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NEUROHUMORAL CONTROL OF CARDIOVASCULAR FUNCTION

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

¹Department of Cardiovascular Medicine, Bispebjerg University Hospital, Copenhagen; ²Department of Medical Physiology, University of Copenhagen, Copenhagen; ³Department of Cardiovascular Medicine, Frederiksberg University Hospital, Copenhagen; ⁴Department of Medical Endocrinology, Herlev University Hospital, Copenhagen; ⁵Department of Physiology and Pharmacology, University of Southern Denmark, Odense; and ⁶Department of Clinical Physiology and Nuclear Medicine, Bispebjerg University Hospital, Copenhagen, Denmark

Submitted 18 October 2005 ; accepted in final form 11 December 2005

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 -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.

dietary sodium; plasma volume; exercise

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