Routine determination of plasma catecholamines using reversed-phase, ion-pair high-performance liquid chromatography with electrochemical detection

We hypothesized that the muscle vasodilatation during mental stress and exercise would vary among humans who are polymorphic at alleles 16 and 27 of the β2-adrenoceptors. From 216 preselected volunteers, we studied 64 healthy, middle-aged normotensive women selected to represent three genotypes: homozygous for the alleles Arg16 and Gln27 (Arg16/Gln27, n = 34), Gly16 and Gln27 (Gly16/Gln27, n = 20), and Gly16 and Glu27 (Gly16/Glu27, n = 10). Forearm blood flow (plethysmography) and muscle sympathetic nerve activity (microneurography) were recorded during 3-min Stroop color-word test and 3-min handgrip isometric exercise (30% maximal voluntary contraction). Baseline muscle sympathetic nerve activity, forearm vascular conductance, mean blood pressure, and heart rate were not different among groups. During mental stress, the peak forearm vascular conductance responses were greater in Gly16/Glu27 group than in Gly16/Gln27 and Arg16/Gln27 groups (1.79 ± 0.66 vs. 0.70 ± 0.11 and 0.58 ± 0.12 units, P = 0.03). Similar results were found during exercise (0.80 ± 0.25 vs. 0.28 ± 0.08 and 0.31 ± 0.08 units, P = 0.02). Further analysis in a subset of subjects showed that brachial intra-arterial propranolol infusion abolished the difference in vasodilatory response between Gly16/Glu27 ( n = 6) and Arg16/Gln27 ( n = 7) groups during mental stress (0.33 ± 0.20 vs. 0.46 ± 0.21 units, P = 0.50) and exercise (0.08 ± 0.06 vs. 0.03 ± 0.03 units, P = 0.21). Plasma epinephrine concentration in Arg16/Gln27 and Gly16/Glu27 groups was similar. In conclusion, women who are homozygous for Gly16/Glu27 of the β2-adrenoceptors have augmented muscle vasodilatory responsiveness to mental stress and exercise.

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“…Plasma epinephrine and norepinephrine concentrations were determined by high-pressure liquid chromatography (1,3).…”

Section: Measurements and Proceduresmentioning

confidence: 99%

Gly¹⁶ + Glu²⁷ β₂-adrenoceptor polymorphisms cause increased forearm blood flow responses to mental stress and handgrip in humans

Trombetta¹,

Batalha²,

Rondon³

et al. 2005

Journal of Applied Physiology

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“…Concentrations of noradrenaline and dopamine following lesioning with either 6-hydroxydopamine (50 pg ICV) or DSP-4 (50 mg/kg x 2) were measured in whole brain by HPLC with electrochemical detection using the method of Davies and Molyneux (1982). 6-Hydroxydopamine lesioning resulted in a loss of approximately 80% of noradrenaline and 65 % of dopamine in mouse brain (Table 6).…”

Section: -Meodmtmentioning

confidence: 99%

The influence of central noradrenergic function on 5-HT2-mediated head-twitch responses in mice: Possible implications for the actions of antidepressant drugs

et al. 1986

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This study has investigated the influence of central noradrenergic function on 5-HT2-mediated head-twitch responses in mice. Central injection of low doses of the alpha 1-adrenoceptor agonists phenylephrine or methoxamine, or peripheral administration of the antagonist prazosin had no effect on the head-twitches induced by 5-methoxy-N,N-dimethyltryptamine (5-MeODMT). High doses of both alpha 1-adrenoceptor agonists and antagonists markedly inhibited this response. Head-twitches induced by 5-MeODMT were potently inhibited by low doses of the alpha 2-adrenoceptor agonist clonidine, and potentiated by the antagonists idazoxan and yohimbine. Clonidine also potently inhibited this response when produced by 5-hydroxytryptophan (5-HTP) and carbidopa. The action of the beta-adrenoceptor agonist clenbuterol on head-twitches was paradoxical, this drug enhancing the responses to precursor loading (5-HTP/carbidopa) but inhibiting those induced by direct agonists (5-MeODMT, quipazine). Lesioning noradrenergic neurons by central injection of 6-hydroxydopamine (6-OHDA) or peripheral administration of DSP-4 resulted in enhanced head-twitch behaviour. 6-Hydroxydopamine lesioning did not alter the inhibition of head-twitch responses by clonidine but prevented their enhancement following withdrawal from repeated desmethylimipramine (DMI) administration. It is therefore suggested that head-twitch behaviour may be under tonic control by a population of alpha 2-adrenoceptors which are not on presynaptic noradrenergic terminals, but are postsynaptic and located "down-stream" of the 5-HT2 receptor. In addition, the enhancement of this behaviour produced by withdrawal from repeated DMI administration probably also resulted from alterations in central noradrenergic function.

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“…5) Determination of plasma norepinephrine levels: Blood samples were collected by venous puncture, using an iced syringe, after the patient had rested in a reclined position for 30 min. Catecholamines were extracted from the plasma with aluminum oxide and quantified using high-performance liquid chromatography with electrochemical detection [11].…”

Section: Methodsmentioning

confidence: 99%

The effect of β-adrenergic receptor antagonism in cardiac sympathetic neuronal remodeling in patients with heart failure

Chizzola

Freitas

Marinho

et al. 2006

International Journal of Cardiology

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Routine determination of plasma catecholamines using reversed-phase, ion-pair high-performance liquid chromatography with electrochemical detection

Cited by 87 publications

References 32 publications

Gly¹⁶ + Glu²⁷ β₂-adrenoceptor polymorphisms cause increased forearm blood flow responses to mental stress and handgrip in humans

Gly¹⁶ + Glu²⁷ β₂-adrenoceptor polymorphisms cause increased forearm blood flow responses to mental stress and handgrip in humans

The influence of central noradrenergic function on 5-HT2-mediated head-twitch responses in mice: Possible implications for the actions of antidepressant drugs

The effect of β-adrenergic receptor antagonism in cardiac sympathetic neuronal remodeling in patients with heart failure

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Routine determination of plasma catecholamines using reversed-phase, ion-pair high-performance liquid chromatography with electrochemical detection

Cited by 87 publications

References 32 publications

Gly16 + Glu27 β2-adrenoceptor polymorphisms cause increased forearm blood flow responses to mental stress and handgrip in humans

Gly16 + Glu27 β2-adrenoceptor polymorphisms cause increased forearm blood flow responses to mental stress and handgrip in humans

The influence of central noradrenergic function on 5-HT2-mediated head-twitch responses in mice: Possible implications for the actions of antidepressant drugs

The effect of β-adrenergic receptor antagonism in cardiac sympathetic neuronal remodeling in patients with heart failure

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Gly¹⁶ + Glu²⁷ β₂-adrenoceptor polymorphisms cause increased forearm blood flow responses to mental stress and handgrip in humans

Gly¹⁶ + Glu²⁷ β₂-adrenoceptor polymorphisms cause increased forearm blood flow responses to mental stress and handgrip in humans