Abstract
Peripheral neurological mechanisms involved in hyperuricemia following ventromedial hypothalamic electrical stimulation was studied in the conscious rat. The intensity of 0.2 mA was near the maximum intensity of stimulation current producing a linear increase in plasma uric acid throughout the 15-min period of stimulation, as well as a subsequent rise and fall of plasma allantoin. Bilateral adrenal demedullation abolished the stimulation-induced hyperuricemia and markedly impaired the accompanying rise of allantoin. Prior treatment of the animal with hexamethonium significantly inhibited the uric acid increase, but did not reduce the allantoin elevation so markedly. Moreover, propranolol eliminated both responses of these plasma purine metabolites, whereas phentolamine greatly increased the response. It is concluded therefore that the hypothalamic stimulation-induced rise of plasma uric acid is the result of acceleration of epinephrine release from the adrenal medulla and that, whereas some unknown extra-adrenal mechanism may be partially involved, the primary part of the accompanying allantoin elevation is explained by the combined effects of the increased uric acid and the hepatic uricase.
Publisher
American Physiological Society
Subject
Physiology (medical),Physiology,Endocrinology, Diabetes and Metabolism
Cited by
12 articles.
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