抄録
Zinc deficient rats are known to drink 0.3 M NaCl, avoided by normal animals, in preference to water. We have indicated in the deficient rats that serum sodium has a tendency to decrease and circulating aldosterone significantly increased and suggested that abnormal salt intake reflects increases in sodium appetite. In order to confirm this view, we analyzed angiotensin II in cerebrospinal fluid and serum calcium (involved in the generation of salt appetite) in zinc deficient rats. Animals were given access to either a zinc deficient diet (group 1) or its normal control diet (group 2) ad libitum for one or four weeks. A group 3 was pair-fed with the group 1. Although aldosterone levels were higher in the group 1 than in the group 3, as described in our previous report, angiotensin II levels of both serum and cerebrospinal fluid varied little between these two groups. On the other hand, with the progress of the deficiency, serum calcium concentrations decreased to levels near those of rickets animals. However, there was no significant difference in the calcium levels between the groups 1 and 3 because of the variance within the group 1. These results suggest that unusual salt intakes of zinc deficient rats are mainly due to salt appetite stimulated by a combination of low calcium and high aldosterone in blood. Serum and brain angiotensin II seem not to contribute to the generation of salt appetite of zinc deficient rats. [J Physiol Sci. 2007;57 Suppl:S185]
