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.
authors.affiliation: Danish Aerospace Medical Centre of Research, National University Hospital (Rigshospitalet), 7805, 20 Tagensvej, DK-2200 Copenhagen, Denmark.
authors.forename: A
authors.initials: A
authors.lastname: Gabrielsen
authors.forename: P
authors.initials: P
authors.lastname: Bie
authors.forename: N H
authors.initials: NH
authors.lastname: Holstein-Rathlou
authors.forename: N J
authors.initials: NJ
authors.lastname: Christensen
authors.forename: J
authors.initials: J
authors.lastname: Warberg
authors.forename: H
authors.initials: H
authors.lastname: Dige-Petersen
authors.forename: E
authors.initials: E
authors.lastname: Frandsen
authors.forename: S
authors.initials: S
authors.lastname: Galatius
authors.forename: B
authors.initials: B
authors.lastname: Pump
authors.forename: V B
authors.initials: VB
authors.lastname: Sørensen
authors.forename: J
authors.initials: J
authors.lastname: Kastrup
authors.forename: P
authors.initials: P
authors.lastname: Norsk
mesh_terms: D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000097:blood; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology; D009320:Atrial Natriuretic Factor / Q000097:blood; D001794:Blood Pressure / Q000502:physiology; D001810:Blood Volume / Q000502:physiology*; D002303:Cardiac Output, Low / Q000503:physiopathology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D018495:Fluid Shifts / Q000502:physiology; D005919:Glomerular Filtration Rate / Q000502:physiology; D006339:Heart Rate / Q000502:physiology; D006801:Humans; D007101:Immersion; D007668:Kidney / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009318:Natriuresis / Q000502:physiology*; D012964:Sodium / Q000378:metabolism; D014556:Urine / Q000737:chemistry; D014667:Vasopressins / Q000097:blood; D014882:Water-Electrolyte Balance / Q000502:physiology*
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D004791:Enzyme Inhibitors; D014667:Vasopressins; D000804:Angiotensin II; D000450:Aldosterone; D009320:Atrial Natriuretic Factor; D012964:Sodium