The Distribution of Catecholamines between Platelets and Plasma in Normal Human Subjects

Smith, Christopher; Curtis, L. D.; Delamothe, A.P.; Prichard, B. N. C.; Betteridge, D. J.

doi:10.1042/cs0690001

Cited by 52 publications

(19 citation statements)

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“…All samples were stored at -80°C prior to analysis. Plasma catecholamines were extracted by adsorption to aluminium oxide [26] and analysed by HPLC (Merck Hitachi LaChrom system, Darmstadt, Germany) with electrochemical detection. Catecholamines were separated on a LiChroCART 250-4 column containing LiChrospher 100 RP-18 (5 μm) (Merck, Darmstadt, Germany), using a sodium acetate buffer (pH 4.8) and methanol (8.5 vol%) as eluents [27].…”

Section: Biochemical Analysesmentioning

confidence: 99%

Noradrenaline and cortisol changes in response to low-grade cognitive stress differ in migraine and tension-type headache

et al. 2007

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The goal of this study was to explore the relationship between indicators of sympathoneural, sympathomedullar and hypothalamic-pituitary-adrenocortical (HPA) activity and stressinduced head and shoulder-neck pain in patients with migraine or tension-type headache (TTH). We measured noradrenaline, adrenaline and cortisol levels before and after low-grade cognitive stress in 21 migraineurs, 16 TTH patients and 34 controls. The stressor lasted for 60 min and was followed by 30 min of relaxation. Migraine patients had lower noradrenaline levels in blood platelets compared to controls. Pain responses correlated negatively with noradrenaline levels, and pain recovery correlated negatively with the cortisol change in migraineurs. TTH patients maintained cortisol secretion during the cognitive stress as opposed to the normal circadian decrease seen in controls and migraineurs. There may therefore be abnormal activation of the HPA axis in patients with TTH when coping with mental stress, but no association was found between pain and cortisol. A relationship between HPA activity and stress in TTH patients has to our knowledge not been reported before. In migraine, on the other hand, both sympathoneural activation and HPA activation seem to be linked to stress-induced muscle pain and recovery from pain respectively. The present study suggests that migraineurs and TTH patients cope differently with low-grade cognitive stress.

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Section: Biochemical Analysesmentioning

confidence: 99%

Noradrenaline and cortisol changes in response to low-grade cognitive stress differ in migraine and tension-type headache

et al. 2007

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“…Rosen et al 3 recently reported that platelets concentrate epinephrine during increases in plasma epinephrine levels in humans following intravenous inftision of this catecholamine. However, Smith et al 4 found no changes in platelet catecholamines after 10 minutes of exercise despite marked increments in plasma catecholamines. Probably a longer period of time with high plasma catecholamines would have been necessary to increase platelet concentrations.…”

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confidence: 99%

Sodium depletion increases platelet and plasma catecholamines in hypertensive men.

et al. 1988

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SUMMARY The catecholamine content in blood platelets is considerably higher than that in plasma, and platelet catecholamines must be taken up from plasma, since blood platelets lack enzymes for catecholamine synthesis. However, it is unknown whether platelets take up and store catecholamines during physiological in vivo increments in plasma catecholamines. Previously untreated 50-year-old men (n = 17) with mild to moderate essential hypertension were given a low sodium diet for 2 weeks. Urinary excretion of sodium decreased from 201 ±11 (SE) to 24 ± 5 and 19 ± 4 mmol/24 hr after 1 and 2 weeks, respectively. During the first week, the blood platelet concentration of norepinephrine increased from 27.2 ± 2.9 to 39.6 ± 4.7 pg/mg (p<0.005) and venous plasma norepinephrine increased from 254 ± 22 to 347 ± 28 pg/ml (p<0.001). The platelet concentration of dopamine increased from 3.7 ± 0.4 to 5.6 ± 0.5 pg/ml (p<0.005), and venous plasma dopamine increased from 26 ± 4 to 41 ± 5 pg/ml (p<0.05). During the second week, both plasma and platelet norepinephrine and dopamine remained elevated. Platelet epinephrine showed a small increase from baseline to the second week (p<0.05), but no concomitant increase in plasma epinephrine occurred. Thus, sodium depletion increases both platelet and plasma catecholamines and blood platelets may take up catecholamines in vivo. Platelet catecholamine content may be an integrated measure of plasma catecholamine concentrations during variations caused by sodium depletion. (Hypertension 11: 477-482, 1988) KEY WORDS • blood pressure * electrolytes • epinephrine * norepinephrine * sympathetic tone • thrombocytes S OME of the knowledge about platelet 5-hydroxytryptamine (5-HT) and catecholamine content has been summarized by Da Prada and Picotti.1 The platelet levels of these monoamines are much higher than corresponding plasma concentrations. However, the molar contents of norepinephrine, dopamine, and epinephrine are several thousand times lower than the molar content of 5-HT. Platelet catecholamines are essentially free (unconjugated), and the subcellular localization in the platelets seems to be the 5-HT organelles (dense granules). Since platelets lack enzymes for catecholamine synthesis, it may be that the catecholamines can be actively transported and taken up through the platelet 5-HT carrier mechanism, although at a relatively low receptor/carrier affinity.

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“…The concentra tion of noradrenaline is substantially higher in platelets than in plasma, with a ratio of plate let to plasma concentration of 1855:1 (REF. 3). This ratio indicates that intra organ platelet destruction is an important source of regional noradrenaline spillover.…”

Section: Shi-sheng Zhou and Yiming Zhoumentioning

confidence: 99%

Renal denervation for resistant hypertension: the wrong target?

Zhou

2016

Nat Rev Cardiol

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We read with interest the article by Gulati et al. (Opinion: The rise, fall, and possible resurrec tion of renal denervation. Nat. Rev. Cardiol. 13, 238-244; 1 . The authors discussed the results of the SYMPLICITY HTN trials and concluded that current evidence is insuffi cient to declare renal denervation a failure for the treatment of resistant hypertension. In their Perspectives article, however, they have not considered the possibility that the current theoretical basis for renal denervation therapy for resistant hypertension might be erroneous.Based on the finding of increased renal noradrenaline spillover in patients with hypertension, it is widely accepted that there is renal sympathetic hyperactivity in hyper tension, which is used as the theoretical basis for renal denervation therapy 2 . However, this basis is questionable because the contribution of platelets to renal noradrenaline spillover has not been taken into account. The plate lets are an important factor that determines plasma noradrenaline levels. They collect, store, and degrade (through monoamine oxi dase) noradrenaline from plasma, but release undegraded noradrenaline during their activa tion (FIG. 1). Given that the lifespan of platelets is around 10 days, ~10% of circulating plate lets are destroyed every day. The concentra tion of noradrenaline is substantially higher in platelets than in plasma, with a ratio of plate let to plasma concentration of 1855:1 (REF. 3). This ratio indicates that intra organ platelet destruction is an important source of regional noradrenaline spillover.Patients with hypertension have platelet abnormalities, including increased platelet vol ume and elevated platelet noradrenaline levels. In vitro evidence has shown that a high diastolic blood pressure correlates with a rapid efflux of noradrenaline from platelets 4 , suggesting an overload of noradrenaline in patients with hypertension. Importantly, increased plate let destruction can be observed in both renal disorders and severe hypertension. The biopsy findings of renal thrombotic microangiopathy in the context of severe hypertension 5 show evidence of intrarenal platelet destruction. The increased destruction of platelets that have high levels of noradrenaline might subsequently trigger the release of more noradrenaline into the renal circulation. Moreover, hyper tension is associated with renal insufficiency, including renal disease and reduced nephron number. As shown in FIG. 1, renal insufficiency might decrease noradrenaline clearance and thus increase the burden on platelets. Indeed, an inverse correlation between estimated glomerular filtration rate and mean platelet volume has been demonstrated 6 . Therefore, an alternative and likely explanation for the increased renal noradrenaline spillover in hypertension is attributable to a combination of renal insufficiency and increased platelet destruction, accounting for the neutral results of the SYMPLICITY HTN 3 study.Platelet overload or increased platelet vol ume can be caused by many factors, incl...

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The Distribution of Catecholamines between Platelets and Plasma in Normal Human Subjects

Cited by 52 publications

References 0 publications

Noradrenaline and cortisol changes in response to low-grade cognitive stress differ in migraine and tension-type headache

Noradrenaline and cortisol changes in response to low-grade cognitive stress differ in migraine and tension-type headache

Sodium depletion increases platelet and plasma catecholamines in hypertensive men.

Renal denervation for resistant hypertension: the wrong target?

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