Direct evidence for erythropoietin-induced release of endothelin from peripheral vascular tissue

Katoh, Kiyoshi; Mizuno, Kenji; Hashimoto, Shigeatsu; K, Okazaki; Asahi, Koichi; Kuriki, Minoru; Yamada, Daishiro; Fukuchi, Soitsu

doi:10.1016/0024-3205(94)00842-6

Cited by 24 publications

(4 citation statements)

References 16 publications

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“…74 In addition, intra-arterial infusion of erythropoietin increases ET-1 release in the isolated rat limb. 75 Finally, erythropoietin-induced hypertension in experimental animals is ameliorated by blockade of the endothelin A receptor. 76 Erythropoietin treatment upregulates levels of messenger RNA for renin and angiotensinogen in rat renal and vascular tissues, but this therapy does not raise plasma renin activity or angiotensinogen levels either in rats 77 or in patients with ESRD.…”

Section: Effects On Endothelin Renin and Angiotensin And Prostaglanmentioning

confidence: 99%

Anemia and anemia correction: surrogate markers or causes of morbidity in chronic kidney disease?

Vaziri

2008

Nat Rev Nephrol

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Observational studies have shown a strong positive correlation between the severity of anemia and the risk of poor outcomes in patients with chronic kidney disease (CKD). This observation was initially taken to imply that adverse outcomes in CKD are caused by anemia. However, the assumption of causality ignores the possibility that anemia and adverse outcomes might be unrelated and that both are caused by underlying inflammation, oxidative stress and comorbid conditions. Randomized clinical trials of anemia correction have revealed an increased risk of adverse cardiovascular outcomes in patients assigned to normal, rather than subnormal, hemoglobin targets. As a result, correction of anemia is now considered potentially hazardous in patients with CKD. Notably, individuals who did not reach the target hemoglobin level in the clinical trials, despite receiving high doses of erythropoietin and iron, experienced a disproportionately large share of the adverse outcomes. These observations point to overdose of erythropoietin and iron, rather than anemia correction per se, as the likely culprit. This Review explores the reasons for the apparent contradiction between the findings of observational studies and randomized clinical trials of anemia treatment in CKD. I have focused on data from basic and translational studies, which are often overlooked in the design and interpretation of clinical studies and in the formulation of clinical guidelines.

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Section: Effects On Endothelin Renin and Angiotensin And Prostaglanmentioning

confidence: 99%

Anemia and anemia correction: surrogate markers or causes of morbidity in chronic kidney disease?

Vaziri

2008

Nat Rev Nephrol

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“…EPO stimulates the release of Endothelin-1 (ET-1) in endothelial cells in culture [140], in isolated rat hind legs [156] and in mice with overexpression of EPO [157]. High ET-1 levels have been found in some [158], but not all [159], studies on patients treated with EPO.…”

Section: Erythropoietin and Shockmentioning

confidence: 97%

From the Oxygen to the Organ Protection: Erythropoietin as Protagonist in Internal Medicine

Buemi¹,

Nostro²,

Giacobbe³

et al. 2006

CHAMC

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Erythropoietin (EPO), already known as the stimulating hormone for erythropoiesis, has shown different and interesting pleiotropic actions. It does not only affect erythroid cells, but also myeloid cells, lymphocytes and megakaryocytes. This hormone can also enhance phagocytic function of the polymorphonuclear cells and reduce the activation of macrophages, thus modulating the inflammatory process.Moreover, hematopoietic and endothelial cells probably have the same cellular origin, and the discovery of erythropoietin receptors (EPO-R) also on mesangial and myocardial cells, smooth muscle fibrocells and neurons has prompted the study of the non-erythropoietic functions of this hormone.The interaction between EPO and VEGF may be of particular importance in neovascularization and wound healing. Different studies have demonstrated that EPO has an important direct hemodynamic and vasoactive action, which does not depend exclusively on any increase in hematocrit and viscosity. Moreover EPO showed protective effects on myocardial cells against apoptosis induced by ischemia/repefusion injury, but it could negatively affect pulmonary hypertension in patient with chronic cor pulmonale.This review aims to stress the importance of the increasing interest in EPO applications and the necessity of further studies to gain a deeper knowledge of this hormone and its pleiotropic and complex actions.

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“…The rationale is illusmolecular mechanisms may be involved, e.g. enhancetrated by the CAST study, which led to the completely ment of the vasoconstrictor endothelin I and constrictor prostanoids [45,46 ], activation of the local Table 3. Effect of r-HuEPO treatment on eight dialysis patients with renin system [47] and expression of growth factors angina pectoris [39] mediated via the angiotensin II-AT-l-pathway [48].…”

Section: Et Al In Los Angeles It Is Known That Cognitivementioning

confidence: 99%

Optimal haemoglobin during treatment with recombinant human erythropoietin

Ritz¹,

Amann²

1998

Nephrology Dialysis Transplantation

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The optimal target haemoglobin during treatment with recombinant human erythropoietin (r-HuEPO) is still controversial. The impact of haemoglobin on cardiovascular function or survival, on physical performance and on medical rehabilitation have to be taken into consideration. Although currently there is no solid evidence to show that haemoglobin beyond that recommended by the ad hoc committee of the National Kidney Foundation improves survival, sound theoretical arguments can be offered for this proposition, particularly in cardiac patients. It is sensible to individualize the target haemoglobin and to avoid rapid correction of anaemia.

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Direct evidence for erythropoietin-induced release of endothelin from peripheral vascular tissue

Cited by 24 publications

References 16 publications

Anemia and anemia correction: surrogate markers or causes of morbidity in chronic kidney disease?

Anemia and anemia correction: surrogate markers or causes of morbidity in chronic kidney disease?

From the Oxygen to the Organ Protection: Erythropoietin as Protagonist in Internal Medicine

Optimal haemoglobin during treatment with recombinant human erythropoietin

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