title: Chronic potassium depletion induces renal injury, salt sensitivity, and hypertension in young rats.
abstract: BACKGROUND
  Chronic hypokalemia has been associated with renal hypertrophy, interstitial disease, and hypertension in both adult animals and humans. However, the effects of potassium (K(+)) depletion on the rapidly growing infant have not been well studied. The purpose of this study was to determine the effects of severe chronic dietary K(+) depletion on blood pressure (BP) and renal structural changes in young rats.
  
  
  METHODS
  Sprague-Dawley rats (50 +/- 5 g) were fed either a control or a potassium-deficient diet (<0.05% K(+)) for 14 to 21 days. At the end of this period, the blood pressure (BP) was measured in all rats, and six rats in each group were sacrificed to determine changes in renal histology and renin-angiotensin system (RAS) activity. The remaining rats in each group were then switched to a high-salt (6% NaCl)--normal-K(+) (0.5%) diet or were continued on their respective control or K(+)-deficient diet for an additional six days. Blood pressure measurements were done every three days until the end of the study.
  
  
  RESULTS
  K(+)-depleted animals had significant growth retardation and increased RAS activity, manifested by high plasma renin activity, recruitment of renin-producing cells along the afferent arterioles, and down-regulation of angiotensin II receptors in renal glomeruli and ascending vasa rectae. K(+)-depleted kidneys also showed tubulointerstitial injury with tubular cell proliferation, osteopontin expression, macrophage infiltration, and early fibrosis. At week 2, K(+)-depleted rats had higher systolic BP than control rats. Switching to a high-salt (6% NaCl)--normal-K(+) diet resulted in further elevation of systolic BP in K(+)-depleted rats, which persisted even after the serum K(+) was normalized.
  
  
  CONCLUSIONS
  Dietary potassium deficiency per se increases the BP in young rats and induces salt sensitivity that may involve at least two different pathogenic pathways: increased RAS activity and induction of tubulointerstitial injury.
authors.affiliation: Center for Molecular Physiology Research, Children's Research Institute, Children's National Medical Center, Washington DC 20010, USA. pray@cnmc.org
authors.forename: P E
authors.initials: PE
authors.lastname: Ray
authors.forename: S
authors.initials: S
authors.lastname: Suga
authors.forename: X H
authors.initials: XH
authors.lastname: Liu
authors.forename: X
authors.initials: X
authors.lastname: Huang
authors.forename: R J
authors.initials: RJ
authors.lastname: Johnson
mesh_terms: D000818:Animals; D001794:Blood Pressure; D002908:Chronic Disease; D004351:Drug Resistance; D006130:Growth Disorders / Q000209:etiology; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology; D007008:Hypokalemia / Q000150:complications* / Q000473:pathology / Q000503:physiopathology; D007668:Kidney / Q000293:injuries* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D017419:Potassium, Dietary / Q000008:administration & dosage; D051381:Rats; D017207:Rats, Sprague-Dawley; D012084:Renin-Angiotensin System / Q000502:physiology; D012965:Sodium Chloride / Q000494:pharmacology
chemical_list: D017419:Potassium, Dietary; D012965:Sodium Chloride