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.

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

“…Despite a higher CI, MAP remained unchanged because of compensatory peripheral vasodilatation (Table 3). Our results are in accordance with recent studies of medically treated patients with compensated HF in which acute central intravascular volume expansion elicited a hemodynamic, neuroendocrine, and renal response similar to that of normal controls (7,8).…”

“…These findings oppose the results of previous studies, in which untreated and conventionally (digoxin) treated patients with HF have been shown to accumulate sodium and water in excess during dietary sodium loading (2, 4, 14, 27, 30). However, it was recently demonstrated that monotherapy with ACE inhibitors restores renal sodium excretion during acute volume expansion in compensated HF (7). Hence, it is conceivable that the neuroendocrine link, which senses the intravascular volume expansion induced by high sodium intake and promotes renal sodium excretion, is preserved in medically treated HF patients.…”

“…Throughout the past two decades, medical treatment of HF has improved, and today most patients receive ␤-adrenoreceptor blockers and inhibitors of the renin-angiotensin-aldosterone system (RAAS). In such patients it has recently been demonstrated that acute central intravascular volume expansion elicits a hemodynamic, neuroendocrine, and renal response similar to that of normal controls (7,8). Thus the intact baroreflex-mediated response to increased cardiac and arterial filling leads to decreased systemic vascular resistance and suppressed neuroendocrine mediators, thereby promoting renal sodium excretion.…”

Vasorelaxation in Space

“…Compared with the upright seated control position, water immersion increased stroke volume index and decreased vascular resistance. 20,21 Thus, the circulatory condition in the heart failure patients improved. Because our results presented here from parabolic flights and spaceflight are in compliance with those of water immersion, 20,21 it is fair to conclude that gravity is a constant burden for heart failure patients and that it aggravates their condition.…”

Biophysiologic Effects of Warm Water Immersion

“…E-mail khildenbrand@wsu.edu. heart injury (Gabrielsen et al, 2001;Gabrielsen, Sorensen et al, 2000;Hanna, Sheldahl, & Tristani, 1993;Heigenhauser, Boulet, Miller, & Faulkner, 1977;Jiang et al, 1994;Magder, Linnarsson, & Gullstrand, 1981;McMurray, Avery, & Sheps, 1988;Meyer & Leblanc, 2008).…”