Stimulation of erythropoietin release by hypoxia and hypoxemia: similar but different

Lee, Chang Joon; Smith, David W.; Gardiner, Bruce S.; Evans, Roger G.

doi:10.1016/j.kint.2018.09.025

Cited by 6 publications

(7 citation statements)

References 9 publications

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“…Under these conditions, oxygen diffusion from the arterial tree results in a more pronounced reduction in the PO 2 of blood, as it flows to the microvasculature, compared with normal conditions. 23 As we show herein, the change in P k O 2 is proportional to the change in C a O 2 . The consequence of this physiologic system is that the EPO-producing cells in the kidney are in an ideal place to sense changes in C a O 2 and thus regulate red cell production in response to acute anemia.…”

Section: Kidney Microvascular P K O 2 Valuessupporting

confidence: 50%

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Renal microvascular oxygen tension during hyperoxia and acute hemodilution assessed by phosphorescence quenching and excitation with blue and red light

Chin

Cazorla-Bak

Liu

et al. 2020

Can J Anesth/J Can Anesth

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PurposeThe kidney plays a central physiologic role as an oxygen sensor. Nevertheless, the direct mechanism by which this occurs is incompletely understood. We measured renal microvascular partial pressure of oxygen (P k O 2 ) to determine the impact of clinically relevant conditions that acutely change P k O 2 including hyperoxia and hemodilution.Methods We utilized two-wavelength excitation (red and blue spectrum) of the intravascular phosphorescent oxygen sensitive probe Oxyphor PdG4 to measure renal tissue PO 2 in anesthetized rats (2% isoflurane, n = 6) under two conditions of altered arterial blood oxygen content (C a O 2 ): 1) hyperoxia (fractional inspired oxygen 21%, 30%, and 50%) and 2) acute hemodilutional anemia (baseline, 25% and 50% acute hemodilution). The mean arterial blood pressure (MAP), rectal temperature, arterial blood gases (ABGs), and chemistry (radiometer) were measured under each condition. Blue and red light enabled measurement of Kyle Chin and Melina P. Cazorla-Bak contributed equally to this manuscript.

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Section: Kidney Microvascular P K O 2 Valuessupporting

confidence: 50%

“…Third, these measurements were performed under anesthesia, which is known to impact renal oxygen delivery. 23 Indeed, increased F I O 2 and hyperoxia have been shown to restore renal oxygen tension in experimental models potentially supporting the use of hyperoxia in patients under general anesthesia to preserve renal function.…”

Section: Limitationsmentioning

confidence: 97%

Renal microvascular oxygen tension during hyperoxia and acute hemodilution assessed by phosphorescence quenching and excitation with blue and red light

Chin

Cazorla-Bak

Liu

et al. 2020

Can J Anesth/J Can Anesth

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“…As described earlier (see Reason 3), through its role in the production of erythropoietin, and thus the production of erythrocytes, the kidney is the body's "critmeter" (Donnelly, 2003). Renal hypoxia provides the signal for production of erythropoietin (Lee et al, 2019;Montero and Lundby, 2019). Moreover, through its role in the excretion of fluid and electrolytes, the kidney determines extracellular fluid volume and, thus, plasma volume (Bie, 2009).…”

Section: Reason 4: the Kidney Is Not Very Good At Defending Itself Frmentioning

confidence: 89%

“…The kidney regulates hematocrit both through release of erythropoietin and, thus, stimulation of erythrocyte production, and through control of salt and water excretion and, thus, plasma volume. In response to either hypoxemia or anemia, the resultant renal hypoxia increases the renal production and circulating levels of erythropoietin (Lee et al, 2019;Montero and Lundby, 2019), which in turn stimulates erythropoiesis. Hypoxia also acutely stimulates diuresis and natriuresis (Goldfarb-Rumyantzev and Alper, 2014), promoting hemoconcentration.…”

Section: Reason 3: the Poor Capacity For Angiogenesis In The Adult Kimentioning

confidence: 99%

What Makes the Kidney Susceptible to Hypoxia?

Evans

Smith

Lee

et al. 2019

The Anatomical Record

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Per gram of tissue, the kidneys are among our most highly perfused organs. Yet the renal cortex and, in particular, the renal medulla are susceptible to hypoxia. In turn, hypoxia is a major pathophysiological feature of both acute kidney injury and chronic kidney disease. We identify seven factors that render the kidney susceptible to hypoxia: (1) the large metabolic demand imposed by active reabsorption of sodium; (2) limitations on oxygen delivery to cortical tissue imposed by the density of peritubular capillaries; (3) the poor capacity for angiogenesis in the adult kidney; (4) the limited ability of the renal vasculature to dilate in response to hypoxia; (5) diffusive oxygen shunting between arteries and veins in the cortex and descending and ascending vasa recta in the medulla; (6) the physiological requirement for low medullary blood flow to facilitate urinary concentration; and (7) the topography of vascular‐tubular arrangements in the outer medulla that limit oxygen delivery to the thick ascending limb of Henle's loop. Recent collaborative efforts between anatomists, physiologists, and mathematicians have improved our understanding of the roles of these factors in both physiological regulation of intrarenal oxygenation and development of renal hypoxia under pathophysiological conditions. We are also better able to understand these apparent maladaptations in the context of evolution. That is, they can be explained by the combined effects of historical contingency (our ancestral life in the sea) and selection pressures imposed by the multiple functions of the kidney to regulate extracellular fluid volume, retain water, and control erythrocyte production.

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“…It has been suggested that hypoxia does not interfere with angiogenesis in kidney endothelial cells to prevent the impairment of hematocrit regulatory mechanisms [189], a balance between the erythropoietin stimulation of erythrocyte production and also control of the blood volume by modulating salt and water excretion. Hypoxia elicits renal production of erythropoietin [205,206] and also acutely stimulates diuresis and natriuresis [207,208], promoting hemoconcentration. The exact link between cysteine metabolism and this mechanism remains to be clarified.…”

Section: Cysteine Contribution For Kidney Adaptation To Hypoxiamentioning

confidence: 99%

Cysteine as a Multifaceted Player in Kidney, the Cysteine-Related Thiolome and Its Implications for Precision Medicine

et al. 2022

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In this review encouraged by original data, we first provided in vivo evidence that the kidney, comparative to the liver or brain, is an organ particularly rich in cysteine. In the kidney, the total availability of cysteine was higher in cortex tissue than in the medulla and distributed in free reduced, free oxidized and protein-bound fractions (in descending order). Next, we provided a comprehensive integrated review on the evidence that supports the reliance on cysteine of the kidney beyond cysteine antioxidant properties, highlighting the relevance of cysteine and its renal metabolism in the control of cysteine excess in the body as a pivotal source of metabolites to kidney biomass and bioenergetics and a promoter of adaptive responses to stressors. This view might translate into novel perspectives on the mechanisms of kidney function and blood pressure regulation and on clinical implications of the cysteine-related thiolome as a tool in precision medicine.

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Stimulation of erythropoietin release by hypoxia and hypoxemia: similar but different

Cited by 6 publications

References 9 publications

Renal microvascular oxygen tension during hyperoxia and acute hemodilution assessed by phosphorescence quenching and excitation with blue and red light

Renal microvascular oxygen tension during hyperoxia and acute hemodilution assessed by phosphorescence quenching and excitation with blue and red light

What Makes the Kidney Susceptible to Hypoxia?

Cysteine as a Multifaceted Player in Kidney, the Cysteine-Related Thiolome and Its Implications for Precision Medicine

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