title: Interactions between sodium intake, calcium supplement, renal excretion and blood pressure in Sprague-Dawley rats.
abstract: BACKGROUND
  The mechanisms responsible for genesis of salt-induced hypertension and its prevention by dietary calcium supplementation are still not clear. Hence, the effect of salt (NaCl) and calcium supplement on blood pressure and renal excretion were investigated.
  
  
  METHODS
  Daily food consumption, water, salt and calcium intake, as well as urine volume and pH were determined. At the end of the feeding period, animals were anaesthetised and the electrocardiographic and blood pressure measurements were done.
  
  
  RESULTS
  Salt-loaded rats (SR) consumed more salt and water but less calcium, and excreted more urine and hydrogen ion than control rats (NR). There was elevation of mean arterial pressure (MAP) in SR (132.63 +/- 2.3 mmHg) compared with NR (94.00 +/- 2.2 mmHg) but there was no significant difference in their heart rates (HR) (395 +/- 11.7 vs. 429 +/- 15.4 beats/min). However, salt-loaded-calcium-fed rats (SCaR) had similar MAP as NR (99.29 +/- 1.8 mmHg) and a lower HR (379 +/- 14.9 beats/min). A reduction in water consumption and an increase in urine output as well as urinary hydrogen ion were noted in SCaR compared with SR. Calcium alone (CaR) did not have any effect on MAP (88.01 +/- 1.3 mmHg) and HR (413 +/- 7.98 beats/min). There was no difference in the organ/body-weight ratios of the aortae among the experimental rats. However, there was renal hypertrophy in SR and SCaR. Also, the hearts of SR were bigger than CaR. The mean electrical axis of hearts showed a tendency towards left ventricular hypertrophy in SR, which was greater than SCaR.
  
  
  CONCLUSIONS
  The results suggest that salt loading caused renal hypertrophy and a tendency towards left ventricular hypertrophy. There are associated salt and water retention resulting in alteration of some cardiovascular function. Dietary calcium supplementation reversed these functional defects.
authors.affiliation: Department of Physiology, College of Medicine, University of Lagos, Idi-Araba, Lagos, Nigeria, Lagos, Nigeria. chrisladipo@yahoo.co.uk
authors.forename: C O
authors.initials: CO
authors.lastname: Oladipo
authors.forename: P E
authors.initials: PE
authors.lastname: Egbe
authors.forename: J O
authors.initials: JO
authors.lastname: Ibu
authors.forename: G
authors.initials: G
authors.lastname: Pamson
mesh_terms: D000818:Animals; D001769:Blood; D001794:Blood Pressure / Q000187:drug effects* / Q000502:physiology; D002136:Calcium, Dietary / Q000008:administration & dosage / Q000494:pharmacology*; D004562:Electrocardiography; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006984:Hypertrophy; D017379:Hypertrophy, Left Ventricular / Q000503:physiopathology; D007668:Kidney / Q000187:drug effects* / Q000473:pathology / Q000502:physiology; D008297:Male; D023421:Models, Animal; D009929:Organ Size / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D012982:Sodium, Dietary / Q000008:administration & dosage / Q000494:pharmacology*; D014556:Urine
chemical_list: D002136:Calcium, Dietary; D012982:Sodium, Dietary