Neuroendocrine and renal effects of intravascular volume expansion in compensated heart failure.

A Gabrielsen; P Bie; N H Holstein-Rathlou; N J Christensen; J Warberg; H Dige-Petersen; E Frandsen; S Galatius; B Pump; V B Sørensen; J Kastrup; P Norsk

Neuroendocrine and renal effects of intravascular volume expansion in compensated heart failure.

A Gabrielsen, P Bie, N H Holstein-Rathlou, N J Christensen, J Warberg, H Dige-Petersen, E Frandsen, S Galatius, B Pump, V B Sørensen, J Kastrup, P Norsk

Department of Biomedical Sciences

35 Citations (Scopus)

Abstract

To examine if the neuroendocrine link between volume sensing and renal function is preserved in compensated chronic heart failure [HF, ejection fraction 0.29 +/- 0.03 (mean +/- SE)] we tested the hypothesis that intravascular and central blood volume expansion by 3 h of water immersion (WI) elicits a natriuresis. In HF, WI suppressed ANG II and aldosterone (Aldo) concentrations, increased the release of atrial natriuretic peptide (ANP), and elicited a natriuresis (P < 0.05 for all) compared with seated control. Compared with control subjects (n = 9), ANG II, Aldo, and ANP concentrations were increased (P < 0.05) in HF, whereas absolute and fractional sodium excretion rates were attenuated [47 +/- 16 vs. 88 +/- 15 micromol/min and 0.42 +/- 0.18 vs. 0.68 +/- 0.12% (mean +/- SE), respectively, both P < 0.05]. When ANG II and Aldo concentrations were further suppressed (P < 0.05) during WI in HF (by sustained angiotensin-converting enzyme inhibitor therapy, n = 9) absolute and fractional sodium excretion increased (P < 0.05) to the level of control subjects (108 +/- 34 micromol/min and 0.70 +/- 0.23%, respectively). Renal free water clearance increased during WI in control subjects but not in HF, albeit plasma vasopressin concentrations were similar in the two groups. In conclusion, the neuroendocrine link between volume sensing and renal sodium excretion is preserved in compensated HF. The natriuresis of WI is, however, modulated by the prevailing ANG II and Aldo concentrations. In contrast, renal free water clearance is attenuated in response to volume expansion in compensated HF despite normalized plasma AVP concentrations.

Original language	English
Journal	American Journal of Physiology: Regulatory, Integrative and Comparative Physiology
Volume	281
Issue number	2
Pages (from-to)	R459-67
ISSN	0363-6119
Publication status	Published - 2001

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Gabrielsen, A., Bie, P., Holstein-Rathlou, N. H., Christensen, N. J., Warberg, J., Dige-Petersen, H., Frandsen, E., Galatius, S., Pump, B., Sørensen, V. B., Kastrup, J., & Norsk, P. (2001). Neuroendocrine and renal effects of intravascular volume expansion in compensated heart failure. American Journal of Physiology: Regulatory, Integrative and Comparative Physiology, 281(2), R459-67.

Gabrielsen, A, Bie, P, Holstein-Rathlou, NH, Christensen, NJ, Warberg, J, Dige-Petersen, H, Frandsen, E, Galatius, S, Pump, B, Sørensen, VB, Kastrup, J & Norsk, P 2001, 'Neuroendocrine and renal effects of intravascular volume expansion in compensated heart failure.', American Journal of Physiology: Regulatory, Integrative and Comparative Physiology, vol. 281, no. 2, pp. R459-67.

@article{680eb810ab6311ddb5e9000ea68e967b,

title = "Neuroendocrine and renal effects of intravascular volume expansion in compensated heart failure.",

abstract = "To examine if the neuroendocrine link between volume sensing and renal function is preserved in compensated chronic heart failure [HF, ejection fraction 0.29 +/- 0.03 (mean +/- SE)] we tested the hypothesis that intravascular and central blood volume expansion by 3 h of water immersion (WI) elicits a natriuresis. In HF, WI suppressed ANG II and aldosterone (Aldo) concentrations, increased the release of atrial natriuretic peptide (ANP), and elicited a natriuresis (P < 0.05 for all) compared with seated control. Compared with control subjects (n = 9), ANG II, Aldo, and ANP concentrations were increased (P < 0.05) in HF, whereas absolute and fractional sodium excretion rates were attenuated [47 +/- 16 vs. 88 +/- 15 micromol/min and 0.42 +/- 0.18 vs. 0.68 +/- 0.12% (mean +/- SE), respectively, both P < 0.05]. When ANG II and Aldo concentrations were further suppressed (P < 0.05) during WI in HF (by sustained angiotensin-converting enzyme inhibitor therapy, n = 9) absolute and fractional sodium excretion increased (P < 0.05) to the level of control subjects (108 +/- 34 micromol/min and 0.70 +/- 0.23%, respectively). Renal free water clearance increased during WI in control subjects but not in HF, albeit plasma vasopressin concentrations were similar in the two groups. In conclusion, the neuroendocrine link between volume sensing and renal sodium excretion is preserved in compensated HF. The natriuresis of WI is, however, modulated by the prevailing ANG II and Aldo concentrations. In contrast, renal free water clearance is attenuated in response to volume expansion in compensated HF despite normalized plasma AVP concentrations.",

author = "A Gabrielsen and P Bie and Holstein-Rathlou, {N H} and Christensen, {N J} and J Warberg and H Dige-Petersen and E Frandsen and S Galatius and B Pump and S{\o}rensen, {V B} and J Kastrup and P Norsk",

note = "Keywords: Aldosterone; Angiotensin II; Angiotensin-Converting Enzyme Inhibitors; Atrial Natriuretic Factor; Blood Pressure; Blood Volume; Cardiac Output, Low; Enzyme Inhibitors; Fluid Shifts; Glomerular Filtration Rate; Heart Rate; Humans; Immersion; Kidney; Male; Middle Aged; Natriuresis; Sodium; Urine; Vasopressins; Water-Electrolyte Balance",

year = "2001",

language = "English",

volume = "281",

pages = "R459--67",

journal = "American Journal of Physiology - Regulatory Integrative and Comparative Physiology",

issn = "0363-6119",

publisher = "American Physiological Society",

number = "2",

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TY - JOUR

T1 - Neuroendocrine and renal effects of intravascular volume expansion in compensated heart failure.

AU - Gabrielsen, A

AU - Bie, P

AU - Holstein-Rathlou, N H

AU - Christensen, N J

AU - Warberg, J

AU - Dige-Petersen, H

AU - Frandsen, E

AU - Galatius, S

AU - Pump, B

AU - Sørensen, V B

AU - Kastrup, J

AU - Norsk, P

N1 - Keywords: Aldosterone; Angiotensin II; Angiotensin-Converting Enzyme Inhibitors; Atrial Natriuretic Factor; Blood Pressure; Blood Volume; Cardiac Output, Low; Enzyme Inhibitors; Fluid Shifts; Glomerular Filtration Rate; Heart Rate; Humans; Immersion; Kidney; Male; Middle Aged; Natriuresis; Sodium; Urine; Vasopressins; Water-Electrolyte Balance

PY - 2001

Y1 - 2001

N2 - To examine if the neuroendocrine link between volume sensing and renal function is preserved in compensated chronic heart failure [HF, ejection fraction 0.29 +/- 0.03 (mean +/- SE)] we tested the hypothesis that intravascular and central blood volume expansion by 3 h of water immersion (WI) elicits a natriuresis. In HF, WI suppressed ANG II and aldosterone (Aldo) concentrations, increased the release of atrial natriuretic peptide (ANP), and elicited a natriuresis (P < 0.05 for all) compared with seated control. Compared with control subjects (n = 9), ANG II, Aldo, and ANP concentrations were increased (P < 0.05) in HF, whereas absolute and fractional sodium excretion rates were attenuated [47 +/- 16 vs. 88 +/- 15 micromol/min and 0.42 +/- 0.18 vs. 0.68 +/- 0.12% (mean +/- SE), respectively, both P < 0.05]. When ANG II and Aldo concentrations were further suppressed (P < 0.05) during WI in HF (by sustained angiotensin-converting enzyme inhibitor therapy, n = 9) absolute and fractional sodium excretion increased (P < 0.05) to the level of control subjects (108 +/- 34 micromol/min and 0.70 +/- 0.23%, respectively). Renal free water clearance increased during WI in control subjects but not in HF, albeit plasma vasopressin concentrations were similar in the two groups. In conclusion, the neuroendocrine link between volume sensing and renal sodium excretion is preserved in compensated HF. The natriuresis of WI is, however, modulated by the prevailing ANG II and Aldo concentrations. In contrast, renal free water clearance is attenuated in response to volume expansion in compensated HF despite normalized plasma AVP concentrations.

AB - To examine if the neuroendocrine link between volume sensing and renal function is preserved in compensated chronic heart failure [HF, ejection fraction 0.29 +/- 0.03 (mean +/- SE)] we tested the hypothesis that intravascular and central blood volume expansion by 3 h of water immersion (WI) elicits a natriuresis. In HF, WI suppressed ANG II and aldosterone (Aldo) concentrations, increased the release of atrial natriuretic peptide (ANP), and elicited a natriuresis (P < 0.05 for all) compared with seated control. Compared with control subjects (n = 9), ANG II, Aldo, and ANP concentrations were increased (P < 0.05) in HF, whereas absolute and fractional sodium excretion rates were attenuated [47 +/- 16 vs. 88 +/- 15 micromol/min and 0.42 +/- 0.18 vs. 0.68 +/- 0.12% (mean +/- SE), respectively, both P < 0.05]. When ANG II and Aldo concentrations were further suppressed (P < 0.05) during WI in HF (by sustained angiotensin-converting enzyme inhibitor therapy, n = 9) absolute and fractional sodium excretion increased (P < 0.05) to the level of control subjects (108 +/- 34 micromol/min and 0.70 +/- 0.23%, respectively). Renal free water clearance increased during WI in control subjects but not in HF, albeit plasma vasopressin concentrations were similar in the two groups. In conclusion, the neuroendocrine link between volume sensing and renal sodium excretion is preserved in compensated HF. The natriuresis of WI is, however, modulated by the prevailing ANG II and Aldo concentrations. In contrast, renal free water clearance is attenuated in response to volume expansion in compensated HF despite normalized plasma AVP concentrations.

M3 - Journal article

C2 - 11448848

SN - 0363-6119

VL - 281

SP - R459-67

JO - American Journal of Physiology - Regulatory Integrative and Comparative Physiology

JF - American Journal of Physiology - Regulatory Integrative and Comparative Physiology

IS - 2

ER -

Neuroendocrine and renal effects of intravascular volume expansion in compensated heart failure.

Abstract

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