Fenoterol but not dobutamine increases erythropoietin production in humans

Gleiter, Christoph H.; T, Becker; Schreeb, K H; Freudenthaler, Stefan M.; Gundert‐Remy, Ursula

doi:10.1016/s0009-9236(97)90102-8

Cited by 16 publications

(43 citation statements)

References 19 publications

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“…We have shown that theophylline [5,6] and fenoterol [7] increase the EPO concentration in humans after a controlled haemorrhage compared to placebo treatment. We have shown that theophylline [5,6] and fenoterol [7] increase the EPO concentration in humans after a controlled haemorrhage compared to placebo treatment.…”

Section: Introductionmentioning

confidence: 89%

“…As in earlier studies [2,5,6,7] the following commercially available assay kits were used. EPO in plasma was analysed using a monoclonal enzyme-linked immunosorbent assay (ELISA, catalogue number 500, Medac, Hamburg, Germany), PRA was measured with a radioimmunoassay kit for angiotensin I [ 125 I]RIA (RENK P2510, Sorin Biomedica, Saluggia, Italy), and A II in plasma was determined using a radioimmunoassay (number 40-6005, Nichols Institute Diagnostics, San Juan Capistrano, USA).…”

Section: Methodsmentioning

confidence: 99%

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Dose-dependent effect of angiotensin II on human erythropoietin production

Freudenthaler

Lucht

Schenk

et al. 2000

Pfl�gers Archiv European Journal of Physiology

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Current evidence suggests that angiotensin II may be involved in the regulation of renal erythropoietin (EPO) production. The present study assessed the role of angiotensin II (A II) in different doses in the control of EPO production in humans. In a parallel, randomized, placebo-controlled open design, 60 healthy male volunteers received a 6-h intravenous infusion of: placebo (placebo, electrolyte solution), a pressor dose of A II (1-3 microg/min; A II press), a combination of a pressor dose of A II and the selective AT1-receptor blocker losartan, 50 mg (A II press + L), a subpressor dose of A II (0.0375-0.15 microg/min; A II subpress) and a combination of a subpressor dose of A II and losartan (A II subpress + L). A II press treatment resulted in a significant increase of the maximum EPO concentration (CmaxEPO, 41% higher versus placebo) and the amount of EPO produced in 24 h (AUCEPO(0-24 h), 61% larger versus placebo), A II subpress treatment increased CmaxEPO (35% higher versus placebo) and AUC(EPO)(0-24 h) (34% larger versus placebo). A II press + L and A II subpress + L treatments did not significantly increase CmaxEPO and AUCEPO(0-24 h) compared to placebo. A II affects EPO production in a dose-dependent manner. The signal seems to be mediated via AT1-receptors. A II appears to be one modulator EPO production in humans.

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Section: Introductionmentioning

confidence: 89%

Section: Methodsmentioning

confidence: 99%

Dose-dependent effect of angiotensin II on human erythropoietin production

Freudenthaler

Lucht

Schenk

et al. 2000

Pfl�gers Archiv European Journal of Physiology

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“…As in earlier studies [4][5][6][7]18], the following commercially available assay kits were used. Epo in plasma was analysed using a monoclonal enzyme-linked immunosorbent assay (ELISA, catalogue no.…”

Section: Methodsmentioning

confidence: 99%

“…In systematic examinations we have shown that theophylline increases Epo concentrations in humans after a controlled stimulus with haemorrhage [4][5][6]. These findings may be interpreted as an indirect effect, via the increase of plasma renin activity (PRA) with a subsequent increase of AII levels as it occurs during theophylline infusion.…”

Section: Introductionmentioning

confidence: 95%

Do alterations of endogenous angiotensin II levels regulate erythropoietin production in humans?

Freudenthaler¹,

Benöhr

Grenz

et al. 2003

Brit J Clinical Pharma

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Aims Recent evidence suggests a potential role of angiotensin II in the physiological regulation of erythropoietin (Epo) production. While the administration of exogenous angiotensin II (AII) has been used so far to study its effects, the role of endogenous AII has remained unclear. Methods To alter endogenous AII in humans experimentally we used furosemide bolus injection as a short-term (study 1) and dietary salt as a long-term modulator (study 2). In an open crossover design, 12 healthy male volunteers received furosemide (F) 0.5 mg kg -1 intravenously or placebo (P) in random order (study 1). With the same design, 12 volunteers received high-salt (HS), normal-salt (NS) and lowsalt (LS) diet (study 2). Plasma renin activity (PRA) was analysed along with AII. Inulin and paraaminohippurate (PAH) clearances were used to indicate glomerular filtration rate (GFR) and renal plasma flow (RPF), respectively. Results While F stimulated AII and PRA and decreased GFR and RPF significantly, no concomitant alteration of Epo was observed [AUCEpo: placebo 5709 ± 243 (% of baseline ¥ h), furosemide: 5833 ± 255 (% of baseline ¥ h); 95% confidence interval (CI) -608.4, 856.0; P = 0.73]. F decreased GFR (from 103.6 ± 4.0 to 90.6 ± 4.8 ml min -1 1 -1 73 m -2 ; 95% CI 1.1, 24.9; P < 0.05), but not RPF (study 1). Correspondingly, LS stimulated and HS decreased AII and PRA significantly. HS increased GFR and RPF. Again, Epo concentrations were not affected (AUCEpo: normal sodium 44 ± 6.7 mIU ¥ day ml -1 , low sodium 39 ± 2.4 mIU ¥ day ml -1 , high sodium 48.5 ± 6.1 mIU ¥ day ml -1 ; normal salt/low salt 95% CI -11.9, 21.9, P = 0.54; normal salt/high salt 95% CI -14.4, 23.3, P = 0.63; study 2). Conclusions We conclude that, at least in the physiological setting in healthy volunteers, increased concentrations of endogenous AII may not be a major factor of Epo regulation.

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“…However, Jelkmann et al (1979) could not confirm these findings, since his group reported unchanged EPO levels following long-term administration of a selective ␤2-adrenergic agonist in rabbits (Jelkmann et al, 1979). Studies in humans showed that EPO secretion was higher following administration of fenoterol, a ␤2-adrenergic receptor agonist following hemorrhage and under normoxic conditions (Gleiter et al, 1997(Gleiter et al, , 1998Freudenthaler et al, 1999a).…”

mentioning

confidence: 99%

Role of Renal Nerves and Salt Intake on Erythropoietin Secretion in Rats following Carbon Monoxide Exposure

Gebhard

Petroktistis²,

Zhang³

et al. 2006

J Pharmacol Exp Ther

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Because the data from the literature contain conflicting results regarding the role of renal nerves and angiotensin II in hypoxiainduced erythropoietin (EPO) secretion, we evaluated the effect of renal nerves and salt intake in rats on EPO secretion stimulated by carbon monoxide (CO). Serum levels and renal mRNA content of EPO were similarly elevated by exposure to different CO concentrations in a dose-dependent manner in rats with bilateral renal denervation (DNX) and in sham-denervated controls (INN). However, at 600 ppm CO, serum concentrations and mRNA of EPO were significantly higher in DNX compared with INN rats (p Ͻ 0.05). This increase of EPO secretion in DNX rats could be blocked by administration of neuropeptide Y (NPY) (p Ͻ 0.05), whereas the NPY receptor antagonist did not enhance EPO secretion in INN rats after CO exposure. Agonists and antagonists of ␤-adrenergic receptors had no effect on EPO secretion. High-salt (HS) diet reduced EPO secretory response at 600 ppm CO by 55% compared with INN rats on normal salt diet (p Ͻ 0.01). In addition, DNX increased EPO secretion in rats on low-salt and HS diet, whereas plasma renin activity did not correlate with EPO levels under these experimental conditions. In summary, our data suggest that renal nerves contribute to the half-maximal EPO secretory response to CO exposure, possibly via NPY receptors.Erythropoietin (EPO), a glycoprotein hormone, is an essential growth factor that regulates erythropoiesis, and in adult laboratory animals and in humans, it is predominantly synthesized in the kidneys (Jelkmann, 1992;Jelkmann and Metzen, 1996). EPO secretion and renal mRNA content are inversely correlated to renal oxygen supply (Scholz et al., 1991). Because renal ischemia in isolated perfused kidneys elicited a much weaker EPO secretory response compared with systemic hypoxia in vivo, it was postulated that additional factors such as nerves and humoral factors may contribute to EPO secretory response to hypoxia (Pagel et al., 1989).Despite that multiple studies have investigated the role of renal nerves on EPO secretion, the published data are contradictory. Beynon (1977). reported increased EPO levels in rats exposed to 6 h of hypoxia (10% O 2 ) following denervation (DNX) of the left kidney and after contralateral nephrectomy compared with control rats with intact renal nerves. In contrast Fink and Fisher (1976) found reduced EPO levels in rabbits exposed to 5 h of hypoxia (0.42 atmospheres) following bilateral renal denervation in control animals. Eckardt et al. (1992) showed in rats that denervation of one kidney does not effect EPO mRNA following systemic exposure to hypoxia, hemorrhage, and carbon monoxide (CO) compared with the contralateral innervated control kidney.Moreover, combination of renal denervation and ␤-adrenergic receptor blockade showed to inhibit the hypoxia-stimulated EPO secretion compared with controls (Fink and Fisher, 1976). However, Jelkmann et al. (1979) could not confirm these findings, since his group reported unchanged ...

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Fenoterol but not dobutamine increases erythropoietin production in humans

Cited by 16 publications

References 19 publications

Dose-dependent effect of angiotensin II on human erythropoietin production

Dose-dependent effect of angiotensin II on human erythropoietin production

Do alterations of endogenous angiotensin II levels regulate erythropoietin production in humans?

Role of Renal Nerves and Salt Intake on Erythropoietin Secretion in Rats following Carbon Monoxide Exposure

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