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PubMed1981

Regulation of human leukocyte beta receptors by endogenous catecholamines: relationship of leukocyte beta receptor density to the cardiac sensitivity to isoproterenol.

High levels of beta receptor agonist have previously been shown to down-regulate beta receptor density on circulating leukocytes in man; however, the factors controlling receptor density under physiological conditions have not previously been defined. To determine whether beta receptor density is normally down-regulated by circulating, physiological levels of catecholamines we have examined the relationship between receptor density and catecholamine levels. Urinary epinephrine and norepinephrine were significantly reciprocally correlated to lymphocyte receptor density. A similar relationship existed between beta receptor density and supine plasma epinephrine, norepinephrine, upright epinephrine, and norepinephrine levels. Change in sodium intake from 10 to 400 meq/d caused a 52% increase in lymphocyte and a 48% increase in polymorphonuclear beta receptor density. The changes in receptor density were accompanied by an increase in the sensitivity to isoproterenol measured as a fall in the dose of isoproterenol required to raise the heart rate by 25 beats per minute. Beta receptor density on both lymphocyte and polymorphonuclear cells was significantly correlated to the cardiac sensitivity to isoproterenol. Propranolol administration resulted in an increase in the density of beta receptors on lymphocyte and polymorphonuclear cells that correlated with the subject's pretreatment catecholamine levels. These findings, therefore, suggest that physiological levels of catecholamines normally down-regulate beta receptors in man and that blockade of this down-regulation by propranolol allows receptor density to increase.

Adult↗
PubMed1987

Effect of fetal adrenalectomy on catecholamine release and physiologic adaptation at birth in sheep.

Plasma catecholamine levels increase dramatically at birth. To determine the contribution of adrenal catecholamine secretion to the surge in catecholamines at birth and the role in newborn adaptation, we performed surgical adrenalectomy or sham operation on near-term ovine fetuses. After recovery in utero, the animals were delivered and supported by mechanical ventilation. Plasma catecholamine levels, heart rate, blood pressure, cardiac output, pulmonary function, surfactant secretion, and release of free fatty acids (FFA) and glucose were compared in control and adrenalectomized animals. Plasma epinephrine increased rapidly at birth in controls but was undetectable in adrenalectomized animals. Norepinephrine levels were not statistically different. Heart rate, blood pressure, cardiac output and contractility increased abruptly after cord cutting in controls but did not increase in adrenalectomized animals. Lung compliance, pulmonary function, surfactant pool size, glucose and FFA levels were significantly decreased in adrenalectomized animals. These results suggest that adrenal epinephrine secretion is vital to many of the adaptive events at birth.

Adaptation, Physiological↗
PubMedDate not supplied

Catecholamine-secreting infratemporal fossa paraganglioma.

Extraadrenal paragangliomas are tumors of the paraganglion system, usually arising from the carotid bodies, the glomus jugulare, or the glomus tympanicum. These tumors are capable of secreting catecholamines which can cause severe hypertensive crises. This paper reports a case of a patient who suffered a cerebral vascular accident due to hypertension resulting from a catecholamine-secreting infratemporal fossa paraganglioma. Any patient with a history of paroxysmal hypertension, headaches, and palpitations should be evaluated for a catecholamine-secreting tumor. Diagnosis and management of these tumors is best accomplished by a team including a radiologist, an endocrinologist, an anesthesiologist, a pathologist, an otolaryngologist--head and neck surgeon, and when the tumor invades the cranial cavity, a neurosurgeon. In this case, precise radiographic mapping of the tumor extent and its blood supply, control of hypertension with adrenergic blocking agents, and depletion of catecholamine stores using alpha-methyl-p-tyrosine allowed total extirpation through a craniofacial approach and a successful outcome.

Catecholamines↗
PubMed1988

Neuroblastoma--when are urinary catecholamines and their metabolites 'normal'?

The overproduction of catecholamines and their metabolites is a well recognised feature of neuroblastoma. Published data are scarce for their urinary excretion in children with neuroblastoma and in ill children in whom this diagnosis may be considered. We have determined a graphical upper reference limit for total catecholamines, total metadrenalines and HMMA in urine, expressed as a ratio to the creatinine concentration, for a group of 174 children with neuroblastoma and 704 hospitalised children with other disorders. This graph has been determined by examining the overlap region between the results for the two groups of children and avoids the irregularities caused by statistical outliers. The sensitivity and specificity of the individual tests indicate that total catecholamines is marginally the best single test to perform when trying to diagnose neuroblastoma, with the best clinical sensitivity being achieved by examining both total catecholamines and HMMA. Only two of the 174 children with neuroblastoma would not have been detected using these two tests. Total metadrenalines did not appear to add any further information and could be dropped from the repertoire in favour of the other two measurements.

Adolescent↗
PubMed1995

Urinary catecholamine levels in children with and without dental caries.

Urinary catecholamines have been used to measure emotionally stressful states which may affect the development of dental caries. This study investigates the hypothesis that children with and without dental caries do not differ significantly in the mean values of urinary catecholamines such as epinephrine, norepinephrine, and dopamine. As a test of this hypothesis, 314 children, males and females, aged from 6 to 8 years, were included in the study. Dental caries were recorded clinically and radiographically, and oral hygiene was evaluated by the recording of dental plaque. A 24-hour urine sample was collected for each subject, and a representative sample (25 mL) was analyzed by the HPLC technique to assay the catecholamine content. Socioeconomic factors such as parental age, education, and profession were recorded by a questionnaire distributed to the parents. Of the examined children, 38 (14 males and 24 females) were free of dental caries and constituted the case group. Two control groups, A and B, of 38 children each (14 males and 24 females) with dental caries were matched by age and gender. Differences in the quantitative and qualitative data were tested by the paired t test and the X2-test, respectively, while a regression analysis was applied to measure the effects of norepinephrine and dopamine on epinephrine. The logistic multiple-regression analysis was used to test, in the entire population, the impact of catecholamines and other related factors on the probability of subjects' developing dental caries. The 95% probability was used. The results showed statistically significant differences in epinephrine values between the case group and control groups A and B. The data suggest, therefore, that children with emotionally stressful states have higher probability of developing dental caries.

Case-Control Studies↗
PubMed1999

Plasma catecholamines, pharmacotherapy and mood of subjects with cardiovascular disorder.

This study investigated whether drug therapy explains why the concentration of arterial plasma catecholamines in patients who have received an orthotopic heart transplant (OHT) or coronary bypass and graft (CABG) is greater than in those with heart failure (HF). The results suggest that the differences in plasma catecholamine concentrations in these groups of patients could not be attributed to administration of any of the drugs studied here. An additional finding is that the use of aspirin is associated with a higher concentration of plasma noradrenaline, but not adrenaline. Patients who were taking aspirin also had a more positive mood, as rated by the Profile of Mood States; this was mainly because they had a lower fatigue score than did patients who were not taking this drug. In contrast, several agents (warfarin, Ca2+-channel blockers and 'mixed cardiac' drugs), which had no effects on catecholamine overspill, were linked with negative mood; this was expressed consistently as a higher tension score. These findings suggest that drugs which are administered for their effects in the periphery could also influence patients' psychological status. With the possible exception of aspirin, this does not involve changes in spillover of catecholamines in the periphery.

Adult↗
PubMed1997

Adverse cardiovascular effects of ketamine infusion in patients with catecholamine-dependent heart failure.

The longterm effects of ketamine on haemodynamic parameters and exogenous catecholamine requirements were studied in twenty-five critically ill patients with catecholamine-dependent heart failure. Following sedation with midazolam (0.15 +/- 0.07, mg.kg-1.h-1) and sufentanil (0.88 +/- 0.33 microgram.kg-1.h-1), patients with impaired left ventricular function (left ventricular ejection fraction area 30 +/- 7%) were randomly assigned to receive ketamine (2.5 +/- 0.9 mg.kg-1.h-1) and midazolam (Group A) or remained on sufentanil/midazolam (Group B). Haemodynamic measurements were performed throughout the first 24 hours after randomization. In group A cardiac index decreased by 21% (P = 0.01), mean arterial pressure increased by 13% (P = 0.01), mean pulmonary artery pressure by 14% (P = 0.04), pulmonary capillary wedge pressure by 20% (P = 0.03), and systemic vascular resistance index by 38% (P < 0.001). No significant cardiovascular effects were observed in Group B. Neither group had significant changes of exogenous catecholamine requirement. In conclusion, ketamine exhibits potential negative cardiovascular effects in patients with catecholamine-dependent heart failure. Therefore, ketamine should not be considered a first line drug for longterm sedation of patients with impaired left ventricular function.

Aged↗
PubMedDate not supplied

An experimental analysis of the catecholamines in hyperglycemia and acidosis induced rat brain.

Hyperglycemia and acidosis are the hallmark of diabetes. Since these factors play an important role in the diabetic complications, we have studied the brain catecholamine levels in hyperglycemic and acidotic conditions per se. Experimentally induced hyperglycemia and acidosis are accompanied by significant alterations in the catecholamine levels in discrete areas of the brain. We and others have shown that chronic or acute diabetes in animals as well as in human results in altered neurotransmitter levels. In the present study, hyperglycemia maintained by daily external administration of glucose for thirty days showed increased level of dopamine in striatum and hippocampus, elevation of norepinephrine in hippocampus, and increased level of epinephrine in hypothalamus, midbrain and pons medulla. The ammonium chloride induced acidosis demonstrated significant elevation of dopamine in midbrain and significant increase of norepinephrine in hypothalamus and midbrain, and increased level of epinephrine in hypothalamus, pons medulla and cerebral cortex. On the other hand, sodium acetoacetate induced acidosis did not show any significant change in the level of catecholamines in any of the areas studied. In conclusion, the changes in catecholamine levels observed in experimentally induced hyperglycemic as well as in acidotic conditions are closely related to the changes observed in spontaneous or alloxan or streptozotocin diabetic animals, thereby suggesting that these conditions may be responsible for the changes observed in diabetic animals.

Acidosis↗
PubMed2006

Human CD4+CD25+ regulatory T cells selectively express tyrosine hydroxylase and contain endogenous catecholamines subserving an autocrine/paracrine inhibitory functional loop.

CD4+CD25+ regulatory T lymphocytes (Tregs) are specialized T cells playing a key role in the control of immune homeostasis. Here, we show that human Tregs constitutively express tyrosine hydroxylase (TH, EC 1.14.16.2), the rate-limiting enzyme in the synthesis of catecholamines, and contain substantial amounts of dopamine, norepinephrine, and epinephrine, which are released upon treatment with reserpine. Catecholamine release results in reduced production of interleukin-10 and transforming growth factor-beta by Tregs, and in down-regulation of Treg-dependent inhibition of effector T-lymphocyte (Teff) proliferation, which occurs without affecting the production of tumor necrosis factor-alpha or interferon-gamma. Tregs and Teffs express on the cell membrane both D1-like and D2-like dopaminergic receptors to a similar extent (12%-29% of the cells). Catecholamine-dependent down-regulation of Tregs is, however, selectively reversed by pharmacological blockade of dopaminergic D1-like receptors, which in Tregs only (and not in Teffs) are also expressed at the level of mRNA and are functionally coupled to intracellular production of cAMP. These findings indicate that in human Tregs endogenous catecholamines subserve an autocrine/paracrine loop involving dopaminergic pathways and resulting in down-regulation of Treg function.

Autocrine Communication↗
PubMed2006

Arginine-vasopressin in catecholamine-refractory septic versus non-septic shock in extremely low birth weight infants with acute renal injury.

INTRODUCTION: The aim of this study was to assess the efficacy of arginine-vasopressin (AVP) as a rescue therapy in catecholamine-refractory septic and non-septic shock in extremely low birth weight (ELBW) infants with acute renal injury. METHODS: Prospective assessment of AVP therapy in three ELBW infants with catecholamine-refractory septic shock and acute renal injury (mean birth weight 600 +/- 30 g) and three ELBW infants with non-septic shock and acute renal injury (mean birth weight 770 +/- 110 g) at a University hospital. The main outcome measures were restoration of blood pressure with adequate organ perfusion and survival at discharge. RESULTS: In all three ELBW infants with catecholamine-resistant septic shock, systemic arterial blood pressure increased substantively with restoration of urine output after AVP administration (dosage, 0.035 to 0.36 U/kg/h; length, 70 +/- 21 hours). In the three ELBW infants with non-septic shock, only a transient stabilization in mean arterial pressure with restoration of urine output was observed after AVP therapy (dosage, 0.01 to 0.36 U/kg/h; length, 30 +/- 16 hours). The mortality rate was 1/3 in the sepsis group versus 3/3 in the non-septic group. CONCLUSION: AVP may be a promising rescue therapy in catecholamine-resistant shock in ELBW infants with acute renal injury. Larger prospective clinical trials are warranted to assess the efficacy and safety of AVP as a pressor adjunct in septic versus non-septic shock in ELBW infants.

Acute Kidney Injury↗
PubMed2004

Fight or flight, forbearance and fortitude: the spectrum of actions of the catecholamines and their cousins.

Catecholamines are recognized to play an important part in the fight-or-flight response to impending stress. Catecholamine and other phase-reactant levels are raised in the first 24 h following acute stress, but the bigger picture of their action on the organism is unavailable. In this article, we examine their actions in light of the theory of phase transitions borrowed from the numerate sciences. Phase transitions involve changes in the state of matter or an organism with a common example of what is termed a first-order phase transition (sudden change) being provided by the popular expression "the straw that broke the camel's back." We propose that the response to catecholamines follows a triphasic response: a Phase I response is the fight-or-flight response to impending stress that protects the animal. With mild to intermediate stress, the Phase II or forbearance response allows it to tolerate the physiological upset. With severe stress, however, severe vital organ vasoconstriction leads to a quick death. The present theory has value in understanding the clinical picture in acute stress. Phase II or Forbearance Phase corresponds to Classes I, II, and III of hemorrhagic shock, and Phase III or Fortitude Phase to Class IV. Thus, a Phase III or fortitude response is to the animal what apoptosis is to the individual cell and has social implications. The present framework provides a fresh perspective on the action of the catecholamines and their cousins.

Animals↗
PubMed2006

Catecholamine-secreting metastatic carcinoid as differential diagnosis in pheochromocytoma: clinical, laboratory, and imaging clues in the search for the lurking neuroendocrine tumor (NET).

Catecholamine-secreting metastatic carcinoid should be considered in differential diagnosis of malignant pheochromocytoma. Paroxysmal functioning or hormonally silent gastroenteropancreatic neuroendocrine tumors (GEP NETs) require repeat biochemical measurements and sensitive anatomic and functional imaging studies overlapping those for malignant pheochromocytoma. This report presents clinical, laboratory, and radiologic findings in a patient presenting with heart rate variability; vasoactive headaches reactive to ethanol, tyramine and tryptophan; labile blood pressure; diaphoresis; diarrhea; abdominal pain; unexplained pancreatitis; joint pain; and paroxysmal flushing with pallor. GI studies (including endoscopic ultrasound) and multiple imaging modalities (including 2D CT, MRI with gadolinium, [18]FDG PET/CT, [123I]MIBG, and SRS [111In]Octreotide [OctreoScan]) were not diagnostic. 24-h BP, Holter and 30-day cardiac event monitors plus urinary biochemical studies consistently suggested catecholamine-synthesizing NET. NIH plasma metanephrines studies and [6]-[18F]Fluorodopamine PET ruled out malignant pheochromocytoma (pheo). Repeated studies showed persistently abnormal GEP NET biomarkers and urinary catecholamines. Capsule endoscopy revealed suspicious submucosal lesions throughout the small intestine. Dual-phase 64-slice multidetector computed tomography (MDCT) with 3D volumetric reconstruction of the abdomen and pelvis revealed multiple diffuse liver metastases and three extrahepatic lesions consistent with metastatic carcinoid. In combination, intensive biochemical testing repeated over time, dual-phase 64-slice MDCT with 3D image reconstruction and volume-rendering (VR) technique, and advanced radionuclide imaging are required to detect NETs' sporadic or paroxysmal functioning, rule out extra-adrenal pheochromocytoma, and localize and characterize metastatic carcinoid. If pheochromocytoma is ruled out, yet symptoms and biochemical markers for catecholamine excess are present, then carcinoid and other amine-precursor-uptake decarboxylation (APUD) tumors must remain in the differential diagnosis.

Adrenal Gland Neoplasms↗
PubMed1987

Indomethacin does not alter the circulating catecholamine response to asphyxia in the neonatal piglet.

The response of circulating catecholamines to asphyxia in unanesthetized, spontaneously breathing neonatal piglets was measured before and after treatment with indomethacin. Prior to treatment with indomethacin, baseline levels [geometric mean, pg/ml (95% confidence limits)] of D, E, and N were 162 (99-266), 174 (52-579), and 380 (286-506), respectively. Inhalation of 10% O2/9% CO2 for 20 min caused significant increases in arterial levels of all three catecholamines to 389 (230-659, 1514 (993-2306), and 3802 (2731-5293), respectively. Treatment with indomethacin (5 mg/kg, intravenous) did not significantly alter either baseline levels of the catecholamines or the levels after 20 min of the asphyxiating gas. In time control piglets, baseline levels and the response to asphyxia were similar before and after placebo. These results suggest that the circulating catecholamine response to asphyxia of the neonatal piglet is independent of the prostaglandin system.

Animals↗
PubMed1995

Anaphylactic reactions to bee-sting challenges in allergic children are not modified by endogenous catecholamines.

To investigate the role of basal catecholamine levels and the response of the adrenergic system to expected bee stings, plasma catecholamines were measured before and 1 and 2 min after bee-sting challenges. Twenty-one children (aged 4-15 y) with bee-sting allergies were selected for sequential challenges to establish the need for venom immunotherapy. The time interval between the challenges varied from 2 to 6 wk. Epinephrine, norepinephrine, and dopamine plasma levels were measured using a simultaneous single-isotope radioenzymatic assay. On the first challenge, 33% of the children experienced a normal local reaction, 29% a large local reaction, and 38% a systemic reaction. On the second challenge in 18 out of 21 subjects, 67% experienced a normal normal local reaction, 22% a large local reaction, and 11% a systemic reaction. Epinephrine and norepinephrine plasma levels increased significantly on the first and second challenges. Dopamine plasma levels showed a significant increase on the first challenge only. Plasma catecholamine levels after the second challenge revealed a significant positive correlation between epinephrine increases measured 1 and 2 min after the challenge and the concomitant sting reaction. Basal epinephrine, norepinephrine, and dopamine plasma levels did not differ significantly between patients who experienced different types of sting reactions. Based on our data, we conclude that clinical reactions to in-hospital insect-sting challenges are not affected by early increases in plasma catecholamine levels produced by the expected stress situation.

Adolescent↗
PubMed2004

Stimulation of catecholamine synthesis by environmental estrogenic pollutants.

Environmental estrogenic pollutants are compounds that have been shown to have estrogenic effects on fetal development and reproductive systems. Less attention, however, has been paid to their influence on neuronal functions. We report here the effects of estrogenic pollutants on catecholamine synthesis in bovine adrenal medullary cells used as a model system of noradrenergic neurons. Treatment of cultured bovine adrenal medullary cells with p-nonylphenol and bisphenol A at 10 nM for 3 d stimulated [14C]catecholamine synthesis from [14C]tyrosine and tyrosine hydroxylase activity, an effect that was not inhibited by ICI 182,780, an antagonist of estrogen receptors. Significant effects of p-nonylphenol on [14C]catecholamine synthesis were observed at 0.1 nM, which is 45 times lower than that of the international regulatory standard (4.5 nM), and the maximum effects were around 10-100 nM. The concentrations (0.1-10 nM) used in the present study are similar to the range observed in rivers in the United States or Europe. On the other hand, short-term treatment of cells with 10 nM p-nonylphenol for 10 min also activated tyrosine hydroxylase, which was suppressed by U0126, an inhibitor of MAPK kinase. Furthermore, treatment of cells with p-nonylphenol for 5 min increased the phospho-p44/42MAPK in a concentration-dependent (1-1000 nM) manner, whereas p-nonylphenol (100 nm, 2 d) enhanced both levels of non-phospho- and phospho-p44/42MAPK. These findings suggest that short-term and long-term treatment of cells with estrogenic pollutants at environmental concentrations stimulates catecholamine synthesis and MAPK through an estrogen receptor-independent pathway.

Adrenal Medulla↗
PubMed2005

Regulatory roles of bone morphogenetic proteins and glucocorticoids in catecholamine production by rat pheochromocytoma cells.

We here report a new physiological system that governs catecholamine synthesis involving bone morphogenetic proteins (BMPs) and activin in the rat pheochromocytoma cell line, PC12. BMP type I receptors, including activin receptor-like kinase-2 (ALK-2) (also referred to as ActRIA) and ALK-3 (BMPRIA), both type II receptors, ActRII and BMPRII, as well as the ligands BMP-2, -4, and -7 and inhibin/activin subunits were expressed in PC12 cells. PC12 cells predominantly secrete dopamine, whereas noradrenaline and adrenaline production is negligible. BMP-2, -4, -6, and -7 and activin A each suppressed dopamine and cAMP synthesis in a dose-dependent fashion. The BMP ligands also decreased 3,4-dihydroxyphenylalanine decarboxylase mRNA expression, whereas activin suppressed tyrosine hydroxylase expression. BMPs induced both Smad1/5/8 phosphorylation and Tlx2-Luc activation, whereas activin stimulated 3TP-Luc activity and p38 MAPK phosphorylation. ERK signaling was not affected by BMPs or activin. Dexamethasone enhanced catecholamine synthesis, accompanying increases in tyrosine hydroxylase and 3,4-dihydroxyphenylalanine decarboxylase transcription without cAMP accumulation. In the presence of dexamethasone, BMPs and activin failed to reduce dopamine as well as cAMP production. In addition, dexamethasone modulated mitotic suppression of PC12 induced by BMPs in a ligand-dependent manner. Furthermore, intracellular BMP signaling was markedly suppressed by dexamethasone treatment and the expression of ALK-2, ALK-3, and BMPRII was significantly inhibited by dexamethasone. Collectively, the endogenous BMP/activin system plays a key role in the regulation of catecholamine production. Controlling activity of the BMP system may be critical for glucocorticoid-induced catecholamine synthesis by adrenomedullar cells.

Activins↗
PubMed1975

Potentiation of suckling-induced release of prolactin by inhibition of brain catecholamine synthesis.

The effects of a catecholamine synthesis inhibitor, alpha-methyl-p-tyrosine (alpha-MT), on the accumulation of newly synthesized brain catecholamines and plasma prolactin concentration were studied in lactating rats. [3H]tyrosine was administered to rats 10 minutes before decapitation, and the rate of its incorporation into [3H]dopamine and [3H]norepinephrine was measured in whole brain. Injection of alpha-MT (3.15--12.50 mg/kg) via a carotid cannula increased plasma prolactin levels and decreased the accumulation of newly synthesized brain catecholamines in nonsuckled, lactating rats compared to rats injected with .9% saline solution. Mother rats pretreated with saline solution were suckled for 20 minutes by pups which previously were separated from the mother rats for 5 hours. This treatment resulted in significantly increased plasma prolactin levels compared to nonsuckled controls. In rats pretreated with alpha-MT for 20 minutes, suckling resulted in a further increase in plasma prolactin levels which was significantly greater than the increase caused by suckling or alpha-MT alone. These results suggest that inhibition or catecholamine synthesis had a facilitatory effect on the brain mechanisms responsible for prolactin release in response to suckling.

Animals↗
PubMed1993

Endogenous glucocorticoids restrain catecholamine synthesis and release at rest and during immobilization stress in rats.

Cardiovascular and metabolic adjustments during stress involve participation of the sympatho-adrenal and hypothalamic-pituitary-adrenocortical systems, which interact at several levels. The present study investigated the effects of removal of endogenous glucocorticoids on indices of norepinephrine release and metabolism and of catecholamine biosynthesis in sympathetic nerves, at baseline and in response to immobilization stress (IMMO) in rats. Plasma levels of the catecholamine precursor dihydroxyphenylalanine, norepinephrine (NE), the NE metabolites dihydroxyphenylglycol and methoxyhydroxyphenylglycol, dopamine, and the dopamine metabolites dihydroxyphenylacetic acid and homovanillic acid were measured in adrenalectomized, adrenal-medullectomized, or sham-operated conscious rats, with or without glucocorticoid treatment (25 mg/kg.24 h cortisol for 7 days by osmotic minipumps), at rest and after 5, 20, 60, and 120 min of IMMO. Adrenalectomy eliminated plasma levels of epinephrine and corticosterone and augmented IMMO-induced increments in levels of NE, dihydroxyphenylglycol, methoxyhydroxyphenylglycol, dihydroxyphenylalanine, dihydroxyphenylacetic acid, and homovanillic acid. Adrenal-medullectomy reduced plasma epinephrine, but not corticosterone, to undetectable levels at baseline and did not augment stress-induced responses of any of the measured compounds. Cortisol administration (plasma levels approximately 600 pmol/ml) reversed the augmentation of catecholaminergic responses in adrenalectomized rats. The results indicate that adrenalectomy stimulates several aspects of sympatho-neural function, including stress-induced increments in NE release, reuptake, metabolism, and turnover and in catecholamine biosynthesis. This augmentation was absent in adreno-medullectomized rats, indicating that the loss of adrenomedullary hormones after adrenalectomy does not appear to contribute to the augmentation. Since cortisol treatment reversed or prevented this augmentation, loss of feedback inhibition by endogenous glucocorticoids appears to be the basis of the enhanced responses. Thus, the results suggest that endogenous glucocorticoids restrain responses of catecholamine turnover, synthesis, release, reuptake, and metabolism in sympathetic nerves in this stress model.

3,4-Dihydroxyphenylacetic Acid↗