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Am J Physiol Regul Integr Comp Physiol 281: R459-R467, 2001;
0363-6119/01 $5.00
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Vol. 281, Issue 2, R459-R467, August 2001

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

Anders Gabrielsen1, Peter Bie2, Niels Henrik Holstein-Rathlou3, Niels Juel Christensen4, Jørgen Warberg3, Harriet Dige-Petersen5, Erik Frandsen5, Søren Galatius6, Bettina Pump1, Vibeke B. Sørensen6, Jens Kastrup6, and Peter Norsk1

1 Danish Aerospace Medical Centre of Research, National University Hospital (Rigshospitalet), DK-2200 Copenhagen; 2 Department of Physiology and Pharmacology, University of Southern Denmark, DK-5000 Odense; 3 Department of Medical Physiology, Panum Institute, University of Copenhagen, DK-2200 Copenhagen; 4 Department of Internal Medicine and Endocrinology, Herlev Hospital, University of Copenhagen, DK-2730 Herlev; 5 Department of Clinical Physiology and Nuclear Medicine, Glostrup Hospital, University of Copenhagen, DK-2600 Glostrup; and 6 Department of Cardiology, The Heart Centre, National University Hospital (Rigshospitalet), DK-2100 Copenhagen, Denmark

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 µmol/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 µmol/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.

renin-angiotensin system; aldosterone; vasopressin; water-electrolyte balance


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