title: Renal, endocrine, and cardiovascular responses to bed rest in male subjects on a constant diet.
abstract: BACKGROUND
  Exposure to actual and simulated microgravity induces cardiovascular deconditioning through a variety of factors. Although the mechanisms involved remain uncertain, one involves alterations in volume-regulating systems--the hypothesis being tested in this study. To maximize our ability to detect subtle changes in the volume-regulating systems, subjects were studied on a high-average salt intake to maximally suppress these systems basally.
  
  
  METHODS
  Fourteen healthy male subjects underwent 14-day head-down tilt bed rest (HDTB) during which a constant 200 mEq sodium, 100 mEq potassium diet was maintained. Daily 24-hour urine collection was performed; plasma renin activity, serum aldosterone, plethysmography, and cardiovascular system identification were performed during a control period (pre-HDTB) and at the end of HDTB (end HDTB).
  
  
  RESULTS
  Sodium excretion increased initially (pre-HDTB = 182.8 +/- 10.4 mEq/total volume; early HDTB = 236.4 +/- 13.0; p = .002) and then returned to baseline values. Potassium excretion increased 4 days after the initiation of HDTB and remained elevated thereafter (pre-HDTB = 82.2 +/- 2.4/total volume; mid- to late HDTB = 89.4 +/- 2.1; p = .02). Plasma renin activity increased significantly with HDTB (pre-HDTB = 1.28 +/- 0.21 ng/mL/h; end HDTB = 1.69 +/- 0.18; p = .01), but serum aldosterone did not change. A significant decrease in autonomic responsiveness and an increase in leg compliance were observed.
  
  
  CONCLUSIONS
  We conclude that even in the presence of a high-average salt intake diet, simulated microgravity leads to renal, cardioendocrine, and cardiovascular system alterations that likely contribute to cardiovascular deconditioning.
authors.affiliation: Division of Endocrinology, Brigham and Women's Hospital, Boston, MA 02115, USA.
authors.forename: S Marlene
authors.initials: SM
authors.lastname: Grenon
authors.forename: Natalie
authors.initials: N
authors.lastname: Sheynberg
authors.forename: Shelley
authors.initials: S
authors.lastname: Hurwitz
authors.forename: Grace
authors.initials: G
authors.lastname: Xiao
authors.forename: Craig D
authors.initials: CD
authors.lastname: Ramsdell
authors.forename: Michael D
authors.initials: MD
authors.lastname: Ehrman
authors.forename: C Lan
authors.initials: CL
authors.lastname: Mai
authors.forename: Siri Rostoft
authors.initials: SR
authors.lastname: Kristjansson
authors.forename: Grete H
authors.initials: GH
authors.lastname: Sundby
authors.forename: Richard J
authors.initials: RJ
authors.lastname: Cohen
authors.forename: Gordon H
authors.initials: GH
authors.lastname: Williams
mesh_terms: D000328:Adult; D001510:Bed Rest; D018493:Cardiovascular Deconditioning / Q000502:physiology*; D004703:Endocrine System / Q000502:physiology*; D018475:Head-Down Tilt / Q000502:physiology; D006439:Hemodynamics; D006801:Humans; D007103:Immobilization / Q000502:physiology*; D007668:Kidney / Q000502:physiology*; D007866:Leg / Q000098:blood supply; D008297:Male; D010991:Plethysmography; D011188:Potassium / Q000652:urine; D012084:Renin-Angiotensin System / Q000502:physiology; D012964:Sodium / Q000652:urine; D017673:Sodium Chloride, Dietary; D014680:Veins / Q000502:physiology; D014893:Weightlessness / Q000009:adverse effects*
chemical_list: D017673:Sodium Chloride, Dietary; D012964:Sodium; D011188:Potassium