The influence of the autonomic nervous system in the control of erythropoietin secretion in the hypoxic rat.

Beynon, G. P. J.

doi:10.1113/jphysiol.1977.sp011771

Cited by 29 publications

(16 citation statements)

References 9 publications

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“…However, DNX rats revealed a significant higher EPO secretory response after exposure to 600 ppm compared with INN rats. In previous studies, animals were exposed to only severe and nearly maximal hypoxic stimuli (1000 ppm, 10% O 2 or 0.42 atmospheres over 4, 6, or 5 h, respectively) (Fink and Fisher, 1976;Beynon, 1977;Eckardt et al, 1992). Therefore, an effect of renal nerves on EPO secretion at half-maximal stimulation could not be detected in these experiments.…”

Section: Discussionmentioning

confidence: 85%

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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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Section: Discussionmentioning

confidence: 85%

“…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.…”

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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“…Indeed, renal denervation in animal models led to a loss of EPO production in response to hypoxic stimuli [14, 15]. Furthermore, EPO deficiency has recently been observed in anemic type 1 diabetic patients with severe symptomatic diabetic autonomic neuropathy [16, 17, 18].…”

Section: Pathophysiology Of Anemia In Diabetic Patientsmentioning

confidence: 99%

Anemia and Diabetes

et al. 2004

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World Health Organization statistics identify 150 million people with diabetes mellitus worldwide and suggest that this figure may double by 2025. In countries with a western lifestyle, the number of patients admitted for renal replacement therapy with diabetes as a co-morbid condition has increased significantly up to three to four times in a period of 10 years. Diabetes and renal failure are thus tightly linked diseases, and so is anemia. However, whether anemia may be worsened and/or directly, at least in part, caused by diabetes is not clearly elucidated yet. In this article, we review the prevalence, pathophysiology and consequences of anemia in diabetic patients.

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“…Es war zunächst nicht klar, ob sich dieser Sauerstoffsensor in der Niere selbst befindet: daher lag es auf der Hand, die Rolle der klassischen Chemorezep toren in der Regulation der EPO-Produktion zu untersu chen. Es scheint jedoch, dass weder die Funktion der Karotiskörperchen noch irgendein anderer neuraler In put in die Niere erforderlich ist, um die EPO-Syntheseals Reaktion auf Hypoxie zu steigern [29,30]. Andererseits kann die selektive Reduktion des renalen Blutstroms die EPO-Bildung erhöhen [31 -33].…”

Section: Der Renale Sauerstoffsensorunclassified