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  • Title: Cardiovascular deconditioning through head-down tilt bed rest increases blood pressure variability and plasma renin activity.
    Author: Schmedtje JF, Liu WL, Taylor AA.
    Journal: Aviat Space Environ Med; 1996 Jun; 67(6):539-46. PubMed ID: 8827135.
    Abstract:
    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.
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