TY - JOUR T1 - UPTAKE, STORAGE AND RELEASE OF H<sup>3-</sup>α-METHYLNOREPINEPHRINE JF - Journal of Pharmacology and Experimental Therapeutics JO - J Pharmacol Exp Ther SP - 175 LP - 182 VL - 158 IS - 2 AU - Arvid Carlsson AU - Per Lundborg AU - Robert Stitzel AU - Bertil Waldeck Y1 - 1967/11/01 UR - http://jpet.aspetjournals.org/content/158/2/175.abstract N2 - H3-α-methyl-norepinephrine (H3-α-Me-NE) is taken up by and stored in sympathetically innervated tissue such as heart and skeletal muscle. The initial uptake of this compound by cardiac muscle appears to be of the same magnitude as that previously reported for H3-norepinephrine and H3-metaraminol. The uptake and subsequent loss of H5-α-Me-NE by skeletal muscle, however, was considerably lower than that found in the heart. This may be due to a lower density of adrenergic innervation or a greater proportion of extracellular binding in skeletal muscle. Unlike norepinephrine, the initial accumulation of α-Me-NE in animals pretreated with reserpine is essentially normal. Reserpine partially inhibits the incorporation of H3-α-Me-NE by subcellular particles and therefore greatly reduces the retention of this amine. The incorporation of some H3-α-Me-NE into the particulate fraction of cardiac tissue of mice pretreated with high doses of reserpine may be evidence for a reserpine-resistant uptake mechanism in adrenergic granules. Protriptyline, a membrane pump inhibitor, blocks the uptake of H3-α-methyl-norepinephrine into both heart and skeletal muscle, although the blockade is less complete in the latter tissue. H3-α-methylnormentanephrine appears to be the principal metabolite of injected H3-α-Me-NE. © 1967 by The Williams &amp; Wilkins Company ER -