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1 ificant trend to increase cortical levels of normetanephrine.
2 ce with the non-glucocorticoid OCT3 blocker, normetanephrine.
3 clusively high plasma concentrations of only normetanephrine.
4 to levels of plasma metanephrine but not to normetanephrine.
5 h venlafaxine (10 mg/kg, i.p.), at a dose of normetanephrine (10 mg/kg, i.p.) that did not produce ch
8 is study we evaluated measurements of plasma normetanephrine and metanephrine for detecting pheochrom
9 The sensitivity of measurements of plasma normetanephrine and metanephrine for the detection of tu
10 e high sensitivity of measurements of plasma normetanephrine and metanephrine was accompanied by a hi
12 d to the hypothesis that increased levels of normetanephrine, and consequently inhibition of uptake 2
13 creatinine-adjusted cortisol, metanephrine, normetanephrine, and total metanephrines were measured i
14 on Hippel-Lindau disease had a normal plasma normetanephrine concentration; this patient had a very s
16 l cortex to monitor extracellular changes in normetanephrine following chronic administration of the
17 e (NE), dopamine (DA), serotonin (5-HT), and normetanephrine (NM) in rat brain microdialysates is to
18 ndicate that inhibition of glial uptake 2 by normetanephrine or other inhibitors of uptake 2 would en
19 rugs or other agents that increase levels of normetanephrine or otherwise inhibit the extraneuronal m
22 ns administration of the uptake(2) inhibitor normetanephrine potentiated cocaine-induced reinstatemen
23 th uptake 1 and uptake 2 via venlafaxine and normetanephrine, respectively, elicits a greater increas
24 rter (NET/uptake 1) and increases in urinary normetanephrine, the O-methylated NE metabolite and pote
25 examined the abilities of corticosterone and normetanephrine to potentiate cocaine-primed reinstateme
26 Additional studies revealed that combining normetanephrine with venlafaxine (10 mg/kg, i.p.), at a
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