title: Treatment of secondary hyperparathyroidism by high calcium diet is associated with enhanced resistance artery relaxation in experimental renal failure.
abstract: BACKGROUND
  Vasorelaxation is impaired in renal failure (RF) and hypertension. A high calcium diet enhances vasodilatation and reduces blood pressure in experimental hypertension. Oral calcium salts are used as phosphate binders in RF. However, the effect of increased calcium intake on arterial tone in RF is unknown.
  
  
  METHODS
  We investigated the influence of an 8-week high calcium diet (0.3 vs 3.0%) on resistance artery tone in 5/6 nephrectomized (NTX) rats. Calcium was supplemented as carbonate salt, blood pressure measured by tail-cuff, urine collected in metabolic cages, and samples taken for blood chemistry and parathyroid hormone (PTH). Functional studies of isolated third-order branches of the mesenteric artery in vitro were performed using the Mulvany multimyograph.
  
  
  RESULTS
  Plasma urea was elevated 1.6-fold and systolic blood pressure by 10 mmHg after NTX, while increased calcium intake was without effect on these variables. Plasma PTH and phosphate were raised following NTX, and suppressed by high calcium diet. Vasorelaxations induced by K(+) channel agonists 11,12-epoxyeicosatrienoic acid and levcromakalim were impaired after NTX. Vasorelaxation induced by acetylcholine was also reduced following NTX, and experiments with N(G)-nitro-L-arginine methyl ester, diclofenac and charybdotoxin + apamin suggested that the K(+) channel-mediated component of endothelium-dependent relaxation was deficient after NTX. Increased calcium intake corrected all impairments of vasodilatation in NTX rats.
  
  
  CONCLUSIONS
  Deficient vasorelaxation via K(+) channels was normalized by high calcium diet in experimental RF. This effect was independent of the degree of renal impairment and blood pressure, but was associated with improved calcium metabolism: plasma levels of PTH and phosphate were decreased and ionized calcium was increased.
authors: Department of Pharmacological Sciences, Medical School, University of Tampere, FIN-33014 Tampere, Finland.
authors: Pasi
authors: P
authors: Jolma
authors: Peeter
authors: P
authors: Kööbi
authors: Jarkko
authors: J
authors: Kalliovalkama
authors: Heikki
authors: H
authors: Saha
authors: Meng
authors: M
authors: Fan
authors: Jarkko
authors: J
authors: Jokihaara
authors: Eeva
authors: E
authors: Moilanen
authors: Ilkka
authors: I
authors: Tikkanen
authors: Ilkka
authors: I
authors: Pörsti
mesh_terms: D000818:Animals; D001158:Arteries / Q000187:drug effects*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002119:Calcium Carbonate / Q000494:pharmacology*; D002136:Calcium, Dietary / Q000494:pharmacology*; D006961:Hyperparathyroidism / Q000178:diet therapy* / Q000209:etiology; D008297:Male; D009392:Nephrectomy; D010760:Phosphorus Metabolism Disorders / Q000178:diet therapy / Q000209:etiology; D015221:Potassium Channels / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D051437:Renal Insufficiency / Q000150:complications / Q000503:physiopathology*; D014664:Vasodilation / Q000187:drug effects*
chemical_list: D002136:Calcium, Dietary; D015221:Potassium Channels; D002119:Calcium Carbonate