著者

井奈波 良一

出版者

The Japanese Society for Hygiene

雑誌

日本衛生学雑誌 (ISSN:00215082)

巻号頁・発行日

vol.38, no.4, pp.748-757, 1983-10-30 (Released:2009-02-17)

参考文献数

25

---

In an effort to clarify the mechanism underlying stress-induced hyperuricemia, rises in uric acid in the plasma of rats which had been subjected to immobilization stress were investigated. Two types of stress were investigated-fixation in a supine position for 3mins and immobilization in a Ballman cage for 6mins.Immobilization in a supine position caused immediate increases of up to 400% in uric acid levels. This hyperuricemic response could be enhanced slightly by pre-treatment with propranolol, or depressed to approximately 50% that of the control level with phentolamine, or to 60% by adrenal demedullation. In demedullated rats, although hexamethonium markedly inhibited the rise of uric acid, it did not eliminate it entirely. Neither phentolamine nor atropine had any significant effects. Such results indicate that two different mechanisms are involved in the hyperuricemic response-the adrenal epinephrine-dependent reaction mediated via α-receptors, and the epinephrine-independent reaction in which autonomic nerves other than the adrenal medulla might be involved.The uric acid levels in the liver markedly increased in response to stress, however those in other tissues did not change. As with changes in plasma, increases in liver uric acid went only as far as 60% of the levels of the control group after adrenal demedullation. These results support the view that the stress-induced increases of plasma uric acid levels are due to raised production of uric acid occurring only in the liver.Stress did not cause changes in liver adenine nucleotides-ATP, ADP and AMP. Although tissue lactate levels had increased following stress, they did not parallel changes in tissue uric acid, which may exclude the possibility that increased dproduction of liver uric acid is caused by decreases in adenine nucleotides or by non-specific effects, such as tissue hypoxia.Immobilization in a Ballman cage did not raise the levels of uric acid in plasma. However, after treating rats with phentolamine, the amount of plasma uric acid doubled after stress. Propranolol had no such effects. In demedullated rats, stress failed to cause increases in uric acid even after phentolamine-treatment. It can be concluded therefore that the hyperuricemic response is caused by adrenal epinephrine and that in sharp contrast to the stress caused by immobilization in a prone position, the action of epinephrine is mediated via β-receptors.