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Title: Accumulation of [3H]norepinephrine in canine saphenous vein: influence of plasma. Author: Freas W, Muldoon SM, Haddy FJ. Journal: Am J Physiol; 1982 Sep; 243(3):H424-33. PubMed ID: 7114274. Abstract: This study was designed to systematically characterize the neuronal and extraneuronal uptake systems for norepinephrine (NE) in isolated nerve-rich vascular tissue and then to explore the possibility that circulating factors may alter these uptake systems. Strips from canine saphenous vein were incubated in Krebs-Ringer solution containing L-[3H]NE, and both tissue and medium were analyzed for total tritium, [3H]NE, and [3H]metabolite content. Under these conditions neuronal uptake (uptake1) played the dominant role in NE disposition. The addition of cocaine, ouabain, or potassium or the reduction of sodium decreased the activity of uptake1, and extraneuronal uptake (uptake 2) then played a major role in NE metabolism. The addition of 30, 60, and 90% plasma reduced NE accumulation and 3,4-dihydroxyphenylglycol (DOPEG) formation to 71 and 62% of control values, respectively; the formation of normetanephrine (NMN) and O-methylated deaminated compounds (OMDA) was not significantly different. In the presence of cocaine and uptake 1 inhibitor, 30% plasma did not cause a further significant decrease in neuronal accumulation of NE. The inhibitory activity of plasma on NE accumulation was not significantly affected by boiling or standing at room temperature for 45 min. These studies show that in the isolated canine saphenous vein the addition of plasma, like low sodium, cocaine, or ouabain, decreases neuronal uptake. The identity of the component in plasma responsible for inhibition of NE uptake appears to be a nonprotein, heat-stable molecule.[Abstract] [Full Text] [Related] [New Search]