BACKGROUND: The renin-angiotensin-aldosterone system may be of primary importance in the mechanism of bed rest cardiovascular deconditioning. HYPOTHESIS: This study was designed to test the hypothesis that bed rest cardiovascular deconditioning does not result simply from plasma volume loss, but is also at least partially attributable to a persistent disequilibrium of the neuroendocrine mediators of plasma volume homeostasis. We examined whether changes in the renin-angiotensin-aldosterone system occur in association with the cardiovascular deconditioning and hemodynamic instability induced by antiorthostatic 6 degrees head-down tilt bed rest. METHODS: Normal male volunteers (n = 10) were tested before, during, and after 14 d of head-down tilt with a high (150 mEq.d-1) salt intake, using head-down tilt as a model of cardiovascular deconditioning and lower body negative pressure (LBNP) as a model of orthostatic stress. RESULTS: Resting plasma renin activity was 2.22 +/- 0.85 ng.ml-1.h-1 (+/- SD) at baseline and increased to 4.14 +/- 1.21 ng.ml-1.h-1 at the end of head-down tilt (p < 0.05), but urine aldosterone, plasma aldosterone, and urine sodium did not change with head-down tilt. Although the plasma norepinephrine response to LBNP was accentuated, resting adrenergic tone did not change during head-down tilt. Cardiovascular deconditioning was associated with an increase in blood pressure variability during LBNP as assessed by both beat-to-beat standard deviation and spectral analysis. CONCLUSIONS: These data support a proposed link between blood pressure variability and the renin-angiotensin system in cardiovascular deconditioning.
BACKGROUND: The renin-angiotensin-aldosterone system may be of primary importance in the mechanism of bed rest cardiovascular deconditioning. HYPOTHESIS: This study was designed to test the hypothesis that bed rest cardiovascular deconditioning does not result simply from plasma volume loss, but is also at least partially attributable to a persistent disequilibrium of the neuroendocrine mediators of plasma volume homeostasis. We examined whether changes in the renin-angiotensin-aldosterone system occur in association with the cardiovascular deconditioning and hemodynamic instability induced by antiorthostatic 6 degrees head-down tilt bed rest. METHODS: Normal male volunteers (n = 10) were tested before, during, and after 14 d of head-down tilt with a high (150 mEq.d-1) salt intake, using head-down tilt as a model of cardiovascular deconditioning and lower body negative pressure (LBNP) as a model of orthostatic stress. RESULTS: Resting plasma renin activity was 2.22 +/- 0.85 ng.ml-1.h-1 (+/- SD) at baseline and increased to 4.14 +/- 1.21 ng.ml-1.h-1 at the end of head-down tilt (p < 0.05), but urine aldosterone, plasma aldosterone, and urine sodium did not change with head-down tilt. Although the plasma norepinephrine response to LBNP was accentuated, resting adrenergic tone did not change during head-down tilt. Cardiovascular deconditioning was associated with an increase in blood pressure variability during LBNP as assessed by both beat-to-beat standard deviation and spectral analysis. CONCLUSIONS: These data support a proposed link between blood pressure variability and the renin-angiotensin system in cardiovascular deconditioning.
Authors: Michael B Stenger; Joyce M Evans; Charles F Knapp; Stuart M C Lee; Tiffany R Phillips; Sondra A Perez; Alan D Moore; William H Paloski; Steven H Platts Journal: Eur J Appl Physiol Date: 2011-05-29 Impact factor: 3.078
Authors: Jessica K Lee; Vincent Koppelmans; Ofer Pasternak; Nichole E Beltran; Igor S Kofman; Yiri E De Dios; Edwin R Mulder; Ajitkumar P Mulavara; Jacob J Bloomberg; Rachael D Seidler Journal: Cereb Cortex Commun Date: 2021-03-30