Effect of copper deficiency on blood pressure and plasma and lung angiotensin converting enzyme activity in rats

Moore, R.J.; Klevay, L.M.

Nutrition Research 8(5): 489-498

1988


ISSN/ISBN: 0271-5317
DOI: 10.1016/s0271-5317(88)80070-8
Accession: 005229356

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Abstract
The effect of copper deficiency on plasma and lung angiotensin I-converting enzyme (ACE) activity and on blood pressure was investigated in weanling rats. Rats were fed for 32 d a Cu-deficient diet (0.8 .mu.g Cu/g) and were given drinking water containing 10 .mu.g Zn/ml, either with (CuS) or without (CuD) 2 .mu.g Cu/ml. Combined results for experiments 1 and 2 (25 rats per group) showed that CuD rats were hypercholesterolemic and that Cu in lung and liver were lower (p < 0.001) than in organs from CuS rats. ACE activity was 28% lower in plasma from CuD rats (234 units) than in plasma from CuS rats (325 units, p < 0.05). In vitro lung ACE activity was unaffected by Cu status. In experiment 3, plasma cholesterol was higher (p < 0.01) and liver (p < 0.001) and lung (p < 0.05) Cu were lower in CuD rats than in CuS rats. Lung ACE activity was not affected by Cu deficiency. Cu deficiency decreased plasma ACE from 365 units to 273 units (p < 0.001) and lowered systolic blood pressure from 113 mm Hg to 98 mm Hg (p < 0.001). However, there was not a significant correlation between plasma ACE activity and blood pressure in CuS or CuD rats. The results show that Cu deficiency lowers plasma ACE activity but does not affect lung ACE activity. It is not known if plasma levels of angiotensin II or bradykinin are affected by Cu status, but these data suggest that reduced metabolism of angiotensin I and bradykinin as a consequence of lower plasma ACE activity could contribute to the lower systolic blood pressure observed in rats made Cu-deficient at weaning.