Author
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Saari, Jack |
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Submitted to: Trace Elements in Man and Animals International Symposium
Publication Type: Abstract Only Publication Acceptance Date: 5/19/1996 Publication Date: N/A Citation: N/A Interpretive Summary: Technical Abstract: Prior studies have indicated that dietary copper (Cu) restriction causes high blood pressure in adult rats. The aim of this study was to determine the cause of this Cu deficiency-induced hypertension by examination of nitric oxide-mediated blood vessel responses and by measurement of kidney variables related to blood pressure regulation. Male Sprague-Dawley rats (180-200 g) were fed a Cu-deficient (0.4-0.6 ug/g diet) or Cu-adequate diet (5.5-6.0 ug/g diet) for 28 weeks. Blood pressure was measured periodically by tail cuff, blood and urine variables were measured to assess renal function and reactivity of isolated aortas to the nitric oxide donor Na nitroprusside (10**-9-10**-6 M) was assessed at termination of the experiment. Cu deficiency was confirmed by observation of reduced liver and heart Cu concentrations and by enlarged hearts and anemia. Blood pressure measurements taken between weeks 12 and 28 were in the range of 125-140 mm Hg and at no time showed a relative hypertension in Cu-deficient rats. Isolated aortas of Cu-deficient rats showed a reduced relaxation to nitroprusside. Although glomerular filtration rate was unchanged in Cu-deficient rats, both renal sodium clearance and sodium excretion were about 4.5-fold higher than in Cu-adequate rats. The depressed blood vessel reactivity to nitroprusside in Cu-deficient rats suggested that higher blood vessel resistance should have produced higher blood pressures than in Cu-adequate rats. However, the finding of higher sodium clearance and sodium excretion in Cu-deficient rats suggests that absence of high blood pressure may be explainable in part by renal compensation in the form of pressure natriuresis. |