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PubMed1976

The metabolism and binding of catecholamines by the hepatic microsomal mixed-function oxidase of the rat.

Noradrenaline and adrenaline were metabolized by an NADPH- and oxygen-dependent process located within the hepatic microsomal fraction of the rat. Metabolism was inhibited by CO and compound SKF 525A, but not by pargyline, an inhibitor of monoamine oxidase, or by 3,4-dimethoxy-5-hydroxybenzoic acid, an inhibitor of catechol O-methyltransferase. It is concluded that the enzyme system responsible for the metabolism of the catecholamines was the microsomal mixed-function oxidase. The Km for noradrenaline was 2.4 mM and for adrenaline 1.0 mM, and V 15.6 and 3.6 nmol/min per mg of microsomal protein respectively. Both catecholamines bound to the microsomal fraction, producing a type II spectral change, with a Ks for noradrenaline of 0.9 mM and for adrenaline of 1.0 mM, and showed other characteristics of type II compounds by inhibited the reduction of cytochrome P-450 by NADPH and exhibiting an enhanced metabolism in the presence of acetone. The major product of catecholamine metabolism was an as yet unidentified alkali-labile compound, which did not correspond to any of the recognized catecholamine metabolites.

Animals↗
PubMed1979

Catecholamines and haemodynamics in fixed essential hypertension.

1. Arterial plasma catecholamines and haemodynamic status were simultaneously studied in 27 patients with fixed essential hypertension (WHO I-II). 2. Total arterial plasma catecholamines were found to be directly related to mean arterial pressure and to calculated total peripheral resistance, and they were inversely related to stroke index. 3. The degree of total peripheral resistance reduction after alpha-receptor blockade (phentolamine 10 mg intravenously) and the degree of mean arterial pressure reduction after combined alpha- and beta- receptor blockade (labetalol 100 mg intravenously) were directly related to pretreatment plasma catecholamine concentrations. 4. These findings support the view that the sympathetic nervous system, as evaluated by plasma catecholamine concentration, may have an important role in maintaining hypertension in a subgroup of patients, contributing mainly to the degree of peripheral vasoconstriction.

Adult↗
PubMed1985

The distribution of catecholamines between platelets and plasma in normal human subjects.

We have used high-performance liquid chromatography with electrochemical detection to measure content of adrenaline and noradrenaline in platelets in 13 normal subjects at rest. Subjects were exercised to raise plasma catecholamine levels and promote the platelet release reaction. There was a significant positive correlation between plasma noradrenaline concentrations and platelet noradrenaline content. Platelet/plasma concentration ratios were 1855 for noradrenaline and 268 for adrenaline at rest and 473 and 152 respectively after exercise. Plasma noradrenaline levels positively correlated with age. Determination of platelet factors released to the plasma showed increases of beta-thromboglobulin and platelet factor 4 with exercise, whereas thromboxane B2 remained unchanged. No change in platelet catecholamine levels occurred with exercise and no correlations were observed between platelet catecholamines and released platelet factors. These data suggest that plasma catecholamine levels influence platelet content and that noradrenaline and adrenaline are concentrated in platelets.

Adult↗
PubMed1986

Stimulus-induced release of endogenous catecholamines from human washed platelets.

Using high-performance liquid chromatography with electrochemical detection, we have studied the release of endogenous catecholamines from washed platelets induced to aggregate by ADP and thrombin. Washed platelets exhibit irreversible aggregation with 10 mumol/l ADP and 0.3 unit of thrombin/ml, extents of aggregation being 27% and 76% respectively. ADP (10 mumol/l) increased noradrenaline release to the medium by 20% and adrenaline by 28%. As observed with aggregation, 0.3 unit of thrombin/ml produced a more marked effect on release than ADP, noradrenaline and adrenaline being increased by 570% and 169% respectively. Values for platelet noradrenaline content were found to mirror those for the release from platelets induced by thrombin. A correlation was observed between catecholamine release and the concentration of thrombin present in incubations. These data reflect the changes observed with platelet aggregation. This is the first study to determine catecholamine release from platelets by direct measurement. Local catecholamine release after platelet aggregation in vivo may have important consequences for tissue perfusion.

Adenosine Diphosphate↗
PubMed1996

Middle cerebral artery blood velocity and plasma catecholamines during exercise.

During dynamic exercise, mean blood velocity (Vmean) in the middle cerebral artery (MCA) demonstrates a graded increase to work rate and reflects regional cerebral blood flow. At a high work rate, however, vasoactive levels of plasma catecholamines could mediate vasoconstriction of the MCA and thereby elevate Vmean at a given volume flow. To evaluate transcranial Doppler-determined Vmean at high plasma catecholamine levels, seven elite cyclists performed a maximal performance test on a bicycle ergometer. Results were compared with those elicited during five incremental exercise bouts and during rhythmic handgrip when plasma catecholamines are low. During rhythmic handgrip the Vmean was elevated by 21 +/- 3% (mean +/- SE), which was not statistically different from that established during moderate cycling. However, at the highest submaximal and maximal work intensities on the bicycle ergometer. Vmean increased by 31 +/- 3% and 48 +/- 4%, respectively, and this was significantly higher compared to handgrip (P < 0.05). During maximal cycling, plasma adrenaline increased from 0.21 +/- 0.04 nmol L-1 at rest to 4.18 +/- 1.46 nmol L-1, and noradrenaline increased from 0.79 +/- 0.08 to 12.70 +/- 1.79 nmol L-1. These levels were 12- to 16-fold higher than those during rhythmic handgrip (adrenaline: 0.34 +/- 0.03 nmol L-1; noradrenaline: 0.78 +/- 0.05 nmol L-1). The increase in Vmean during intense ergometer cycling conforms to some middle cerebral artery constriction elicited by plasma catecholamines. Such an influence is unlikely during rhythmic handgrip compared with low intensity cycling.

Adult↗
PubMed1998

Changes in plasma catecholamine concentrations and haemodynamic effects of rocuronium and vecuronium in elderly patients.

Rocuronium administration may cause tachycardia and an increase in cardiac index. Pancuronium, another steroidal non-depolarizing muscle relaxant, augments release of, and blocks re-uptake of catecholamines at adrenergic nerve endings. This study compared the haemodynamic effects of, and changes in catecholamine concentrations following administration of vecuronium (0.12 mg kg-1) or rocuronium (0.9 mg kg-1) to elderly patients. Thirty patients, 65 years or older, not receiving beta-blockers, were studied. During thiopentone, fentanyl, nitrous oxide anaesthesia, either rocuronium (0.9 mg kg-1) or vecuronium (0.12 mg kg-1) was administered, according to random allocation. In all 30 patients, blood pressure and heart rate were measured before induction of anaesthesia, immediately and 1 min after induction, 1 and 2 min after muscle relaxant administration, and immediately, 1 and 2 min after tracheal intubation. In the latter 20 patients, samples for plasma catecholamine estimation were obtained prior to, and 1 min after muscle relaxant administration and 1 min after tracheal intubation. Blood pressure and heart rate were similar in the two groups throughout the study. Plasma noradrenaline concentrations were similar in the vecuronium and rocuronium groups prior to muscle relaxant administration (589(SD240) and 444(SD213) pg mL-1, respectively), 1 min after muscle relaxant administration (602(SD220) and 520(SD392) pg mL-1, respectively) and 1 min after tracheal intubation (597(SD351) and 440(SD181) pg mL, respectively). There was no significant change in either plasma noradrenaline or adrenaline concentrations in either group following muscle relaxant administration or tracheal intubation. The use of rocuronium (0.9 mg kg-1) in elderly patients does not result in a clinically significant change in heart rate, blood pressure or plasma catecholamine concentration.

Adrenergic Agonists↗
PubMed1999

Metformin inhibits catecholamine-stimulated lipolysis in obese, hyperinsulinemic, hypertensive subjects in subcutaneous adipose tissue: an in situ microdialysis study.

AIMS: Metformin has been reported to decrease the plasma concentrations of non-esterified fatty acids in Type 2 diabetic subjects. This study investigated the effects of metformin on basal and catecholamine-stimulated lipolysis in abdominal subcutaneous adipose tissue of obese, hyperinsulinaemic, hypertensive subjects. METHODS: Fourteen subjects with severe obesity (12 female, twomale, age 35.4 +/- 4 years, body mass index 48.2 +/- 2 kg/m2, body fat mass 63.3 +/- 5 kg) were recruited. Glycerol and lactate concentrations were determined in the presence of metformin and after administration of catecholamines using microdialysis. Simultaneously, blood flow was assessed with the ethanol escape method. RESULTS: Glycerol release was lowered by metformin during the 3-h experiment (P<0.01). The lipolytic activity of catecholamines was suppressed when adipose tissue was pre-treated with metformin (P<0.001). Lactate concentration increased after application of metformin (P<0.01) and catecholamines (P<0.001). Blood flow was decreased in the presence of adrenaline (P < 0.01), but this effect was abolished by metformin. CONCLUSIONS: The present data demonstrate the effects of metformin on lipolysis in subcutaneous adipose tissue in vivo. In the large body fat mass of obese subjects, a reduction of lipolysis in adipose tissue may contribute to a decrease of VLDL synthesis in the liver resulting in a lowered plasma triglyceride concentration.

Adipose Tissue↗
PubMed2003

Catecholamine response during haemodynamically stable upright posture in individuals with and without tilt-table induced vasovagal syncope.

AIM: Changes in circulating catecholamine concentrations during vasovagal faints have been the subject of considerable study. However, whether catecholamines are part of the triggering mechanism, or principally reflect attempted compensation for an evolving circulatory crisis is unknown. To address this issue, we determined whether the circulating catecholamine response to upright posture differs among patients with and without inducible vasovagal faints at a time when there is no detectable haemodynamic compromise. METHODS AND RESULTS: Blood samples for measurement of adrenaline and noradrenaline (Norepi) concentrations were obtained in the baseline state, and at both 2-3 min and 4-6 min of upright posture in 22 patients undergoing head-up tilt-table testing for evaluation of syncope of unknown cause. In 11 individuals tilt-testing induced syncope at >5 min head-up posture (Group 1). In 11 other individuals tilt testing did not result in syncope (Group 2). Supine arterial catecholamine levels were comparable in the two groups. However, adrenaline concentrations during upright posture tended to be greater at 2-3 min and were significantly greater at 4-6 min in Group 1 than in Group 2 (P< 0.01). These differences occurred in the absence of significant intergroup differences in mean arterial pressure or cardiac cycle lengths. Norepi concentrations also increased in both groups, but without significant differences. CONCLUSION: Circulating adrenaline concentrations in posturally induced vasovagal faints rise more rapidly in vasovagal fainters than in comparably posturally stressed non-fainters, and were significantly greater in fainters prior to either detectable haemodynamic compromise or diminution of circulating Norepi levels. These findings suggest that a premonitory rise in adrenaline concentrations occurs in vasovagal fainters unassociated with an evolving circulatory crisis.

Adolescent↗
PubMed2000

Acute triiodothyronine administration does not reverse depressed contractile performance following catecholamine exposure in isolated rat cardiomyocytes.

BACKGROUND: It has been previously suggested that triiodothyronine (T3) may reverse depressed cardiac contractile performance occurring after excessive catecholamine stimulation. We therefore investigated the effects of T3 on intracellular calcium transients and contractile performance in isolated ventricular rat myocytes. METHODS: Isolated rat myocytes were loaded with the calcium indicator FURA-2/AM (50 micromol/L) and superfused with Krebs-Henseleit solution (pH 7.4). Cells were illuminated by ultraviolet light and fluorescent images obtained with a target camera at 340 nm and 380 nm excitation wavelengths (ratio method). Simultaneous measurements of calcium transients and cell shortening (35 degrees C, electrical field stimulation: 0.5 Hz) were done. At steady state conditions, FURA-2 loaded myocytes were superfused for 60 min with epinephrine (0.1 micromol/L). After 60 min the effect of T3 (10 micromol/L) on calcium transients and shortening were measured. As control, only the effect of 10 micromol/L T3 was analyzed. RESULTS: Epinephrine significantly increased cell shortening and FURA-2 signals to 148.6+/-8.8% and 109.5+/-3.1% (p < 0.01: n = 21; 5 min) respectively. With longer epinephrine exposure, the increase in cell shortening continuously declined to 134.6+/-7.9% with no change in FURA-2 fluorescence. Acute administration of T3 after epinephrine exposure lowered contractile performance from 136.2 +/- 15.5% to 102 +/- 8.2 %, after 10 minutes. In control experiments acute administration of T3 increased basal contractile response from 100% to 115.8+/-3.3% (p<0.01; n = 8; 5 min). CONCLUSIONS: This study confirms previous reports of impaired cardiac function after high catecholamine exposure. High catecholamine exposure is associated with a desensitization of contractile proteins for calcium. Acute T3 administration increased contractility in untreated myocytes, but further depressed myocyte shortening in epinephrine-treated cells. Our results show that T3 is ineffective at restoring myocardial contractility after excessive catecholamine stimulation.

Animals↗
PubMed2000

Sepsis and catecholamine support are the major risk factors for critical illness polyneuropathy after open heart surgery'.

BACKGROUND: Critical illness polyneuropathy (CIP) remains a problem after open heart surgery. Recently, we reported about a retrospectively performed study pointing out that sepsis, the application of higher amounts of catecholamines and intervention such as chronic venovenous hemodiafiltration may be involved in the onset of CIP. A prospectively performed study is presented in order to evaluate the significance of risk factors initially after open heart surgery. METHODS: From June 1997 until September 1998, patients undergoing open heart surgery and being ventilated beyond 3 days were prospectively enrolled in the study and underwent a standard protocol of electromyographic investigation in order to determine CIP. Several items were recorded: amount of catecholamines, serum levels of urea, creatinine, albumin, and glucose. The duration of sepsis and chronic venovenous hemodiafiltration were reevaluated. Additionally the age, the left ventricular end-diastolic pressure prior to the operation, the time of ICU stay and the time of ventilatory support were compared. RESULTS: Within the observation period, 37 adult patients could be enrolled in the study, whereas 12 patients did develop CIP and 7 patients did not. Patients developing CIP required significantly different amounts of epinephrine (0.17 +/- 0.02 vs. 0.09 +/- 0.01 mg/kg/day, p < 0.05, t-test) higher amounts of norepinephrine (0.06 +/- 0.02 vs. 0.02 +/- 0.01 mg/kg/day, p<0.05, t-test), and lesser dosages of dobutamine (2.2 +/- 0.5 vs. 4.9 +/- 0.7, p<0.05, t-test). After cardiac surgery, the plasma levels of urea was initially significantly elevated in patients developing CIP (127.4 +/- 10.5 vs 97.3 +/- 18.5, p<0.05, t-test) Patients suffering from CIP stayed significantly longer in the ICU (40.3 +/- 11.7 vs. 19.6 +/- 11.3 days, p < 0.05 t-test) with an extended time of ventilator support. (769.6 +/- 05.0 vs 295.0 +/- 134.0 hours, p<0.05, t-test). Patients of the CIP group were suffering significant longer from sepsis than patients without CIP. CONCLUSIONS: Sepsis and catecholamine support and an increased level of urea were associated with the development of CIP. The prevention of sepsis and a modulation of the catecholamine support in order to improve microcirculatory flow may reduce the onset of CIP in patients undergoing open heart surgery.

Aged↗
PubMed2003

Does Catecholamine Secretion from Head and Neck Paragangliomas Respond to Radiotherapy? Case Report and Literature Review.

We report a 38-year-old woman with a malignant catecholamine-secreting vagal paraganglioma. In the preceding year she had intermittent severe frontoparietal headaches. While she was receiving radiotherapy (35 Gy in 15 fractions) she developed palpitations, which steadily worsened over the following three years. A repeat CT scan showed no change in the size of the tumor. Urinary catecholamines were elevated and a MIBG scan showed increased uptake in the region of the vagal paraganglioma. She underwent near total resection of her tumor via a Fisch type C approach. Pathological examination showed a paraganglioma with metastasis involving a cervical lymph node. The palpitations and headaches resolved completely after surgery. This report and other published case reports suggest that catecholamine secretion from head and neck paragangliomas does not appear to respond to radiotherapy. Patients with cardiovascular symptoms from catecholamine-secreting paragangliomas are best managed surgically.

Case Reports↗
PubMed1980

Catecholamine-induced hyperglycemia in dogs: independence from alterations in pancreatic hormone release.

Although isoproterenol is a very effective hyperglycemic agent in dogs, other species such as rats, baboons and man are resistant to this effect. In each of these species catecholamines exert pronounced effects on insulin and glucagon release from the pancreas. In man, baboons, and rats catecholamine-induced alterations in pancreatic hormone release indirectly influence the hyperglycemic response to these amines: glucagon release supports and insulin release limits hyperglycemic responses. In contrast, the present study demonstrates that in dogs catecholamine-induced hyperglycemic responses are relatively independent of concurrent alterations in pancreatic hormone release. In dogs isoproterenol produces hyperglycemia equal to or greater than responses to epinephrine despite large increases in insulin release produced by isoproterenol. Moreover, catecholamine-induced hyperglycemia is not significantly altered when insulin and glucagon release are blocked with somatostatin.

Animals↗
PubMed2002

Seasonal variation of endothelin-1, angiotensin II, and plasma catecholamines and their relation to outside temperature.

Circannual rhythmicity in plasma catecholamines is well known, but no chronobiologic data are available on endothelin-1 and angiotensin II. This study was designed to investigate in healthy human subjects whether endothelin-1 and angiotensin II exhibit seasonal variations. Furthermore, we assessed the relation of both variables to plasma catecholamines, to environmental temperature, and to relative humidity in northern Germany, a region of a temperate climate. Plasma concentrations of endothelin-1, angiotensin II, epinephrine, and norepinephrine were prospectively determined in venous blood from 10 healthy subjects at monthly intervals during 13 consecutive months. The single-cosinor method was applied to evaluate the seasonal rhythmicity of these parameters and to assess their temporal relation to both relative humidity and ambient temperature. Whereas relative humidity did not significantly change throughout the year, outdoor temperature was lowest in January and highest in August. Endothelin-1 levels displayed a significant variation, with a sinusoid pattern throughout the year: nadir values occurred in January, peak values in July. Angiotensin II demonstrated a significant correlation with endothelin-1 and paralleled its rhythmicity. In contrast, the two plasma catecholamines exhibited an opposite pattern. We noted a significant inverse correlation between endothelin-1 and norepinephrine. Outside temperature correlated positively with endothelin-1 and angiotensin II levels and correlated negatively with levels of both catecholamines. This is the first study to report a seasonal variation of endothelin-1 and angiotensin II in normal subjects. According to our data, environmental temperature is the climate variable most closely related to the rhythmicity of endothelin-1, angiotensin II, epinephrine, and norepinephrine.

Adult↗
PubMed2001

Catecholamines decrease nitric oxide production by cytokine-stimulated hepatocytes.

BACKGROUND: Catecholamines are significantly elevated in inflammatory responses and play a regulatory role in sepsis. Nitric oxide (NO), also a key inflammatory mediator in sepsis, is produced in large amounts by the inducible nitric oxide synthase (iNOS) in the liver. The purpose of this study was to test the hypothesis that catecholamines play a role in the regulation of NO production by hepatocytes. METHODS: Primary hepatocytes were isolated from healthy male Sprague-Dawley rats and either cultured with normal medium or stimulated with cytomix (interleukin-1 beta, interferon-gamma, and tumor necrosis factor-alpha) in the presence or absence of epinephrine or norepinephrine at varying concentrations. Total RNA was isolated 6 hours after treatment and analyzed by Northern blotting for iNOS mRNA. Protein extracts were obtained at 12 hours and were analyzed by Western immunoblotting for iNOS. Cell culture supernatants were analyzed for NO, determined as the stable end-product NO(2)(-), at 24 hours. RESULTS: Epinephrine and norepinephrine significantly decreased NO(2)(-) levels in stimulated hepatocytes but had no effect on iNOS mRNA or protein levels. The decrease in NO(2)(-) was reproduced by the adenylate cyclase stimulator, forskolin. The catecholamine-induced decrease in NO(2)(-) was completely reversed by the protein kinase A inhibitor Rp-8-Br-cyclic adenosine monophosphate. CONCLUSIONS: Catecholamines decrease hepatocyte production of NO in response to cytokine stimulation. This effect seems to be due to post-translational events and appears to be mediated in part by cyclic adenosine monophosphate.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1988

Catecholamine binding and concentrations in acute phase plasma after surgery.

The present study was undertaken to decide whether the bound fractions and/or total concentrations of catecholamines were determinative for the variability of biologically active concentrations in human plasma. The binding and concentrations of noradrenaline (NA) and adrenalin (Adr) were determined in acute phase plasma after major hip surgery in five subjects. The bound fractions before surgery were 23.0% and 18.4% for NA and Adr, respectively. The binding of catecholamines increased in the post-operative period. Five days after surgery the binding of NA and Adr was 30.9% and 24.0%, respectively. The surgical trauma induced an acute phase reaction in plasma with a decrease of albumin (HSA) concentrations whereas the concentrations of alpha-1 acid glycoprotein (AAG) increased. The catecholamine concentrations showed a considerable inter- and intraindividual variability. However, the present work shows that the variability of the biologically active catecholamine concentrations is mainly dependent on the total plasma concentrations and not the plasma protein binding.

Acute-Phase Reaction↗
PubMed1996

Catecholamine concentrations and contractile responses of isolated vessels from hens treated with cyclic phenyl saligenin phosphate or paraoxon in the presence or absence of verapamil.

Blood samples and vascular segments from the ischiadic artery of hens treated with either cyclic phenyl saligenin phosphate (PSP; 2.5 micrograms/kg, im) or paraoxon (PXN; 0.1 micrograms/kg, im) in the presence or absence of verapamil, a calcium channel antagonist (7 micrograms/kg, im, given 4 consecutive days beginning the day before PSP or PXN administration), were examined 1, 3, 7, and 21 d after PSP or PXN administration in order to determine the contribution of catecholamines and peripheral blood vessel physiology and morphology to organophosphorus-induced delayed neuropathy (OPIDN). The levels of plasma catecholamines were measured by high-performance liquid chromatograpy (HPLC) and indicated a different effect with PSP, which causes OPIDN, and PXN, which does not. PSP treatment elevated the levels of norepinephrine and epinephrine throughout the study, while PXN treatment depressed the levels of these catecholamines. Verapamil treatment attenuated the OP response by approximately 50% for both compounds. Ischiadic vessel segments were isolated from OP-treated hens and perfused at a constant flow rate of 12 ml/min, then examined for their response to potassium chloride (KCl, 3 x 10(-3) M), acetylcholine (ACh), phenylephrine (PE), an alpha 1 adrenergic agonist, and salbutamol (SAL), a beta 2 adrenergic agonist. Agents were delivered in concentrations of 10(-8) to 10(-3) M. Vascular segments did not respond to ACh or SAL at any concentration used. Vessels displayed a significant reduction in contractile response to both KCl (3 x 10(-3) M) and PE (10(-8) to 10(-3) M) 3 and 21 d after exposure to either PSP or PXN. This reduced response was not altered by the presence of verapamil. Innervation of the peripheral vasculature was unchanged after OP treatment. This study indicates that plasma catecholamine levels could be differentially altered by treatment with OPs that do and do not cause OPIDN and suggests that the alterations involve intracellular calcium. In contrast, vascular response of the ischiadic artery was altered following OP treatment, but the effect was not specific for the neuropathy-inducing OP, PSP, and response was not mediated by Ca 2+, nor was it the result of autonomic nerve deterioration.

Acetylcholine↗
PubMed2002

The biochemical basis of Parkinson's disease: the role of catecholamine o-quinones: a review-discussion.

This paper reviews the possible role of catecholamine o-quinones (oQs) in the genesis of Parkinson's disease (PD). This disease is characterized by damage caused to the pigmented catecholaminergic cells in various areas of the brain. The pigment involved is neuromelanin that is the end product of catecholamine oxidation by the o-quinone route. Evidence is presented regarding the overproduction in PD of these catecholamine oQs that damage the electron chain in the mitochondria leading to cell death. The roles of glutathione S-transferase and reactive oxygen species in this are also surveyed. A review of all known biochemical properties of these o-quinones is included. The hypothesis is put forward that an important factor in the genesis of PD may be the overload by environmental toxins of enzymes such as glutathione S-transferase that also detoxify catecholamine oQs.

Journal Article↗
PubMed1992

Relationship of catecholamine excretion to body size, obesity, and nutrient intake in middle-aged and elderly men.

Catecholamine release from sympathetic nerves and the adrenal medulla is influenced by diet under controlled research conditions. To test whether diet affects catecholamine excretion in free-living men, the urinary content of dopamine (DA), epinephrine (Epi), or norepinephrine (NE) was measured in 24-h collections provided by 572 participants of the Normative Aging Study of the Veterans Administration. Average daily intakes of energy and macronutrients were assessed by means of a semiquantitative food frequency questionnaire and sodium intake by quantitation of sodium excretion. Catecholamine excretion was also examined in relation to anthropometric variables. Because DA and Epi excretion were inversely related to age, all subsequent analyses included adjustments for age. Although DA and NE were positively related to measures of body size and fatness, Epi was negatively related to body fatness. Excretion rates of all three catecholamines were directly related to total energy intake and inversely related to energy-adjusted CHO consumption.

Adult↗