Abstract
The mechanisms of the actions of catecholamines on plasma purine catabolites were investigated in rats. The elevations of plasma levels of uric acid and allantoin were caused by two types of mechanisms which included either alpha or beta adrenoceptor-mediated actions. The effect, which was blocked by alpha adrenoceptor antagonist, could be mainly observed in the intraperitoneal treatment with epinephrine, norepinephrine or phenylephrin. e. These catecholamines obviously constricted the blood vessels of portal vein system, resulting in a marked increase of plasma purine catabolites in portal vein blood and a considerable reduction of ATP concentration in intestine and liver. The hepatic extracts prepared from animals administered epinephrine were studied on the amounts of adenine nucleotides, nucleosides and bases therein. The results showed the rapid break-down of hepatic ATP into the end product with a transient accumulation of 5' - AMP. On the other hand, the stimulation of purine catabolism mediated by beta adrenoceptor agonist was closely associated with the reduction of myocardial adenine nucleotides, which has been demonstrated by earlier workers. Isoproterenol caused the reduction of ATP concentration in the myocardium. However, neither compensatory increases of ADP and 5'-AMP nor recognizable amounts of nucleosides and bases were observed. The reduced amounts of myocardial adenine nucleotides by isoproterenol corresponded well to the increased amounts of plasma purine catabolites. Our present studies supported that a rapid breakdown of tissue adenine nucleotides should be more essential action of catecholamine on the increase of plasma purine catabolites, although earlier workers have suggested that catecholamine might induce hyperuricemia by promotion of xanthine oxidase reaction or its renal vasoconstricting action.
