Nephrol Dial Transplant (2003) 18: 2560-2569
© 2003 European Renal Association-European Dialysis and Transplant Association
Original Article
Treatment of secondary hyperparathyroidism by high calcium diet is associated with enhanced resistance artery relaxation in experimental renal failure
1Department of Pharmacological Sciences, and 4The Immunopharmacological Research Group, Medical School, University of Tampere, Tampere, 2Department of Anaesthesia and Intensive Care, 3Department of Internal Medicine, and 5Department of Clinical Chemistry, Tampere University Hospital, Tampere, 6Department of Medicine, Helsinki University Central Hospital, Helsinki and 7Minerva Institute for Medical Research, Helsinki, Finland
Correspondence and offprint requests to: Ilkka Pörsti, MD, PhD, Medical School, Department of Internal Medicine, FIN-33014 University of Tampere, Finland. Email: ilkka.porsti{at}uta.fi P. Jolma and P. K\|[ouml ]\|\|[ouml ]\|bi contributed equally to the manuscript.
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 NG-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.
Keywords: arterial smooth muscle; calcium diet; endothelium; phosphate binding; renal failure
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