration have suggested that adenosine may be an important endogenous mediator that may trigger a vasovagal response in susceptible patients. However, little is known regarding endogenous adenosine plasma levels (APLs) during vasovagal syncope provoked by tilt testing. The aim of this study was to determine whether APLs differ in patients with a positive head-up tilt test compared with those with a negative test and whether APLs are modified during tilt-induced vasovagal syncope. Methods and Results-APLs (meanϮSEM) were measured during head-up tilt test in 26 patients who presented with unexplained syncope. In the 15 patients with a negative test, APLs were 0.39Ϯ0.03 mol/L at baseline, 0.22Ϯ0.03 mol/L immediately after tilting, and 0.44Ϯ0.03 mol/L after 45 minutes. APLs were significantly higher in the 11 patients with a positive test (2.66Ϯ0.67 mol/L at baseline and 3.22Ϯ0.85 mol/L immediately after tilting) than in those with a negative test. During tilt testing-induced syncope, APLs increased to reach 4.03Ϯ0.66 mol/L (ie, a 52% increase compared with baseline levels; PϽ0.02). Furthermore, we observed that the higher the APL during syncope, the shorter the time to appearance of symptoms. Conclusions-This study showed that APLs were higher in patients with a positive tilt test than in patients with a negative test and that they increased during tilt testing-induced syncope. These observations suggest that adenosine release may be involved in the triggering mechanism of syncope induced during tilt testing. (Circulation. 2002;106:569-574.)

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Section: Adenosine Plasma Levelsmentioning

confidence: 99%

Section: Adenosine Plasma Levelsmentioning

confidence: 99%

Section: Saadjian Et Al Endogenous Adenosine In Vasovagal Syncopementioning

confidence: 99%

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Role of Endogenous Adenosine as a Modulator of Syncope Induced During Tilt Testing

et al. 2002

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“…Lipids were separated on a Zorbax Eclipse XDB-C8 column, 4. Measurement of Plasma Nucleotide Concentrations-Plasma levels of ATP, ADP, and adenosine were measured using minor adaptations of previously published procedures (35,36). In brief, plasma samples were collected directly into stop solution, deproteinated by extraction with perchloric acid, then neutralized by extraction with a mixture of tri-n-octylamine and Freon.…”

Section: Enpp2-tg and Enpp2mentioning

confidence: 99%

Autotaxin/Lysopholipase D and Lysophosphatidic Acid Regulate Murine Hemostasis and Thrombosis

Pamuklar

Federico

Liu

et al. 2009

Journal of Biological Chemistry

132

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The lipid mediator lysophosphatidic acid (LPA) is a potent regulator of vascular cell function in vitro, but its physiologic role in the cardiovasculature is largely unexplored. To address the role of LPA in regulating platelet function and thrombosis, we investigated the effects of LPA on isolated murine platelets. Although LPA activates platelets from the majority of human donors, we found that treatment of isolated murine platelets with physiologic concentrations of LPA attenuated agonist-induced aggregation. Transgenic overexpression of autotaxin/lysophospholipase D (Enpp2), the enzyme necessary for production of the bulk of biologically active LPA in plasma, elevated circulating LPA levels and induced a bleeding diathesis and attenuation of thrombosis in mice. Intravascular administration of exogenous LPA recapitulated the prolonged bleeding time observed in Enpp2-Tg mice. Enpp2 ؉/؊ mice, which have ϳ50% normal plasma LPA levels, were more prone to thrombosis. Plasma autotaxin associated with platelets during aggregation and concentrated in arterial thrombus, and activated but not resting platelets bound recombinant autotaxin/ lysoPLD in an integrin-dependent manner. These results identify a novel pathway in which LPA production by autotaxin/lysoPLD regulates murine hemostasis and thrombosis and suggest that binding of autotaxin/lysoPLD to activated platelets may provide a mechanism to localize LPA production.

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“…Plasma atrial natriuretic peptide levels have been reported to be similar in hypotensive and normotensive dialysis patients [15,16], but the possible role of this molecule in chronic hypotension in uremia is controversial [6]. In addition, it has been shown that plasma levels of adenosine, a strong hypotensive agent, are increased, while the activity of intracellular adenosine deaminase, the enzyme that metabolizes this agent, is reduced in HD patients, but not in predialysis or peritoneal dialysis patients [17]. However, the possible role of this agent in hypotension in dialysis patients has yet to be fully evaluated.…”

Section: Discussionmentioning

confidence: 99%

Plasma Concentrations of Adrenomedullin and Ghrelin in Hemodialysis Patients with Sustained and Episodic Hypotension

et al. 2005

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Abstract. Sustained and/or episodic hypotension during hemodialysis (HD) is an important clinical issue. Plasma adrenomedullin (AM) is increased in HD patients with sustained hypotension, but little is known about its implications for episodic hypotension. Ghrelin may also contribute to the pathophysiology of hypotension in HD patients. We evaluated plasma levels of AM and total ghrelin in sustained hypotensive (SH; n = 23), episodic hypotensive (EH; n = 30) and normotensive (NT; n = 23) HD patients. In the EH group, the relationship between low blood pressure during HD and circulating levels of AM and ghrelin was also evaluated. Plasma levels of AM were significantly higher in SH (34.3 ± 8.3 fmol/ml, p<0.01) than in NT patients (27.6 ± 5.2 fmol/ml), but not in EH patients (30.8 ± 6.1 fmol/ml). There was no significant difference of plasma total ghrelin in SH (548.1 ± 426.5 fmol/ml) and in EH patients (544.6 ± 174.3 fmol/ml), compared with NT patients (400.0 ± 219.7 fmol/ml). On the other hand, in EH patients, the "suppressed blood pressure ratio" during HD significantly correlated with plasma AM (r = 0.77, p<0.001) and with total ghrelin levels (r = 0.44, p<0.05). Our results suggest that ghrelin, as well as AM, may play an important role as vasodilator local hormones and regulation of blood pressure during HD, especially the occurrence of EH. Further studies are necessary to clarify the implication of these hormones in the control of hypotension during HD.Key words: Adrenomedullin, Chronic hypotension, Episodic hypotension, Ghrelin, Hemodialysis, Sustained hypotension (Endocrine Journal 52: 23-28, 2005) SIGNIFICANT hypotension is a major cardiovascular complication in patients with end-stage renal disease undergoing hemodialysis (HD). Two types of hypotension are recognizable in the setting of maintenance HD: episodic hypotension (EH) during HD is the most common manifestation of hemodynamic instability, and occurs in around 30-40% of the dialysis population [1]. A second form is sustained hypotension (SH), characterized by a systolic blood pressure (SBP) lower than 100 mmHg, during the interdialysis period and is present in approximately 5-10% of patients [2,3]. Both groups of patients require a substantial amount of medical and nursing care during and after HD to control hypotension-related symptoms. Although several clinical factors, such as autonomic dysfunction, reduced pressor response to vasopressor agents and cardiac dysfunction, have been shown to be responsible for the occurrence of EH and SH [1], the pathophysiology of chronic hypotension in dialysis patients has yet to be fully clarified.

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Adenosine and Hemodialysis in Humans

Abstract: These data indicate that chronic HD inhibited MCADA activity and increased ADO plasma concentration. Both high ADO plasma concentration and low MCADA activity may be involved in dialysis-induced immune system failure and thereby favor infectious diseases.

Cited by 15 publications

References 62 publications

Role of Endogenous Adenosine as a Modulator of Syncope Induced During Tilt Testing

Role of Endogenous Adenosine as a Modulator of Syncope Induced During Tilt Testing

Autotaxin/Lysopholipase D and Lysophosphatidic Acid Regulate Murine Hemostasis and Thrombosis

Plasma Concentrations of Adrenomedullin and Ghrelin in Hemodialysis Patients with Sustained and Episodic Hypotension

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