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  • 1
    ISSN: 1432-1912
    Keywords: β-TM10 ; Adrenergic Neurone Blocker ; Sympathetic Denervation ; Noradrenaline Depletion by Reserpine ; Monoamine Oxidase Inhibition ; Pargyline
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The noradrenaline content of the rat submaxillary gland was determined fluorimetrically as various times after sympathetic denervation as well as after the subcutaneous injection of reserpine (300 μg/kg). The effect of an adrenergic neurone blocker (β-TMIO) was compared with that of an inhibitor of monoamine oxidase (pargyline). 2 Both βTM10 (50 mg/kg s.c. given 6 hours and repeated 12 hours after the operation) and pargyline (100 mg/kg i.p. at the operation) delayed the decline of endogenous noradrenaline observed after denervation; the delay was similar for both treatments. 3. Both,β-TM10 (50 mg/kg s.c. 2 hours before reserpine) and pargyline (100 mg/kg s.c. 6 hours before reserpine), caused a similar delay in the reserpine-induced decline of endogenous noradrenaline in the sympathetically decentralized gland. 4. Reserpine induced a higher rate of depletion in normal than in decentralized glands of untreated or pargyline-pretreated rats. However, the relation of depletion rates was reversed afterβ-TM10. 5. It is concluded that the last mentioned effect is at least partly due to the adrenergic neurone blocking effect ofβ-TMIO. The antagonism byβ-TMIO of the depleting effect of sympathetic denervation and of reserpine, on the other hand, is attributed to the ability of adrenergic neurone blocking agents to block monoamine oxidase. The results confirm earlier studies and indicate that the ability of adrenergic neurone blocking agents to block intraneuronal monoamine oxidase accounts for effects which up to now have been ascribed to their ability to prevent the release of noradrenaline by nerve impulses.
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  • 2
    ISSN: 1432-1912
    Keywords: Kidney ; Renal Handling ; Dopamine ; Noradrenaline ; Adrenaline ; Catechol-O-Methyl-Transferase (COMT)
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary In 12 female dogs renal excretion and catabolism of 14C-(±)-adrenaline, 14C-(±)-noradrenaline, 14C-dopamine and 3H-(±)-normetanephrine were investigated using a modified stop-flow technique. Radioactive compounds were infused, together with inulin, into the left renal artery for 10 min. During the first 2 min of the infusion period the left ureter was occluded. Urine samples were serially collected from both kidneys up to the end of the infusion. In the urine the total radioactivity and the pattern of radioactive metabolites were measured. On average, the infused kidney excreted from the infused dose of 14C-adrenaline 9.4% as adrenaline, 27.9% as metanephrine and 5.8% as deaminated or conjugated metabolites. From infused 14C-noradrenaline 7.4% was excreted as noradrenaline, 3.5% as normetanephrine and 1% as deaminated or conjugated compounds. When 3H-normetanephrine was infused the urine contained only radioactive normetanephrine (22.2%). From the infused dose of 14C-dopamine 9.6% was excreted as dopamine, 16.2% as 3-O-methyldopamine and 3.7% as deaminated or conjugated compounds. — Urine from the other kidney contained 1/25 to 1/5 the radioactivity of that from the infused side, but the pattern of radioactive compounds was similar. From the excretion rate of simultaneously infused inulin the filtration fraction of the infused kidney was determined. That part of the infused 14C-catecholamines which was excreted unmetabolized in the urine, corresponds to the filtration fraction in this kidney. Therefore, it is suggested, that in mammals the unmetabolized catecholamines of the urine are mainly excreted by glomerular filtration and not by tubular secretion. On the other hand, the urinary O-methylated radioactive catecholamines, which were excreted by the infused kidney at a high rate, were formed in this organ from the infused catecholamines and were excreted by tubular secretion. Thus, in mammals tubular secretion is linked to an inactivation of these compounds by O-methylation.
    Type of Medium: Electronic Resource
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