Hemodynamic and neuroendocrine responses to changes in sodium intake in compensated heart failure.

Morten Damgaard; Peter Norsk; Finn Gustafsson; Jørgen K Kanters; Niels Juel Christensen; Peter Bie; Lars Friberg; Niels Gadsbøll

doi:10.1152/ajpregu.00738.2005

Hemodynamic and neuroendocrine responses to changes in sodium intake in compensated heart failure.

Morten Damgaard, Peter Norsk, Finn Gustafsson, Jørgen K Kanters, Niels Juel Christensen, Peter Bie, Lars Friberg, Niels Gadsbøll

Department of Biomedical Sciences

70 Citations (Scopus)

Abstract

Patients with untreated heart failure (HF) exhibit a blunted hemodynamic and neuroendocrine response to a high sodium intake, leading to excessive sodium and water retention. However, it is not known whether this is the case for patients with compensated HF receiving angiotensin-converting enzyme inhibitors and beta-adrenoreceptor blockers. Therefore, we determined the hemodynamic and neuroendocrine responses to 1 wk of a low-sodium diet (70 mmol/day) and 1 wk of a high-sodium diet (250 mmol/day) in 12 HF patients and 12 age-matched controls in a randomized, balanced fashion. During steady-state conditions, hemodynamic and neuroendocrine examinations were performed at rest and during bicycle exercise. In seated HF patients, high sodium intake increased body weight (1.6 +/- 0.4%), plasma volume (9 +/- 2%), cardiac index (14 +/- 6%), and stroke volume index (21 +/- 5%), whereas mean arterial pressure was unchanged. Therefore, the total peripheral resistance decreased by 10 +/- 4%. Similar hemodynamic changes were observed during an incremental bicycle exercise test. Plasma concentrations of angiotensin II and norepinephrine were suppressed, whereas plasma pro-B-type natriuretic peptide remained unchanged. In conclusion, high sodium intake was tolerated without any excessive sodium and water retention in medically treated patients with compensated HF. The observation that high sodium intake improves cardiac performance, induces peripheral vasodilatation, and suppresses the release of vasoconstrictor hormones does not support the advice for HF patients to restrict dietary sodium.

Original language	English
Journal	American Journal of Physiology: Regulatory, Integrative and Comparative Physiology
Volume	290
Issue number	5
Pages (from-to)	R1294-301
ISSN	0363-6119
DOIs	https://doi.org/10.1152/ajpregu.00738.2005
Publication status	Published - 2005

Access to Document

10.1152/ajpregu.00738.2005

Cite this

Hemodynamic and neuroendocrine responses to changes in sodium intake in compensated heart failure. / Damgaard, Morten; Norsk, Peter; Gustafsson, Finn et al.

In: American Journal of Physiology: Regulatory, Integrative and Comparative Physiology, Vol. 290, No. 5, 2005, p. R1294-301.

Research output: Contribution to journal › Journal article › Research › peer-review

@article{5b341930acd711ddb538000ea68e967b,

title = "Hemodynamic and neuroendocrine responses to changes in sodium intake in compensated heart failure.",

abstract = "Patients with untreated heart failure (HF) exhibit a blunted hemodynamic and neuroendocrine response to a high sodium intake, leading to excessive sodium and water retention. However, it is not known whether this is the case for patients with compensated HF receiving angiotensin-converting enzyme inhibitors and beta-adrenoreceptor blockers. Therefore, we determined the hemodynamic and neuroendocrine responses to 1 wk of a low-sodium diet (70 mmol/day) and 1 wk of a high-sodium diet (250 mmol/day) in 12 HF patients and 12 age-matched controls in a randomized, balanced fashion. During steady-state conditions, hemodynamic and neuroendocrine examinations were performed at rest and during bicycle exercise. In seated HF patients, high sodium intake increased body weight (1.6 +/- 0.4%), plasma volume (9 +/- 2%), cardiac index (14 +/- 6%), and stroke volume index (21 +/- 5%), whereas mean arterial pressure was unchanged. Therefore, the total peripheral resistance decreased by 10 +/- 4%. Similar hemodynamic changes were observed during an incremental bicycle exercise test. Plasma concentrations of angiotensin II and norepinephrine were suppressed, whereas plasma pro-B-type natriuretic peptide remained unchanged. In conclusion, high sodium intake was tolerated without any excessive sodium and water retention in medically treated patients with compensated HF. The observation that high sodium intake improves cardiac performance, induces peripheral vasodilatation, and suppresses the release of vasoconstrictor hormones does not support the advice for HF patients to restrict dietary sodium.",

author = "Morten Damgaard and Peter Norsk and Finn Gustafsson and Kanters, {J{\o}rgen K} and Christensen, {Niels Juel} and Peter Bie and Lars Friberg and Niels Gadsb{\o}ll",

note = "Keywords: Adrenergic beta-Antagonists; Aged; Angiotensin-Converting Enzyme Inhibitors; Body Weight; Echocardiography; Exercise Test; Heart Failure; Heart Function Tests; Hemodynamics; Humans; Male; Middle Aged; Neurosecretory Systems; Oxygen Consumption; Plasma Volume; Respiratory Function Tests; Sodium; Sodium, Dietary; Vasodilation",

year = "2005",

doi = "10.1152/ajpregu.00738.2005",

language = "English",

volume = "290",

pages = "R1294--301",

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

issn = "0363-6119",

publisher = "American Physiological Society",

number = "5",

}

TY - JOUR

T1 - Hemodynamic and neuroendocrine responses to changes in sodium intake in compensated heart failure.

AU - Damgaard, Morten

AU - Norsk, Peter

AU - Gustafsson, Finn

AU - Kanters, Jørgen K

AU - Christensen, Niels Juel

AU - Bie, Peter

AU - Friberg, Lars

AU - Gadsbøll, Niels

N1 - Keywords: Adrenergic beta-Antagonists; Aged; Angiotensin-Converting Enzyme Inhibitors; Body Weight; Echocardiography; Exercise Test; Heart Failure; Heart Function Tests; Hemodynamics; Humans; Male; Middle Aged; Neurosecretory Systems; Oxygen Consumption; Plasma Volume; Respiratory Function Tests; Sodium; Sodium, Dietary; Vasodilation

PY - 2005

Y1 - 2005

N2 - Patients with untreated heart failure (HF) exhibit a blunted hemodynamic and neuroendocrine response to a high sodium intake, leading to excessive sodium and water retention. However, it is not known whether this is the case for patients with compensated HF receiving angiotensin-converting enzyme inhibitors and beta-adrenoreceptor blockers. Therefore, we determined the hemodynamic and neuroendocrine responses to 1 wk of a low-sodium diet (70 mmol/day) and 1 wk of a high-sodium diet (250 mmol/day) in 12 HF patients and 12 age-matched controls in a randomized, balanced fashion. During steady-state conditions, hemodynamic and neuroendocrine examinations were performed at rest and during bicycle exercise. In seated HF patients, high sodium intake increased body weight (1.6 +/- 0.4%), plasma volume (9 +/- 2%), cardiac index (14 +/- 6%), and stroke volume index (21 +/- 5%), whereas mean arterial pressure was unchanged. Therefore, the total peripheral resistance decreased by 10 +/- 4%. Similar hemodynamic changes were observed during an incremental bicycle exercise test. Plasma concentrations of angiotensin II and norepinephrine were suppressed, whereas plasma pro-B-type natriuretic peptide remained unchanged. In conclusion, high sodium intake was tolerated without any excessive sodium and water retention in medically treated patients with compensated HF. The observation that high sodium intake improves cardiac performance, induces peripheral vasodilatation, and suppresses the release of vasoconstrictor hormones does not support the advice for HF patients to restrict dietary sodium.

AB - Patients with untreated heart failure (HF) exhibit a blunted hemodynamic and neuroendocrine response to a high sodium intake, leading to excessive sodium and water retention. However, it is not known whether this is the case for patients with compensated HF receiving angiotensin-converting enzyme inhibitors and beta-adrenoreceptor blockers. Therefore, we determined the hemodynamic and neuroendocrine responses to 1 wk of a low-sodium diet (70 mmol/day) and 1 wk of a high-sodium diet (250 mmol/day) in 12 HF patients and 12 age-matched controls in a randomized, balanced fashion. During steady-state conditions, hemodynamic and neuroendocrine examinations were performed at rest and during bicycle exercise. In seated HF patients, high sodium intake increased body weight (1.6 +/- 0.4%), plasma volume (9 +/- 2%), cardiac index (14 +/- 6%), and stroke volume index (21 +/- 5%), whereas mean arterial pressure was unchanged. Therefore, the total peripheral resistance decreased by 10 +/- 4%. Similar hemodynamic changes were observed during an incremental bicycle exercise test. Plasma concentrations of angiotensin II and norepinephrine were suppressed, whereas plasma pro-B-type natriuretic peptide remained unchanged. In conclusion, high sodium intake was tolerated without any excessive sodium and water retention in medically treated patients with compensated HF. The observation that high sodium intake improves cardiac performance, induces peripheral vasodilatation, and suppresses the release of vasoconstrictor hormones does not support the advice for HF patients to restrict dietary sodium.

U2 - 10.1152/ajpregu.00738.2005

DO - 10.1152/ajpregu.00738.2005

M3 - Journal article

C2 - 16357094

SN - 0363-6119

VL - 290

SP - R1294-301

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

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

IS - 5

ER -

Hemodynamic and neuroendocrine responses to changes in sodium intake in compensated heart failure.

Abstract

Access to Document

Fingerprint

Cite this