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Publication AbstractsCardiovascular deconditioning through head-down tilt bed rest increased blood pressure variability and plasma remin activitySchmedtje JF Jr., Liu WL, Taylor AA.Aviat Space Environ Med 1996; 67:539-46. AbstractBackground: 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 atleast partially attributable to a persistent disequilibrium of the neuroendocrine mediators of plasma volume homeostasis. We examined wether changes in the renin-angiotensinaldosterone system occur in association with the cardiovascular deconditioning and hemodynamic instability induced by antiorihostatic 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 noreponephrine 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 special analysis. Conclusions: these data support a proposed link between blood pressure variability and the renin-angiotensin system in cardiovascular deconditioning.
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