Author
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Saari, Jack |
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Submitted to: Trace Elements in Man and Animals International Symposium
Publication Type: Proceedings Publication Acceptance Date: 5/19/1996 Publication Date: N/A Citation: N/A Interpretive Summary: 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 high blood pressure. Two ways Cu deficiency may affect blood pressure are by altering blood vessel diameter and by affecting blood volume control by the kidney. These two possibilities were tested by examination of blood vessel dilatory responses and by measurement of kidney variables related to blood pressure regulation. Measurement of blood pressure in adult rats, however, showed no increase in blood pressure after 29 weeks of severe dietary Cu restriction. Assessment of blood vessel response in Cu-deficient rats showed that the vessels' ability to dilate was impaired, which should have led to high blood pressure. Measurement of kidney function revealed that the body's stores of sodium were being released by the kidney. Loss of sodium in turn could lead to loss of blood volume and to a relative reduction of blood pressure. These findings indicate that impairment of blood vessel function tends to cause high blood pressure, but this tendency is compensated for by the loss of sodium and hence blood volume. This information will be useful to scientists and consumers interested in trace element nutrition of the cardiovascular system. 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 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. |