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Title: Brief transient ischemia induces long-term depletion of norepinephrine without affecting the aromatic amino acid decarboxylase and monoamine oxidase activities in the rat kidney. Author: Soares-da-Silva P, Fernandes MH, Albino-Teixeira A, Azevedo I, Pestana M. Journal: J Pharmacol Exp Ther; 1992 Feb; 260(2):902-8. PubMed ID: 1738131. Abstract: Renal artery occlusion (RAO) for 30, 60 or 90 sec was found to reduce norepinephrine tissue levels in both the cortex and medulla of the rat, respectively, by 2 to 5%, 56 to 65% and 92 to 97%, but no significant change in dopamine tissue levels was found to occur. Similar effects were obtained with occlusion of the aorta proximally to the renal arteries for 90 sec. Administration of superoxide dismutase (40 mg/kg) immediately before RAO resulted in a marked protection of the norepinephrine depletion effect as caused by transient ischemia. The sodium-dependent formation of dopamine and 3,4-dihydroxyphenylacetic acid, the deaminated metabolite of dopamine, in renal slices loaded with L-3,4-dihydroxyphenylalanine (50 microM) was found to be similar in denervated and control kidneys. Type A and B monoamine oxidase activities were measured with the deamination of two specific substrates, respectively, [3H]-5-hydroxytryptamine and [14C]-beta-phenylethylamine, in homogenates of the renal cortex and renal medulla; neither type of monoamine oxidase, A or B, was found to be affected by denervation. The renal tissues collected for morphological observation were those in which RAO was performed for 90 sec. The general structure of the renal cortex was not affected by RAO, being similar in the control and the denervated kidney. In conclusion, the results presented suggest that the tissue damaging effect produced by RAO appears to be selective for the renal sympathetic innervation and seems to involve the generation of some reactive oxygen species, namely superoxide.[Abstract] [Full Text] [Related] [New Search]