Reduction in central venous pressure enhances erythropoietin synthesis: role of volume‐regulating hormones

Abstract

Reduction in CVP prompts an increase in plasma EPO concentration independent of hemoconcentration and hence suggests CVP per se as an acute regulator of EPO synthesis. This effect may be explained by changes in volume-regulating hormones.

Unexplained Anemia in the Elderly: Potential Role of Arterial Stiffness

“…In humans, hypervolemic hemodilution increasing CVP paralleled a decrease in circulating EPO seemingly beyond the dilution effect (Breymann et al, 2000). Recently, plasma EPO concentration was found increased independent of hemoconcentration, with moderate head-up tilt redistributing blood toward the lower limbs and thereby reducing CVP (Montero et al, 2016b). Overall, these studies suggest that CVP per-se could be a regulator of EPO production.…”

“…In this line, aging has been associated with a blunted VPN release in response to conditions associated with reduced CVP such as acute post-exercise hypotension (Kirsch et al, 1986; Halliwill et al, 2000; Keck et al, 2000). Importantly, the increase in EPO concentration induced by decreasing CVP is abolished when adjusted for the concomitant increase in copeptin (Montero et al, 2016b), a marker of VPN (Morgenthaler et al, 2008). Indeed, changes in copeptin with experimental manipulation of CVP independently explained simultaneously occurring changes in EPO concentration in healthy adults (Montero et al, 2016b).…”

“…Importantly, the increase in EPO concentration induced by decreasing CVP is abolished when adjusted for the concomitant increase in copeptin (Montero et al, 2016b), a marker of VPN (Morgenthaler et al, 2008). Indeed, changes in copeptin with experimental manipulation of CVP independently explained simultaneously occurring changes in EPO concentration in healthy adults (Montero et al, 2016b). Furthermore, VPN administration is associated with increased plasma EPO levels and red cell mass in hypopituitaric patients (Jepson et al, 1968).…”

New insights into the astonishing diversity of hormone functions

“…A second stimulus for the synthesis of aldosterone is an increase in the plasma K + concentration, whereas hypokalaemia inhibits aldosterone synthesis. 7 A reduction of central venous pressure that is independent of changes in blood volume causes the release of volume-regulating hormones. In primary aldosteronism, synthesis of aldosterone is partially or completely independent of the RAS.…”

“…4 An inappropriately high aldosterone secretion can lead to a disease called primary aldosteronism, which represents the most common cause of secondary hypertension. 7 One antagonist of the RAS-hormone aldosterone is desoxycorticosterone, a descendant of the mineralocorticoid progesterone. Autonomous aldosterone secretion is, for example, caused by recurrent somatic mutations of the Potassium Voltage-Gated Channel Subfamily J Member 5 gene (KCNJ5) which encodes G protein-activated inward rectifier potassium channel 4 located in aldosterone-expressing adenomas.…”