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.
authors.affiliation: Dept. of Cardiovascular Medicine, Bispebjerg University Hospital, Bispebjerg Bakke 23, DK-2400 Copenhagen, Denmark. mdamgaard@dadlnet.dk
authors.forename: Morten
authors.initials: M
authors.lastname: Damgaard
authors.forename: Peter
authors.initials: P
authors.lastname: Norsk
authors.forename: Finn
authors.initials: F
authors.lastname: Gustafsson
authors.forename: Jørgen K
authors.initials: JK
authors.lastname: Kanters
authors.forename: Niels Juel
authors.initials: NJ
authors.lastname: Christensen
authors.forename: Peter
authors.initials: P
authors.lastname: Bie
authors.forename: Lars
authors.initials: L
authors.lastname: Friberg
authors.forename: Niels
authors.initials: N
authors.lastname: Gadsbøll
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000368:Aged; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use; D001835:Body Weight / Q000502:physiology; D004452:Echocardiography; D005080:Exercise Test; D006333:Heart Failure / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000503:physiopathology*; D006334:Heart Function Tests; D006439:Hemodynamics / Q000502:physiology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009490:Neurosecretory Systems / Q000502:physiology*; D010101:Oxygen Consumption; D010953:Plasma Volume; D012129:Respiratory Function Tests; D012964:Sodium / Q000652:urine; D012982:Sodium, Dietary / Q000494:pharmacology*; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology
chemical_list: D000319:Adrenergic beta-Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D012982:Sodium, Dietary; D012964:Sodium