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PubMed1995

No effects of large doses of catecholamines on vascular permeability in isolated blood-perfused dog lungs.

Neurogenic pulmonary oedema (NPO) is believed to be induced by intense activation of the sympathetic nervous system, characterized by massive secretion of catecholamines into the blood stream. There is a possibility that NPO is partly the result of increased vascular permeability. However, the mechanism for an increase in pulmonary vascular permeability is not known. The present study was designed to test the hypothesis that large doses of catecholamines increase pulmonary microvascular permeability directly. Adrenaline or noradrenaline (100 and 300 micrograms) was injected as a bolus into isolated dog lungs perfused with heparinized autologous blood at constant pressure. Adrenaline or noradrenaline produced sustained lung weight loss although both catecholamines increased pulmonary capillary pressure, assessed by double occlusion pressure, by 2-5 mmHG above baseline. Vascular permeability, as measured by the capillary filtration coefficient and the isogravimetric capillary pressure, did not change significantly from baseline at 30 and 60 min after catecholamine. Finally, the final-to-initial wet lung weight ratio of the catecholamine-treated lungs did not differ from that of saline-injected control lungs. Thus, we conclude that circulating catecholamines, even at supraphysiological doses, do not increase permeability in isolated blood-perfused dog lungs.

Animals↗
PubMed1976

Catecholamine-induced changes in ion transport in short-circuited frog skin and the effect of beta-blockade.

1. A method for measuring bidirectional Cl fluxes has been used to estimate net Cl movements in short-circuited frog skin and to compare these with the short-circuit current (Isc) and Na fluxes. 2. In some experiments bidirectional fluxes of both Na and Cl were measured simultaneously. It was found that the algebraic sum of the net fluxes of these two ions did not differ significantly from the values of Isc, either in untreated or catecholamine-treated skins, except for the half-hour period immediately after catecholamine addition. 3. The net effluxes of Cl produced by noradrenaline (1-6 X 10(-5)M), isoprenaline (8 X 10(-7)M) and adrenaline (6 and 15 X 10(-6)M) were of similar magnitude for each catecholamine. The magnitude of the Cl response measured as a flux ratio was related to a certain extent to the precatecholamine Cl conductance. 4. The net Na influx was increased by isoprenaline and reduced by noradrenaline. 5. Addition of the beta-adrenergic blocking agent oxprenolol (4-5 X 10(-5)M) to skins stimulated by catecholamine resulted in the disappearance of the net Cl movement and fall in skin conductance and Isc. This fall was similar in magnitude to, and correlated with the mean rise in Isc produced by isoprenaline, but of significantly greater magnitude in the case of noradrenaline. 6. The changes in Na influx were strongly associated with the changes in Isc following catecholamine addition. Similarly, the changes in Na efflux and Cl efflux were correlated, suggesting the Na fluxes to be dissociated, influx and efflux changes perhaps taking place at different loci. 7. Acetazolamide (1-2 X 10(-4)M), added either before or during the noradrenaline stimulation, had no effect on the Cl efflux response. 8. The tissue exchange of Cl from the outside bathing medium after 4 hr was greater in catecholamine-stimulated skins than in those in which the response had been blocked by oxprenolol. 9. These findings were taken to support a model entailing a neutral NaCl pump resident in the mucous glands and an epithelial Na pump enhanced by beta- and inhibited by alpha-adrenergic stimulation.

Acetazolamide↗
PubMed1993

In vivo evidence for adrenal catecholamine release mediated by nonnicotinic mechanism: local medullary effect of VIP.

The aim of the present study was 1) to develop a model in anesthetized dogs in which local infusion of a given substance could be made to the adrenal gland without any systemic effects and 2) to show in this model the potential existence of a nonnicotinic mechanism involved in adrenal catecholamine secretion. Plasma catecholamine concentrations were determined by an high-performance liquid chromatography method. The local infusion into the left adrenolumbar artery (0.5 ml/min for 1 min) of either dimethylphenylpiperazinium (0.3-3.0 micrograms/ml) or vasoactive intestinal peptide (0.1-10.0 micrograms/ml) resulted in dose-dependent increases in both epinephrine and norepinephrine secretions. Neither aortic pressure nor plasma catecholamine levels altered during the drug infusion. The net increases in adrenal catecholamine secretion obtained with dimethylphenylpiperazinium were abolished by the nicotinic blockade with pentolinium (2 mg/ml, 0.5 ml/min for 2 min). However, the net catecholamine responses to vasoactive intestinal peptide remained unaffected in the presence of the same dose of pentolinium. The results suggest that there exists a nonnicotinic mechanism that may be implicated in the local regulation of medullary catecholamine secretion in the dog adrenal gland. This model may be a useful tool for studying local physiological role(s) of various neurotransmitters and neuromodulators in the adrenal secretory function in vivo.

Adrenal Glands↗
PubMed1994

Nifedipine inhibits adrenal but not circulating catecholamine response to nicotinic stimulation in dogs.

We investigated whether dihydropyridine-sensitive L-type Ca2+ channels are implicated in adrenal and sympathetic neural catecholamine release in response to nicotinic stimulation by 1,1-dimethyl-4-phenylpiperazinium (DMPP), a selective cholinergic nicotinic agonist, in dogs anesthetized with pentobarbital sodium. Plasma epinephrine and norepinephrine concentrations were measured in adrenal venous and aortic blood by a high-performance liquid chromatography-electrochemical method. In the vehicle control group, intravenous injection of DMPP (15 micrograms/kg iv) produced a significant increase in adrenal venous catecholamine output and aortic catecholamine concentration. These increasing responses were highly reproducible on the repetition of DMPP injection given 30 min after the first injection. In dogs receiving nifedipine (100 micrograms/kg iv), the net increase in adrenal venous epinephrine and norepinephrine output in response to DMPP was attenuated by 42% (P < 0.05), while no significant changes were observed in the aortic catecholamine response to DMPP. In dogs treated with pentolinium (1 mg/kg iv), both adrenal epinephrine and norepinephrine responses to DMPP were inhibited by 67% (P < 0.05) and 84% (P < 0.05), respectively. Furthermore, pentolinium inhibited aortic catecholamine response to DMPP by > 95% (P < 0.05). The present study suggests that DMPP-induced release of adrenal catecholamines was mediated, at least in part, through mechanisms involving dihydropyridine-sensitive L-type Ca2+ channels under in vivo conditions. By contrast, however, the results also suggest that dihydropyridine-sensitive L-type Ca2+ channels were not implicated in the neurotransmission at the level of sympathetic ganglions.

Adrenal Glands↗
PubMed1997

Angiotensins stimulate catecholamine release from the chromaffin tissue of the rainbow trout.

Immunohistochemical and pharmacological techniques were utilized to investigate the relationships between angiotensins and catecholamine release from the chromaffin tissue of rainbow trout (Oncorhynchus mykiss). Double labeling with [Asp1, Ile5]angiotensin II-fluorescein isothiocyanate (ANG II-FITC) and anti-dopamine beta-hydroxylase revealed specific ANG II binding sites on chromaffin cells. Injection (1 nmol/kg body wt) of either ANG II-FITC, [Asn1, Val5, Asn9]ANG I, [Asp1, Ile5, His9]ANG I, [Asn1, Val5]ANG II, [Asp1, Val5]ANG II, or [Asp1, Ile5]ANG II elicited catecholamine release from in situ perfusion preparations of the head kidney. Catecholamine release elicited by [Asn1, Val5]ANG II (10(-13) to 10(-7) mol/kg body wt) was dose dependent, and the secretion of epinephrine (Epi) was greater than that of norepinephrine (NE). Relative to the results obtained with the [Asn1, Val5]ANG II treatment (1 nmol/kg body wt), Epi release was 72 and 82% lower in response to injections (1 nmol/kg body wt) of [Asn1, Val5]ANG I [amino acid (AA) positions 1-7] and [Asn1, Val5]ANG I (AA 1-6), respectively. Pretreatment with either losartan (10(-5) M), PD-123319 (10(-5) M), or hexamethonium (10(-3) M) had no effect on [Asn1, Val5]ANG II-elicited catecholamine release. Pretreatment with captopril (10(-4) M) significantly reduced [Asn1, Val5, Asn9]ANG I-elicited Epi and NE release and decreased basal catecholamine release. These results provide direct evidence that angiotensins can elicit catecholamine release from the chromaffin tissue via specific ANG II binding sites and indicate that the synthesis of ANG II may be either local or systemic.

Angiotensin I↗
PubMed2001

Effects of catecholamines on the pulmonary circulation in the ovine fetus.

High levels of circulating catecholamines are found in the fetus, and fetal stress and birth induce a marked surge in catecholamine secretion. Little is known about the role of catecholamines on the fetal pulmonary circulation. To determine the effects of catecholamines on the pulmonary vascular tone, we tested the hemodynamic response to norepinephrine and dopamine infusion in chronically prepared late-gestation fetal lambs. We found that norepinephrine infusion (0.5 microg. kg(-1). min(-1)) increased pulmonary artery pressure (PAP) by 10 +/- 1% (P < 0.01), left pulmonary artery blood flow by 73 +/- 14% (P < 0.01), and decreased pulmonary vascular resistance (PVR) by 33 +/- 6% (P < 0.01). The pulmonary vasodilator effect of norepinephrine was abolished after nitric oxide synthase inhibition. Dopamine infusion at 5 microg. kg(-1). min(-1) did not significantly change PVR. Conversely, dopamine infusion at 10 microg. kg(-1). min(-1) increased PAP (P < 0.01) and progressively increased PVR by 30 +/- 14% (P < 0.01). These results indicate that catecholamines may modulate basal pulmonary vascular tone in the ovine fetus. We speculate that catecholamines may play a significant role in the maintenance of the fetal pulmonary circulation and in mediating changes in the transitional pulmonary circulation.

Adrenergic alpha-Agonists↗
PubMed1977

Catecholamines in coronary sinus during exercise in man before and after training.

Coronary patients exercised on an ergometric bicycle before and after physical training. Plasma catecholamines were sampled simultaneously at the arterial and coronary sinus levels and assayed with a radioenzymatic method. The increase in the level of coronary sinus catecholamines exceeded the increase in the arterial level, indicating a liberation of catecholamines by the myocardium and an activation of the peripheral sympathetic fibers during exercise. With high work loads, these values no longer differed, suggesting that the additional increase in circulating catecholamines originate from extra-myocardial stores, presumably the adrenal medulla. Arterial catecholamine levels were significantly correlated with work loads, heart rate, changes in systolic blood pressure, and rate-pressure product. After physical training, arterial catecholamine increases for various work loads were lower; these lower elevations were associated with diminished responses in heart rate and systolic blood pressure, resulting in a lower rate-pressure product. Physical training results in diminished sympathetic responses for a given level of exercise, which could be associated with the clinical improvement of these patients.

Adult↗
PubMedDate not supplied

Does catecholamine secretion mediate the hypoxia-induced increase in nerve activity?

Catecholamine secretion from carotid body glomus cells is hypothesized to cause the hypoxia-induced increase in nerve activity. To test aspects of this hypothesis, tissue catecholamine and single-fiber nerve activity was measured from rat carotid bodies in vitro. Hypoxia (1-min duration, 0 Torr at nadir) caused a rapid increase in catecholamine release and nerve activity, consistent with the hypothesis, but repetitive hypoxias interspersed with short rest periods resulted in a much greater decline in catecholamine release than nerve activity. Furthermore, pretreatment with reserpine (24 h) nearly abolished catecholamine release, but nerve response was not different than untreated controls. These results suggest that catecholamine secretion is not causal to the increase in nerve activity of rat carotid body.

Action Potentials↗
PubMed1984

Variations in circulating catecholamines fail to alter human platelet alpha-2-adrenergic receptor number or affinity for [3H]yohimbine or [3H]dihydroergocryptine.

A series of studies were performed to determine the relationship between physiologic levels of circulating plasma norepinephrine and epinephrine and human platelet alpha-2 binding site number and the affinity (KD) of these sites for antagonist radioligands. In one study, alpha-2-adrenergic binding site number and affinity were compared using both [3H]yohimbine and [3H]dihydroergocryptine as radioligands. There was good absolute and relative comparison for binding site number, but only a relative relationship for KD. In 46 normal subjects, there was no significant relationship between site number or KD and age, plasma epinephrine, or plasma norepinephrine concentration. Even after plasma epinephrine was raised nearly 20-fold by means of an intravenous infusion for 4 h in seven normal subjects, neither sites (608 +/- 68 vs. 567 +/- 120 sites/platelet) nor KD (2.01 +/- 0.94 vs. 2.14 +/- 1.15 nM) were significantly changed. Similarly, neither sites (445 +/- 55 vs. 421 +/- 53 sites/platelet) nor KD (1.44 +/- 0.29 vs. 2.10 +/- 0.75 nM) were significantly changed in six normal subjects when plasma norepinephrine levels increased during oral administration of prazosin for 1 wk. Thus, in a cross-sectional analysis and after a change in plasma catecholamine concentrations, there was no relationship in normal subjects between platelet alpha-2 binding site number or affinity of these sites for antagonist radioligands and the circulating catecholamine levels to which the platelets were exposed. In a group (n = 7) of patients who lack epinephrine-induced platelet aggregation due to abnormal thrombopoiesis, binding site number was decreased (304 +/- 36 vs. 572 +/- 29 sites/platelet, P less than 0.001) and KD tended to be greater (8.69 +/- 2.44 vs. 5.40 +/- 0.31 nM, P = NS) than in normal subjects (n = 46), despite having similar plasma catecholamine levels. There was no difference in binding site number (491 +/- 116 sites/platelet) and KD (5.61 +/- 0.84 nM) in patients (n = 5) with autonomic insufficiency and low levels of upright plasma norepinephrine when compared with the normal subjects. Two patients were examined before and after the removal of a pheochromocytoma. Their binding site number and KD were normal before the operation and essentially unchanged after the tumor removal and fall of plasma catecholamines. Thus, this study demonstrates that within the physiologic and pathophysiologic range of plasma catecholamines (in men), there is no relationship between the circulating catecholamine concentration and either platelet alpha-2 adrenergic binding site number or the affinity of these sites for antagonist radioligands.

Adult↗
PubMed1997

Novel autocrine feedback control of catecholamine release. A discrete chromogranin a fragment is a noncompetitive nicotinic cholinergic antagonist.

Catecholamine secretory vesicle core proteins (chromogranins) contain an activity that inhibits catecholamine release, but the identity of the responsible peptide has been elusive. Size-fractionated chromogranins antagonized nicotinic cholinergic-stimulated catecholamine secretion; the inhibitor was enriched in processed chromogranin fragments, and was liberated from purified chromogranin A. Of 15 synthetic peptides spanning approximately 80% of chromogranin A, one (bovine chromogranin A344-364 [RSMRLSFRARGYGFRGPGLQL], or catestatin) was a potent, dose-dependent (IC50 approximately 200 nM), reversible secretory inhibitor on pheochromocytoma and adrenal chromaffin cells, as well as noradrenergic neurites. An antibody directed against this peptide blocked the inhibitory effect of chromogranin A proteolytic fragments on nicotinic-stimulated catecholamine secretion. This region of chromogranin A is extensively processed within chromaffin vesicles in vivo. The inhibitory effect was specific for nicotinic cholinergic stimulation of catecholamine release, and was shared by this chromogranin A region from several species. Nicotinic cationic (Na+, Ca2+) signal transduction was specifically disrupted by catestatin. Even high-dose nicotine failed to overcome the inhibition, suggesting noncompetitive nicotinic antagonism. This small domain within chromogranin A may contribute to a novel, autocrine, homeostatic (negative-feedback) mechanism controlling catecholamine release from chromaffin cells and neurons.

Amino Acid Sequence↗
PubMed1982

Decreased response of plasma catecholamine to stress in diabetic rats.

Previously we reported that the heart norepinephrine concentration was markedly increased in diabetic rats. To further study the relationship between a disturbance in the autonomic nervous system and catecholamine metabolism in diabetes mellitus, the plasma catecholamine response to stress and catecholamine concentration of heart and adrenals were measured. Wistar male rats were made diabetic by streptozotocin and kept for 13 weeks. A silicon catheter was placed in the superior V. cava 1 week prior to the experiment. Insulin was injected subcutaneously for 3 days once daily. After an overnight fast and without anesthesia, 1 ml of blood, a control sample, was obtained and then the animals were exsanguinated. The blood was mixed with 1 mM EGTA at a final concentration and centrifuged. The tissue was homogenized with 0.4 N perchloric acid containing 1 mM EGTA and centrifuged at 10,000 x g for 20 minutes. Catecholamines were determined by high performance liquid chromatography. Normal rats responded to blood withdrawal stress, and plasma catecholamines were markedly increased, but almost no increase or an actual decrease was observed in diabetic rats. These abnormal responses were improved by insulin treatment. Heart norepinephrine was increased significantly in the diabetic rats compared with the control rats and was reduced significantly by insulin injections. Adrenal epinephrine was also significantly increased in the diabetic rats compared with the control rats, but was not significantly reduced by insulin. These result suggest a possible disturbance of catecholamine secretion in the diabetic rats.

Adrenal Glands↗
PubMed1979

Catecholamine requirement for hamster sperm motility in vitro.

Homogenates of hamster and bovine glands contain a "sperm motility factor" (SMF) that stimulates the motility of hamster epididymal spermatozoa in vitro. The potency of these adrenal preparations was severely attenuated after gel filtration on a Sephadex G-10 column. This loss of activity was ascribed to the retardation and separation of co-factors for SMF which appeared to be catecholamines. The sperm motility-stimulating activity of the SMF-containing fractions was fully restored by addition of either the 'retarded' fractions or catecholamines (epinephrine or norepinephrine). Neither the catecholamines nor the 'retarded' fractions were able to sustain vigorous sperm motility in the absence of the SMF-containing fractions. The potentiating action of catecholamines on SMF was mimicked by the adrenergic agonists isoproterenol and phenylephrine and inhibited by the alpha-adrenergic antagonist phentolamine, but not by the beta-adrenergic antagonist propranolol. Our results indicate that one or more catecholamines are essential co-factors of SMF and demonstrate that hamster spermatozoa require catecholamines for their motility in vitro.

Adrenal Cortex↗
PubMed1984

Low sodium diet augments plasma and tissue catecholamine levels in pithed rats.

Plasma and tissue (cardiac, vascular, renal, and adrenal) catecholamine concentrations were measured in pithed male Wistar rats maintained on low (10 mEq/kg diet), basal (115 mEq/kg diet), or high (1200 mEq/kg diet) sodium test diets for five weeks. Significant differences in catecholamine disposition were observed only in response to sodium restriction; responses to basal and high sodium intakes were consistently similar. Baseline plasma catecholamine levels (p less than 0.01) as well as those in response to stimulation of the entire sympathetic outflow at 4 Hz were markedly enhanced in low sodium rats (p less than 0.001). The facilitation of stimulation-induced increments in plasma norepinephrine levels in low sodium rats may be related to the finding that norepinephrine content was also elevated in noradrenergically innervated tissues (atria, ventricles, mesenteric artery, and kidneys) (p less than 0.01). Adrenal catecholamine levels, however, were not affected by dietary sodium restriction. Despite the peripheral catecholamine changes associated with a low sodium intake, pressor and tachycardic responses to sympathetic nerve stimulation were similar across dietary sodium groups. The results indicate that a low sodium intake enhances plasma and tissue catecholamine levels, adaptations that may be important in the maintenance of sympathetic responsiveness.

Adrenal Glands↗
PubMed2004

Modification of Cu,Zn-superoxide dismutase by oxidized catecholamines.

Oxidation of catecholamines may contribute to the pathogenesis of Parkinson's disease (PD). The effect of the oxidized products of catecholamines on the modification of Cu,Zn-superoxide dismutase (SOD) was investigated. When Cu,Zn-SOD was incubated with the oxidized 3,4-dihydroxyphenylalanine (DOPA) or dopamine, the protein was induced to be aggregated. The deoxyribose assay showed that hydroxyl radicals were generated during the oxidation of catecholamines in the presence of copper ion. Radical scavengers, azide, N-acetylcysteine, and catalase inhibited the oxidized catecholamine-mediated Cu,Zn-SOD aggregation. Therefore, the results indicate that free radicals may play a role in the aggregation of Cu,Zn-SOD. When Cu,Zn-SOD that had been exposed to catecholamines was subsequently analyzed by an amino acid analysis, the glycine and histidine residues were particularly sensitive. These results suggest that the modification of Cu,Zn-SOD by oxidized catecholamines might induce the perturbation of cellular antioxidant systems and led to a deleterious cell condition.

Animals↗
PubMed1984

[Role of adrenergic receptors in the mechanism of action of catecholamines and DOPA on proliferative processes].

Catecholamines (adrenaline, isoproterenol) and L-DOPA decreased the mitotic index of L-cells in culture. The action of catecholamines was blocked by the beta-adrenergic antagonist propranolol, but was not abolished by the alpha-adrenoblocker phenoxybezamine. The L-DOPA-induced decrease in the mitotic index did not depend on the pretreatment with the adrenoblockers. Catecholamines inhibited the incorporation of 3H-thymidine and 3H-leucine into DNA and total protein of the cells, respectively. Preincubation of the culture with propranolol for 10-20 minutes before catecholamine administration prevented the action of catecholamines. Phenoxybenzamine, an alpha-adrenoreceptor blocker, did not produce such an effect. The data obtained point to the leading role of beta-adrenoreceptors in the mechanism of the effects of catecholamines on proliferative processes. The action of L-DOPA on cell proliferation does not seem to be linked with adrenoreceptor activation.

Adrenergic alpha-Antagonists↗
PubMed1980

[The influence of arterial partial pressure of co2 and of the arterial value of ph on endogenous catecholamines during extracorporal circulation in regard to oxygen consumption of the whole body (author's transl)].

Ten patients with coronary heart diseases were studied during total hypothermic extracorporal circulation relating changes of the endogenous catecholamines epinephrine and nor-epinephrine to arterial partial pressure of CO2 and to the arterial value of pH. Both of the catecholamines increased significantly during respiratory or metabolic acidosis whereas respiratory or metabolic alkalosis was accompanied by significantly lower catecholamine levels in blood. The changes in total peripheral resistance due to the endogenous blood levels of catecholamines depended proprotionally. Total peripheral resistance increased significantly due to increasing arterial level of both of the catecholamines. The results are discussed in consideration of oxygen consumption of the whole body during extracorporal circulation. It is known that the decrease of oxygen consumption of the whole body due to acidosis and due to an increased total peripheral resistance is accompanied by high catecholamine levels in blood. Increased hypothermic sympatho-adrenal activity during extracorporal circulation should not in any case cause in increase of oxygen consumption of the whole body.

Acidosis↗
PubMed1980

[Plasma catecholamines in accidental hypothermia (author's transl)].

The plasma levels of adrenaline and noradrenaline were measured by a radioenzymatic method in 3 patients with accidental hypothermia and followed up until normal body temperature was achieved. In all 3 patients the hypothermia was accompanied by markedly elevated levels of noradrenaline, whereas adrenaline increased considerably only in one of the 3 patients. During normalization of body temperature the elevated catecholamine levels started to decrease. In 2 of the 3 patients nearly normal catecholamine levels were measured, when body temperature had normalized. In spite of the high levels of catecholamines in plasma the heart rate was strikingly low at the lowest temperature. During the increase of the lowered body temperature the heart rate increased in contrast to the decreasing catecholamine levels. The increase of the catecholamine levels in plasma in patients with accidental hypothermia can be explained either by an augmented stimulation of the sympathetic nervous system or by a decreased metabolism. On the basis of the high endogeneous catecholamine levels the use of beta-sympathomimetics appears contraindicated in case a haemodynamic insufficiency develops during the course of accidental hypothermia.

Adult↗
PubMed2005

Different expression of catecholamine transporters in phaeochromocytomas from patients with von Hippel-Lindau syndrome and multiple endocrine neoplasia type 2.

OBJECTIVE: Phaeochromocytomas in patients with multiple endocrine neoplasia type 2 (MEN 2) produce adrenaline, whereas those with von Hippel-Lindau (VHL) syndrome do not. This study assessed whether these distinctions relate to differences in expression of the transporters responsible for uptake and storage of catecholamines - the noradrenaline transporter and the vesicular monoamine transporters (VMAT 1 and VMAT 2). METHODS: Tumour tissue and plasma samples were obtained from 31 patients with hereditary phaeochromocytoma - 18 with VHL syndrome and 13 with MEN 2. We used quantitative PCR, Western blotting, electron microscopy, immunohistochemistry and measurements of plasma and tumour catecholamines to assess differences in expression of the transporters in noradrenaline-producing vs adrenaline-producing hereditary tumours. These differences were compared with those in a further group of 26 patients with non-syndromic phaeochromocytoma. RESULTS: Adrenaline-producing phaeochromocytomas in MEN 2 patients expressed more noradrenaline transporter mRNA and protein than noradrenaline-producing tumours in VHL patients. In contrast, there was greater expression of VMAT 1 in VHL than MEN 2 tumours, while expression of VMAT 2 did not differ significantly. These differences were associated with larger numbers of storage vesicles and higher tissue contents of catecholamines in MEN 2 than in VHL tumours. Differences in expression of the noradrenaline transporter were weaker, and those of VMAT 1 and VMAT 2 stronger, in noradrenaline and adrenaline-producing non-syndromic than in hereditary tumours. CONCLUSIONS: The findings show that, in addition to differences in catecholamine biosynthesis, phaeochromocytomas in MEN 2 and VHL syndrome also differ in expression of the transporters responsible for uptake and vesicular storage of catecholamines.

Adolescent↗