Direct vasopressor effect of recombinant human erythropoietin on renal resistance vessels

Heidenreich, Stefan; Rahn, K. H.; Zidek, Walter

doi:10.1038/ki.1991.31

Cited by 181 publications

(97 citation statements)

References 18 publications

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“…Recombinant human EPO (rHuEPO) causes contraction of isolated resistance vessels of the renal and mesenteric vascular beds. 7 These effects are endothelium independent and are not abolished by calcium antagonists or angiotensin II (AII) receptor antagonists. In cultured human coronary artery cells EPO causes dosedependent inhibition of basal and acetylcholine stimulated nitric oxide (NO) production and eNOS protein expression suggesting that EPO may also alter vascular reactivity by endothelium dependent mechanisms.…”

Section: Discussionmentioning

confidence: 99%

“…1,3 Cortisol treatment also causes suppression of the nitric oxide system as evidenced by reduced plasma nitrate/nitrite concentrations. 5 In the context of these observations, Correspondence 6,7 EPO-induced hypertension has also been demonstrated to be due in part to nitric oxide resistance. 8 The aim of the current study was to examine the role of EPO as a possible mediator of cortisolinduced hypertension.…”

Section: Introductionmentioning

confidence: 99%

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Role of erythropoietin in cortisol-induced hypertension

2000

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The mechanism of cortisol-induced hypertension remains unknown. We investigated a possible role of erythropoietin (EPO) as a mediator of hypertension in healthy male subjects treated with cortisol. In Study 1, blood pressure (BP) and serum EPO concentrations were measured on alternate days in nine subjects treated with 80 mg of cortisol per day for 5 days. In Study 2 the same parameters were measured in eight subjects randomised to cortisol (80 mg/day) or placebo and 10 subjects randomised to cortisol (200 mg/day) or placebo for 5 days. In Study 1, cortisol caused a significant increase in systolic BP (SBP) (115 ؎ 2 vs 126 ؎ 2 mm Hg, control vs day 5, P Ͻ 0.001) and serum EPO

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Role of erythropoietin in cortisol-induced hypertension

2000

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“…The mechanism by which rHuEPO induces hypertension has been in the past explained by an increase of blood viscosity strongly related to the hematocrit (Mayer et al 1988 ;Raine 1988), or vasoconstriction elicited by improvement of hypoxia (Eschbach et al 1987 ;Kamata et al 1991). Recently, Heidenreich et al (1991) have reported that rHuEPO has a direct vasopressor effect on renal and mesenteric resistance vessels of normotensive Wistar-Kyoto rats in vitro and that threshold concentration for a pressor response to rHuEPO is 10 U/ml. They suggest that the vasopressor capacity of rHuEPO may contribute to the development of hypertension seen in rHuEPO-treated dialysis patients and may amplify or aggravate other relevant pathomechanisms of hypertension.…”

Section: Discussionmentioning

confidence: 99%

“…Recently, Heidenreich et al (1991) have reported that rHuEPO has a direct vasopressor effect on proximal resistance vessels taken from Wistar-Kyoto rats without renal failure, which may contribute to the development of hypertension seen in rHuEPO-treated dialysis patients. Therefore, the present study was designed to determine whether rHuEPO has direct effects on mean arterial pressure (MAP) or renal hemodynamics in anesthetized rabbits without renal failure.…”

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confidence: 99%

The Effects of Intrarenal Infusion of Recombinant Human Erythropoietin on Mean Arterial Pressure and Renal Hemodynamics in Anesthetized Rabbits.

Nushiro

Abe²,

S³

et al. 1992

Tohoku J. Exp. Med.

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“…However, complications such as newly originated hypertension, worsening of previous hypertension, thrombosis of arteriovenous fi stula, and hyperkalemia can be caused by the use of rhEPO. [1][2][3][4] Hypertension induced with the use of erythropoietin in therapy is a complication which affects prognosis in patients treated with dialysis. 5,6 The exact mechanism of hypertension caused by rhEPO is not yet known.…”

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confidence: 99%

The influence of erythropoietin on levels of endothelin‐1 and nitric oxide in patients on hemodialysis

Tomić

Gales̃ić

Markota

et al. 2009

Dialysis & Transplantation

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The positive treatment effect with recombinant human erythropoietin (rhEPO) on anemia in patients with chronic renal failure is documented. However, complications such as newly originated hypertension, worsening of previous hypertension, thrombosis of arteriovenous fi stula, and hyperkalemia can be caused by the use of rhEPO. [1][2][3][4] Hypertension induced with the use of erythropoietin in therapy is a complication which affects prognosis in patients treated with dialysis. 5,6 The exact mechanism of hypertension caused by rhEPO is not yet known. The balance irregularities of local endothelin factors, such as endothelin-1 (ET-1) and nitric oxide (NO), are one of the suggested possible mechanisms included in hypertension caused by erythropoietin. [7][8][9][10][11][12][13][14][15] Endothelins are regulatory peptides, distributed in many organic systems with a strong physiological function.In 1988, Yanagisava isolated, sequenced, and cloned 21 amino acids from a fraction of unhomogenized endothelin cells and named them endothelin. 16 Yanagisava also isolated 2 isoforms of endothelin, different from the original endothelin in the second and sixth amino acid, and named them endothelin-2 and endothelin-3. These are the most powerful vasoconstrictive substances known today. [17][18][19][20][21][22] Endothelin-1 is produced in endothelin cells of blood vessels, in the heart, lungs, pancreas, spleen, kidneys, rear hypophysis, and cerebral neurons. Endothelin-1 is mostly produced in endothelin cells of blood vessels, but its concentrations are much higher in tissues than in plasma, where they are found in picomolar concentrations. The half-life of ET-1 in plasma is very short, only 60 to 90 seconds.Nitric oxide is a free gas radical included in various physiological processes such as vasodilatation, neuron transmission, immunological response, and modulation of thrombocyte function. It is synthesized from amino acid L-arginine using the enzymes of NO synthetase which convert arginine and oxygen in citrulline and NO. The relaxation of blood vessels is one of the physiological effects of NO. Nitrogen oxide has an important role in regulating the tone of blood vessels since it mediates in the vasodilatatory effect of many factors, limits the effects of vasoconstrictors, and reduces the aggregation of thrombocytes. 23 Also, higher blood speed, loss of hypoxic vasodilatation after the correction of anemia, and mobilization of vascular calcium OBJECTIVE: Examine the infl uence of the chronic use of erythropoietin on the value of endothelin-1 (ET-1) and nitric oxide (NO), as well as on ET-1/NO ratio in serum, before and after dialysis.METHODS: A total of 30 patients on hemodialysis were included in the study. Different doses of erythropoietin were administered at least 3 weeks before study. All patients had stable blood pressure values, without changes in antihypertensive therapy in the last 3 months, and without signifi cant intradialytic hypertension and hypotension. The concentration of ET-1 and NO was measured before and a...

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Direct vasopressor effect of recombinant human erythropoietin on renal resistance vessels

Cited by 181 publications

References 18 publications

Role of erythropoietin in cortisol-induced hypertension

Role of erythropoietin in cortisol-induced hypertension

The Effects of Intrarenal Infusion of Recombinant Human Erythropoietin on Mean Arterial Pressure and Renal Hemodynamics in Anesthetized Rabbits.

The influence of erythropoietin on levels of endothelin‐1 and nitric oxide in patients on hemodialysis

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