|Nielsen, Forrest - Frosty|
Submitted to: Journal of Federation of American Societies for Experimental Biology
Publication Type: Abstract only
Publication Acceptance Date: 12/10/2000
Publication Date: 3/7/2001
Citation: Yokoi, K., Uthus, E.O., Nielsen, F.H. 2001. Nickel deficiency induces renal damage and hypertension in rats which is augmented by sodium chloride [abstract]. The Federation of American Societies for Experimental Biology Journal. 15:A973. Interpretive Summary:
Technical Abstract: We have found that kidney contains a relatively high concentration of nickel (Ni) and retains an orally-dosed radio-nickel tracer longer than liver. To test the hypothesis that Ni has a physiological role that affects kidney function, weanling male Sprague-Dawley rats were assigned to groups of 8 in a factorially arranged experiment with dietary variables of supplemental sodium chloride (NaCl: 0 or 80 g/kg) and Ni (0 or 1 mg/kg). The basal diet contained 15 ng Ni/kg and 1.1 g Na/kg. Systolic blood pressure (SBP) was measured after 9 weeks of feeding the experimental diets. One week later, 16 h urine was collected while the rats were fasting to assess protein loss and hematuria. Ni deprivation induced albuminuria, hematuria and hypertension. NaCl evoked hypertension. Severe proteinuria was associated with severe hypertension. When SBP exceeded the break point (194 mm Hg) determined by the broken line model, urinary protein excretion was proportionally increased with SBP (R**2 = 0.77, p < 0.0001). These results suggest that Ni has important physiological roles in kidney function and blood pressure control.