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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 66] vs 10.88 [5.78-18.03] nmol/L; P = .001), normetanephrine (1.75 [1.16-4.93] vs 1.25 [0.86-2.56] nm
6 h venlafaxine (10 mg/kg, i.p.), at a dose of normetanephrine (10 mg/kg, i.p.) that did not produce ch
7     Twenty-four-hour cortisol metabolite and normetanephrine (3-methoxynorepinephrine) outputs were h
8                       Measurements of plasma normetanephrine and metanephrine are useful in screening
9 is study we evaluated measurements of plasma normetanephrine and metanephrine for detecting pheochrom
10    The sensitivity of measurements of plasma normetanephrine and metanephrine for the detection of tu
11 e high sensitivity of measurements of plasma normetanephrine and metanephrine was accompanied by a hi
12                 The plasma concentrations of normetanephrine and metanephrine were compared with the
13 d to the hypothesis that increased levels of normetanephrine, and consequently inhibition of uptake 2
14  creatinine-adjusted cortisol, metanephrine, normetanephrine, and total metanephrines were measured i
15 on Hippel-Lindau disease had a normal plasma normetanephrine concentration; this patient had a very s
16                  However, corticosterone and normetanephrine failed to potentiate cocaine-primed rein
17 l cortex to monitor extracellular changes in normetanephrine following chronic administration of the
18 e (NE), dopamine (DA), serotonin (5-HT), and normetanephrine (NM) in rat brain microdialysates is to
19 ndicate that inhibition of glial uptake 2 by normetanephrine or other inhibitors of uptake 2 would en
20 rugs or other agents that increase levels of normetanephrine or otherwise inhibit the extraneuronal m
21         Lower HRV was associated with higher normetanephrine output (r=-0.19; P=0.03).
22 accounted for 37% of the link between MS and normetanephrine output, and 7% to 19% for CAA.
23 ns administration of the uptake(2) inhibitor normetanephrine potentiated cocaine-induced reinstatemen
24 th uptake 1 and uptake 2 via venlafaxine and normetanephrine, respectively, elicits a greater increas
25 rter (NET/uptake 1) and increases in urinary normetanephrine, the O-methylated NE metabolite and pote
26 examined the abilities of corticosterone and normetanephrine to potentiate cocaine-primed reinstateme
27                    Plasma chromogranin A and normetanephrine were the best tumor-marker surrogates an
28   Additional studies revealed that combining normetanephrine with venlafaxine (10 mg/kg, i.p.), at a