title: Effects of potassium supplementation on markers of osmoregulation and volume regulation: results of a fully controlled dietary intervention study.
abstract: OBJECTIVE
  Lifestyle measures including dietary sodium restriction and increased potassium intake are recognized to lower blood pressure (BP). Potassium was found to be effective in reducing BP at higher levels of sodium intake, but to have little effect when sodium intake is restricted. The humoral mechanisms underlying these sodium intake dependent effects of potassium are unknown. We investigated the effects of potassium supplementation on top of a fully controlled sodium-restricted diet on markers of osmoregulation and volume regulation.
  
  
  METHODS
  In this post-hoc analysis, we included 35 (pre)hypertensive individuals participating in a randomized, double-blind, placebo-controlled crossover trial. Individuals received capsules containing sodium [3.0 g (130 mmol)/day], potassium [2.8 g (72  mmol)/day], or placebo for three four-week periods. Linear mixed-effect models were used to estimate the effects of potassium supplementation compared with placebo. Skewed data were ln-transformed before analysis.
  
  
  RESULTS
  Increased potassium intake was associated with a significant decrease in 24-h BP (-3.6/-1.6 mmHg). Furthermore, we found a significant decrease in ln MR-proANP [-0.08 (95% confidence interval -0.15, -0.01) pmol/l, P = 0.03] and significant increases in 24-h heart rate [2.5 (0.9, 4.0) bpm, P = 0.002], ln plasma copeptin [0.11 (0.01, 0.20) pmol/l, P = 0.02], ln renin [0.34 (0.08, 0.60) μIU/ml, P = 0.01], and ln aldosterone [0.14 (0.07, 0.22) nmol/l, P < 0.001] compared with placebo.
  
  
  CONCLUSIONS
  We found that potassium has BP-lowering effects during sodium restriction. These BP-lowering effects, however, seem mitigated by several counter regulatory mechanisms (i.e. increased secretion of vasopressin, stimulation of RAAS, and increased heart rate) that were activated to maintain volume homeostasis and counterbalance the decrease in BP.
authors.affiliation: aTop Institute Food and Nutrition, Wageningen, the NetherlandsbDepartment of Internal Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen, Groningen, the NetherlandscDivision of Human Nutrition, Wageningen University, Wageningen, the NetherlandsdDepartment of Laboratory Medicine, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands*Ineke J. Riphagen and Lieke Gijsbers contributed equally.
authors.forename: Ineke J
authors.initials: IJ
authors.lastname: Riphagen
authors.forename: Lieke
authors.initials: L
authors.lastname: Gijsbers
authors.forename: Maatje D A
authors.initials: MD
authors.lastname: van Gastel
authors.forename: Ido P
authors.initials: IP
authors.lastname: Kema
authors.forename: Ron T
authors.initials: RT
authors.lastname: Gansevoort
authors.forename: Gerjan
authors.initials: G
authors.lastname: Navis
authors.forename: Stephan J L
authors.initials: SJ
authors.lastname: Bakker
authors.forename: Johanna M
authors.initials: JM
authors.lastname: Geleijnse
mesh_terms: D000368:Aged; D000450:Aldosterone / Q000097:blood; D015415:Biomarkers; D001794:Blood Pressure; D004039:Diet, Sodium-Restricted; D019587:Dietary Supplements; D004311:Double-Blind Method; D005260:Female; D006339:Heart Rate; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000178:diet therapy / Q000188:drug therapy*; D008297:Male; D008875:Middle Aged; D064587:Osmoregulation; D011188:Potassium / Q000097:blood; D017419:Potassium, Dietary / Q000627:therapeutic use*; D058246:Prehypertension / Q000097:blood / Q000178:diet therapy / Q000188:drug therapy*; D012083:Renin / Q000097:blood; D012084:Renin-Angiotensin System; D012964:Sodium / Q000097:blood; D017673:Sodium Chloride, Dietary / Q000627:therapeutic use*; D014882:Water-Electrolyte Balance
chemical_list: D015415:Biomarkers; D017419:Potassium, Dietary; D017673:Sodium Chloride, Dietary; D000450:Aldosterone; D012964:Sodium; D012083:Renin; D011188:Potassium