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1
Wang, Wenping, Ximing Wu, Chung S. Yang, and Jinsong Zhang. "An Unrecognized Fundamental Relationship between Neurotransmitters: Glutamate Protects against Catecholamine Oxidation." Antioxidants 10, no. 10 (September 30, 2021): 1564. http://dx.doi.org/10.3390/antiox10101564.
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Neurotransmitter catecholamines (dopamine, epinephrine, and norepinephrine) are liable to undergo oxidation, which copper is deeply involved in. Catecholamine oxidation-derived neurotoxicity is recognized as a pivotal pathological mechanism in neurodegenerative diseases. Glutamate, as an excitatory neurotransmitter, is enriched in the brain at extremely high concentrations. However, the chemical biology relationship of these two classes of neurotransmitters remains largely unknown. In the present study, we assessed the influences of glutamate on the autoxidation of catecholamines, the copper- and copper-containing ceruloplasmin-mediated oxidation of catecholamines, the catecholamine-induced formation of quinoprotein, catecholamine/copper-induced hydroxyl radicals, and DNA damage in vitro. The results demonstrate that glutamate, at a physiologically achievable molar ratio of glutamate/catecholamines, has a pronounced inhibitory effect on catecholamine oxidation, catecholamine oxidation-evoked hydroxyl radicals, quinoprotein, and DNA damage. The protective mechanism of glutamate against catecholamine oxidation could be attributed to its restriction of the redox activity of copper via chelation. This previously unrecognized link between glutamate, catecholamines, and copper suggests that neurodegenerative disorders may occur and develop once the built-in equilibrium is disrupted and brings new insight into developing more effective prevention and treatment strategies for neurodegenerative diseases.
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Padbury, J. F., A. M. Martinez, S. L. Thio, E. E. Burnell, and J. A. Humme. "Free and sulfoconjugated catecholamine responses to hypoxia in fetal sheep." American Journal of Physiology-Endocrinology and Metabolism 257, no. 2 (August 1, 1989): E198—E202. http://dx.doi.org/10.1152/ajpendo.1989.257.2.e198.
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Plasma catecholamines circulate either in conjugated or unconjugated forms. In adult humans, sulfoconjugated catecholamines predominate; however, there is considerable variation between species. In a variety of pathophysiological states catecholamine conjugation is believed to represent an important mechanism of inactivation of high circulating catecholamine levels. To date, there have been few data in developing animals or humans on catecholamine sulfoconjugation. We studied the differences in free and sulfoconjugated catecholamines in full term (141 +/- 1 days) and preterm (123 +/- 1 days) chronically catheterized fetal sheep and determined the changes in free and sulfoconjugated catecholamines in response to hypoxia. The results demonstrate that term and preterm animals have a comparable percentage of basal circulating sulfoconjugated catecholamines (free-to-total ratio 50-60%). In response to hypoxia, both free and sulfoconjugated catecholamines were promptly elevated with significant increases in each by 5 min of hypoxia. This was true for both term and pretern animals. The proportion of free and total catecholamines remained relatively constant during hypoxia despite a 5- to 10-fold increase in circulating levels of each. These data demonstrate that fetal sheep, as early as 80% gestation, have a well developed mechanism for sulfoconjugation and subsequent inactivation of the high circulating levels of catecholamines seen during fetal and newborn life.
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Koller, M. "Results for 74 substances tested for interference with determination of plasma catecholamines by "high-performance" liquid chromatography with electrochemical detection." Clinical Chemistry 34, no. 5 (May 1, 1988): 947–49. http://dx.doi.org/10.1093/clinchem/34.5.947.
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Abstract Various catecholamine metabolites, catecholamine-related compounds, catechols, drugs, amines, and other nitrogen compounds were injected onto an HPLC system ("ClinRep Catecholamine-Plasma" assay kit with a reversed-phase C18 column) used for measuring catecholamines. None of the 74 substances tested co-eluted with any of the catecholamines--norepinephrine, epinephrine, or dopamine--or with the internal standard, 3,4-dihydroxybenzylamine.
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Stein, H. M., A. Martinez, K. Oyama, L. Blount, and J. F. Padbury. "Effect of corticosteroids on free and sulfoconjugated catecholamines at birth in premature newborn sheep." American Journal of Physiology-Endocrinology and Metabolism 268, no. 1 (January 1, 1995): E28—E32. http://dx.doi.org/10.1152/ajpendo.1995.268.1.e28.
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We previously demonstrated that prenatal corticosteroids attenuated the expected exponential increase in circulating catecholamines at birth. The present studies were undertaken to determine if alteration in sulfoconjugation could account for this attenuation. Catheterized fetal lambs received saline (n = 6) or corticosteroids (n = 8) intravenously for 60 h. The lambs were delivered by cesarean section at 130 +/- 1 days gestation. Ventilatory and cardiovascular responses and plasma catecholamine concentrations were measured for 2 h after birth. Although plasma free catecholamines levels were higher in controls than in corticosteroid-treated fetuses, the sulfoconjugated levels were similar in the two groups. Thus the corticosteroid-treated fetuses had a higher proportion of plasma sulfoconjugated catecholamines consistent with the possibility that sulfoconjugation was augmented during intrauterine life. After birth, the corticosteroid-treated animals showed an attenuated increase in plasma free catecholamine levels compared with controls but a similar increase in sulfoconjugated catecholamine levels to the control animals. The proportion of plasma sulfoconjugated catecholamines was higher in the corticosteroid-treated animals; however, the increase in sulfoconjugated catecholamines was insufficient to account for the attenuated overall increase in total catecholamines in the corticosteroid-treated animals.
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Davidson, D. Fraser. "Phaeochromocytoma with Normal Urinary Catecholamines: The Potential Value of Urinary Free Metadrenalines." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 39, no. 6 (November 2002): 557–66. http://dx.doi.org/10.1177/000456320203900603.
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Background Normal urine catecholamine values in patients with phaeochromocytoma is an occasional finding and may lead to a missed diagnosis. Additional urinary free metadrenaline analysis may be of value in this situation. Methods In addition to vanillylmandelic acid, homovanillic acid and the catecholamines, urinary free normetadrenaline (fNMA) and free metadrenaline (fMA) were measured. This report describes six confirmed cases of phaeochromocytoma showing normal urinary catecholamine output and compares fMA results and tumour size with other confirmed cases where the urine catecholamines were increased. Results Urine catecholamines in these patients with, on average, smaller tumours, were all normal. Urinary fNMA and fMA were available on five patients, and were increased in three. The data suggest that, unlike the catecholamines, urinary fNMA and fMA could be a useful predictor of tumour size. Conclusion The inclusion of fNMA and fMA in the test profile is likely to be of additional benefit in tumour detection, particulariy when catecholamines or other metabolites are normal.
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Rosano, T. G., T. A. Swift, and L. W. Hayes. "Advances in catecholamine and metabolite measurements for diagnosis of pheochromocytoma." Clinical Chemistry 37, no. 10 (October 1, 1991): 1854–67. http://dx.doi.org/10.1093/clinchem/37.10.1854.
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Abstract Assessment of catecholamine production and excretion is important in the laboratory detection of pheochromocytoma, a rare but curable cause of hypertension. Advances in catecholamine and metabolite methodologies have enhanced the diagnostic acumen by increasing analytical sensitivity and eliminating many of the interferences observed with earlier methods. Estimation of urinary catecholamines metanephrine and vanillylmandelic acid is routinely used in the biochemical detection of pheochromocytoma and in monitoring the completeness of tumor excision as well as the possibility of recurrence. Traditional spectrophotometric and fluorometric methods for urinary catecholamines and their metabolites are being replaced by highly sensitive and selective chromatographic methods. The ability to quantify individual catecholamines and metanephrines by high-performance liquid chromatography is of particular value for detecting familial forms of the tumor that may secrete epinephrine. Plasma norepinephrine and epinephrine measurements are of additional diagnostic value in determining recent catecholamine release and response to clonidine suppression. For either urine or plasma measurements, appropriate patient preparation, sample collection, and method validation along with an understanding of the variable pattern of catecholamine secretion and metabolism in pheochromocytoma are essential. Advances in laboratory methodology and reference intervals for catecholamines for clinical interpretation are reviewed.
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Zhao, Lin, Xiaoran Zhang, Xu Meng, Ting Zhang, Hua Fan, Qiongyu Zhang, Yecheng Liu, Xianliang Zhou, and Huadong Zhu. "The Clinical Characteristics of Pheochromocytomas and Paragangliomas with Negative Catecholamines." Journal of Clinical Medicine 11, no. 19 (September 23, 2022): 5583. http://dx.doi.org/10.3390/jcm11195583.
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Pheochromocytomas and paragangliomas (PPGLs) associated with negative catecholamines are not uncommon. However, few studies have examined clinical features of patients with these tumors. In the absence of available data, it is difficult to identify characteristics of patients with potential PPGLs and normal serum and urine screens. Therefore, an analysis of patients with PPGLs was conducted retrospectively to compare the clinical features of patients with positive and negative catecholamines. This study included 214 patients, including 69 patients with negative catecholamines. Prevalence rates of diabetes (p < 0.001) and hypertension (p < 0.001) were lower and tumor diameter (p < 0.001) was smaller in the negative-catecholamine group compared with the positive-catecholamine group. Multivariable logistic regression analysis showed that extra-adrenal PPGLs were independently positively associated with negative catecholamines (p = 0.004); hypertension (p = 0.001) and tumor diameter (p = 0.016) were independently negatively associated with negative catecholamines. There was no significant difference in tumor recurrence between the two groups (mean follow-up, 20.54 ± 11.83 months) (p = 0.44). The results demonstrated that PPGL patients with negative catecholamines were more likely to have extra-adrenal tumors and less likely to have comorbidities, and these patients should also be closely monitored for tumor recurrence.
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Oyama, K., J. Padbury, A. Martinez, B. Chappell, H. Stein, L. Blount, and E. Buhl. "Free and sulfoconjugated catecholamine responses at birth in newborn sheep." American Journal of Physiology-Endocrinology and Metabolism 263, no. 1 (July 1, 1992): E23—E27. http://dx.doi.org/10.1152/ajpendo.1992.263.1.e23.
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There have been little data on catecholamine sulfoconjugation in developing animals or humans. We studied the differences in free and sulfoconjugated catecholamines at birth in newborn sheep. Baseline concentrations of sulfoconjugated norepinephrine and epinephrine were the predominant form of circulating catecholamine, representing 77 +/- 4 and 65 +/- 12% of total circulating catecholamines, respectively. At birth the free epinephrine concentration increased 10-fold (49 +/- 27 to 653 +/- 21 pg/ml, respectively), and plasma free norepinephrine concentration rose 4-fold (307 +/- 92 to 1,178 +/- 389 pg/ml). In contrast, there was only a transient twofold increase in the sulfoconjugated epinephrine. There was no increase in the sulfoconjugated form of norepinephrine. These data demonstrate that, while the near-term newborn sheep has a well-developed mechanism for sulfoconjugation of circulating catecholamines, this does not occur rapidly. During the logarithmic increases of circulating catecholamines at birth, there are not commensurate increases in the concentration of sulfoconjugated norepinephrine or epinephrine. Thus sulfoconjugation does not appear to represent a significant mechanism for inactivation of the high circulating levels of catecholamines seen at birth.
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Waele, Jean-Pascal De, Michel Anctil, and Mats Carlberg. "Biogenic catecholamines in the cnidarian Renilla köllikeri: radioenzymatic and chromatographic detection." Canadian Journal of Zoology 65, no. 10 (October 1, 1987): 2458–65. http://dx.doi.org/10.1139/z87-371.
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The presence of biogenic catecholamines in the colonial anthozoan Renilla köllikeri was assessed with a radioenzymatic assay and thin-layer chromatographic separation of extracts from different parts of the colony. Confirmation of catecholamine detection was also obtained using an HPLC technique with electrochemical detection. All three catecholamines, i.e., dopamine, noradrenaline, and adrenaline, were detected to varying degrees in the colonial compartments. Unidentified inhibitory factor(s) endogenous to Renilla tissues prevented the detection of internal catecholamine standards to an extent that was dependent upon time of sampling and part of the colony assayed. Peaks in catecholamine levels fluctuated sharply over the 10-month sampling period. Dopamine was the most frequently detected catecholamine, with levels generally higher than those of the other two amines, especially in the autozooids. The presence of adrenaline is reported for the first time in a coelenterate species. These results suggest that catecholamines are present in the most primitive metazoan phylum known to possess a nervous system. The physiological significance of these findings is discussed.
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Fazio, Francesco, Marina Basova, and Osman Sabri Kesbiç. "Anthropogenic Pollution-Induced Stress: Catecholamine Deposition in Erythrocytes of Scorpaena porcus Linnaeus 1758." Croatian Journal of Fisheries 82, no. 3 (September 1, 2024): 85–90. http://dx.doi.org/10.2478/cjf-2024-0011.
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Abstract The sympathoadrenal system plays an essential role in forming the body’s response to the action of stimuli of various natures and intensities. The content of deposited catecholamines in peripheral blood erythrocytes is one of the most accessible parameters for an adequate description of the functional activity of the sympathoadrenal system in humans and rats. The aim of the work is to assess the accumulation of catecholamines in erythrocytes of sea ruffs Scorpaena porcus L. at various pollution levels in the bays of Sevastopol. The phenomenon of accumulation of catecholamines in erythrocytes of the peripheral blood of fish is revealed. The concentration of erythrocytes with deposited catecholamines was higher in fish from polluted bays. In 2006, fish from Alexander Bay exhibited a significantly higher erythrocyte content of deposited catecholamines (36.04%) compared to those from the background area (28.19%) and Quarantine Bay (30.74%) (P < 0.01). Similar levels were observed between Quarantine Bay and the coast of Balaklava. In 2007, fish from Alexander Bay maintained a high erythrocyte catecholamine content (35.2%), while those from Quarantine Bay exhibited a lower level (23.8%) (P ≤ 0.01). In 2008, the erythrocyte catecholamine content in Quarantine Bay was six times higher than that observed in fish from Martynov Bay. These findings underscore the variability in catecholamine concentrations among fish populations inhabiting different coastal regions, suggesting potential environmental influences on stress responses..
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Kjeldsen, S. E., K. Gjesdal, P. Leren, and I. K. Eide. "Decreased Platelet-Free Dopamine and Unchanged Noradrenaline and Adrenaline in Essential Hypertension." Thrombosis and Haemostasis 60, no. 02 (1988): 251–54. http://dx.doi.org/10.1055/s-0038-1647040.
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SummaryThe content of free-catecholamines in blood platelets is much higher than in plasma and platelet catecholamines must be taken up from plasma, since platelets lack the enzymes for catecholamine synthesis. There is some evidence that platelet catecholamine content under certain circumstances may be an integrated measure of plasma catecholamine concentrations over time. Platelet-free catecholamines were therefore assayed in 18 untreated patients with essential hypertension and in 16 normotensive control subjects. Mean platelet-free dopamine in the hypertensive group was 3.7 ± 0.4 pg/mg platelet weight, i.e. significantly less than the 6.5 ± 0.9 pg/mg found in the normotensive (p <0.005). Platelet contents of noradrenaline and adrenaline did not differ. Decreased platelet-free dopamine and unchanged platelet noradrenaline and adrenaline persisted after adjustment for increased body weight in the hypertensive group. Although the reasons for decreased platelet-free dopamine in the hypertensive group remain unknown, this finding may add to previous result showing facilitated release of granular contents from blood platelets in patients with essential hypertension. Our data do not support platelet levels of free-catecholamines to be a marker of increased sympathetic tone in essential hypertension.
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Shou, Jialong, Shuwang Zhan, Yi Zhang, Bo Liang, and Lu Fang. "Study on Catecholamine Sensors Based on Noble Metal Nanoparticles Modified Ti3C2 Mxene." Journal of Physics: Conference Series 2500, no. 1 (May 1, 2023): 012002. http://dx.doi.org/10.1088/1742-6596/2500/1/012002.
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Abstract Catecholamines are neurotransmitters in the peripheral and central nervous systems, which maintain the normal physiological state of the human body. Studies have shown that the occurrence of many diseases are often accompanied by changes in catecholamine levels. Clinically, the detection of catecholamine levels in human plasma or urine can assist in the diagnosis of endocrine-related diseases and neurological diseases. However, catecholamines are easily oxidized, and the content in human body is very low. So the rapid detection of catecholamines is very important for the prevention and diagnosis of related diseases. In this paper, the electrochemical response characteristics of Ti3C2Tx MXene and noble metal nanoparticles modified Ti3C2Tx to dopamine (one type of catecholamine) were explored. The results shown that Ti3C2Tx would undergo irreversible oxidation at the anode potential and the single Ti3C2Tx modified electrode was not suitable for the detection of dopamine. So we further explored the modification of Pt and Au nanoparticles on the Ti3C2Tx/GCE electrode, and the experimental results shown that Au/Ti3C2Tx/GCE had higher sensitivity for measuring dopamine, while Pt/Ti3C2Tx/GCE had a larger linear range. Both electrodes had good stability and repeatability and could be used for the detection of catecholamines.
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Bhattacharya, Arnab. "Bridging the Gap: Understanding the Significance of Catecholamines in Neurochemistry and Recent Advances in their Detection." Science Reviews - Biology 2, no. 1 (May 12, 2023): 20–26. http://dx.doi.org/10.57098/scirevs.biology.2.1.3.
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The neurochemistry of catecholamines plays a crucial and complex role in human memory, behavior, and cognition, while affecting other organs such as the lungs, heart, liver, and skin. Dopamine, norepinephrine, and epinephrine are three closely-related catecholamines that have been widely studied over the last seven decades for development of medications for life-threatening diseases. Other studies have also suggested a link between drug abuse and catecholamine levels. The determination of catecholamine levels in different parts of the human body has also been a hot topic for research in these years. HPLC, spectrophotometry, fluorescence, electrochemistry and other techniques have been used to quantify catecholamines in mostly in biological samples like serum and urine, although in vivo studies are also possible. This article attempts to present the research on catecholamines from the perspectives of their bodily functions, development of medications for diseases related to these, and the techniques used for their detection and quantification.
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Meijer, Wim G., Sjef C. V. M. Copray, Harry Hollema, Ido P. Kema, Nynke Zwart, Ietje Mantingh-Otter, Thera P. Links, Pax H. B. Willemse, and Elisabeth G. E. de Vries. "Catecholamine-Synthesizing Enzymes in Carcinoid Tumors and Pheochromocytomas." Clinical Chemistry 49, no. 4 (April 1, 2003): 586–93. http://dx.doi.org/10.1373/49.4.586.
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Abstract Background: Serotonin is the principal endocrine product of carcinoid tumors, but simultaneously increased production of catecholamines has been described in these tumors. As it is not clear whether these tumors contain specific enzymes for catecholamine synthesis, we aimed to detect catecholamine-synthesizing enzymes [tyrosine hydroxylase (TH), dopamine-β-hydroxylase (DBH), and phenylethanolamine-N-methyltransferase (PNMT)] in midgut carcinoid tumors and pheochromocytoma and to correlate enzyme expression to serotonin production as well as catecholamines and metabolites excreted in urine. Methods: Paraffin-embedded tumor specimens from 21 midgut carcinoid patients and 20 pheochromocytoma patients (10 sporadic and 10 MEN type IIa-related tumors) were stained for TH, DBH, and PNMT, using a three-step biotin-avidin-peroxidase method. Results: TH was demonstrated in 9 (43%) of 21 carcinoids and in all (100%) of 20 pheochromocytomas, DBH in 8 (38%) carcinoids and in 15 (75%) pheochromocytomas, and PNMT in 7 (33%) carcinoids and in 13 (65%) pheochromocytomas. Increased urinary excretion of catecholamines and metabolites was observed in 10 (48%) carcinoid patients and in all pheochromocytoma patients. No clinically relevant association between enzyme expression and urinary excretion of catecholamines and metabolites was found. Conclusions: Catecholamine-synthesizing enzymes are present in many carcinoid tumors. This finding possibly indicates the existence of a catecholamine-synthesizing pathway in carcinoids similar to that found in pheochromocytoma.
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Boutilier, R. G., G. K. Iwama, and D. J. Randall. "The promotion of catecholamine release in rainbow trout, Salmo gairdneri, by acute acidosis: interactions between red cell pH and haemoglobin oxygen-carrying capacity." Journal of Experimental Biology 123, no. 1 (July 1, 1986): 145–57. http://dx.doi.org/10.1242/jeb.123.1.145.
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A fall in blood pH was generated either by infusion of HCl or by reducing gill ventilation and raising blood PCO2 in rainbow trout, Salmo gairdneri Richardson. The acute acidosis resulting from HCl infusion caused an increase in plasma adrenaline and noradrenaline concentrations, the adrenaline increase being proportional to the decrease in blood pH. Fish subjected to a prolonged respiratory acidosis, caused by a reduction in gill ventilation, showed no increase in catecholamines 24 h after the change in gill ventilation. We suggest that catecholamine levels increase in response to a pH decrease, but if acidotic conditions are maintained, circulating catecholamines return to low levels. There was a much smaller decrease in erythrocytic pH with a fall in plasma pH when catecholamine levels were high. This ameliorating effect of catecholamines on erythrocytic pH during a plasma acidosis maintains the oxygen-carrying capacity of the haemoglobin. If erythrocytic pH was decreased by increasing blood PCO2 in vitro, then there was a fall in haemoglobin oxygen-carrying capacity which was proportional to the reduction in pH. We conclude that catecholamines are released into the blood in proportion to the fall in blood pH but if the pH is maintained the circulating catecholamines return to their initial low levels. The elevated catecholamine concentrations in blood safeguard against any impairment of haemoglobin oxygen-carrying capacity by maintaining erythrocytic pH in the face of a plasma acidosis.
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Kido, Kazuhiko, and Maya Guglin. "Drug-Induced Takotsubo Cardiomyopathy." Journal of Cardiovascular Pharmacology and Therapeutics 22, no. 6 (May 11, 2017): 552–63. http://dx.doi.org/10.1177/1074248417708618.
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Background: The most plausible hypothesis for takotsubo cardiomyopathy (TCM) is a catecholamine surge. Direct administration of catecholamines or medications causing catecholamine surge is frequently used in clinical practice. Methods: A Medline/PubMed database search was conducted for case reports or series of drug-induced TCM. All reported cases of drug-induced TCM were systemically identified and analyzed. Results: We identified 157 cases of drug-induced TCM. Fifty-seven (36.3%) cases were related to the administration of exogenous catecholamines. In 50 (31.9%) other cases, there was potential adrenergic effect. This included drugs with adrenergic vasoconstriction properties (3.2%), hyperadrenergic state due to alcohol or opioid withdrawal (7.7%), inhibitors of catecholamine reuptake (14.7%), anaphylactic reaction that is accompanied by catecholamine release (3.2%), and psychological or somatic stress coinciding with the administration of a drug that was thought to be the culprit (3.2%). Overall, 68.2% of these drug-induced TCM cases were catecholamine related. In 14 (8.9%) cases, the likely etiology of cardiomyopathy was chemotherapy-induced coronary vasospasm. Conclusion: Our systematic review showed that over two-thirds of drug-induced TCM cases were due to direct or indirect catecholamine stimulation. The lowest effective dose and shortest duration of catecholamines should be utilized, and alternative therapies should be considered if feasible.
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Romain, Yveline, Sylvain Demassieux, Giovanni D'Angelo, Martin Gyger, and Serge Carrière. "Is the platelet phenolsulfotransferase involved in the sulfoconjugation of plasma catecholamines?" Canadian Journal of Physiology and Pharmacology 64, no. 9 (September 1, 1986): 1197–201. http://dx.doi.org/10.1139/y86-203.
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Catecholamines are predominantly present in the sulfoconjugated forms in human plasma. Phenolsulfotransferase (EC 2.8.2.1), which catalyses the sulfation of phenolic compounds, is widely distributed in human tissues. In blood, a phenolsulfotransferase, more specific for catecholamine sulfation is found exclusively in platelets. Free and sulfoconjugated catecholamines were measured in plasma and platelets of healthy volunteers and compared with those present in patients with uremia or pheochromocytoma to determine the ability of platelet phenolsulfotransferase to sulfurylate plasma catecholamines. In patients with pheochromocytoma, the rise in free and sulfoconjugated plasma catecholamines is accompanied by a simultaneous rise of these molecules in platelets. In uremia, where the level of plasma catecholamines is normal, the rise in the sulfoconjugates is not accompanied by a concomitant increase in either free or sulfoconjugated catecholamines in platelets. Platelet phenolsulfotransferase activity remains unchanged in pheochromocytoma and uremia. These data indicate that the platelet phenolsulfotransferase is involved in the sulfation of the catecholamines present in platelets, but its contribution, if any, to the high level of sulfoconjugated catecholamines found in plasma is negligible. This assertion is confirmed by our observations in thrombocytopenic patients. Indeed, despite the very low number of platelets and the absence of plasma phenolsulfotransferase activity, thrombocytopenic patients have normal plasma levels of free and sulfoconjugated catecholamines.
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Cuche, J. L., F. Selz, G. Ruget, M. Gentil, and C. Gaudin. "Dilution of plasma with Tris buffer increases measured catecholamines in plasma." Clinical Chemistry 33, no. 3 (March 1, 1987): 408–11. http://dx.doi.org/10.1093/clinchem/33.3.408.
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Abstract We investigated the effects of dilution of plasma samples on the measured concentrations of catecholamines. Diluting samples of human plasma 10-, 50-, and 100-fold with Tris buffer (100 mol/L, pH 8.6) improved analytical recovery of internal standards, suggesting that it decreases the commonly observed inhibition of methylation in radioenzymatic assays of catecholamines in plasma. However, the dilution is not associated with a proportional decrease in counted radioactivity. This extra amount of radioactivity, which is unlikely to be nonspecific in origin, accounts for a significant increase in the calculated catecholamine concentration. Tentatively, we suggest that Tris buffer releases both catecholamines and conjugated catecholamines bound to some unidentified low-molecular-mass component of plasma.
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AOTA, S., K. D. HOLMGREN, P. GALLAUGHER, and D. J. RANDALL. "A Possible Role for Catecholamines in the Ventilatory Responses Associated with Internal Aciosis or External Hypoxia in Rainbow Trout Oncorhynchus Mykiss." Journal of Experimental Biology 151, no. 1 (July 1, 1990): 57–70. http://dx.doi.org/10.1242/jeb.151.1.57.
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Plasma catecholamine levels and gill ventilation were measured in rainbow trout (Oncorhynchus mykiss) during acidosis and hypoxia. There was an increase in both plasma catecholamines and ventilation correlated with the acidosis. Fish exposed to hyperoxia prior to acid infusion did not show significant changes in catecholamines or ventilation. Those treated with the β-adrenergic antagonist propranolol before acidosis showed increases in catecholamines but not ventilation. Hypoxia was also associated with increases in endogenous catecholamines and ventilation, and the increase in ventilation could be partially blocked with propranolol. This increase in ventilation during hypoxia was not inhibited by asaline injection alone. It is proposed that catecholamines act to modulate ventilatory responses in fish under both acidotic and hypoxic conditions. If a central H+ chemoreceptor exists in fish to control breathing, it can be inhibited by hyperoxia or by β-receptor blockade.
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Hugh, D., A. Grennan, M. A. Abugila, and C. Weinkove. "Ascorbic acid as an antioxidant in measurements of catecholamines in plasma." Clinical Chemistry 33, no. 4 (April 1, 1987): 569–71. http://dx.doi.org/10.1093/clinchem/33.4.569.
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Abstract Sodium metabisulfite, commonly used to prevent the oxidation of catecholamines during extraction from plasma onto alkaline alumina, does not prevent their subsequent degradation in acetic acid eluates. However, ascorbic acid, a potent antioxidant, is extracted with the catecholamines onto the alumina and prevents such destruction. However, ascorbic acid may interfere with the electrochemical measurement of catecholamines, unless sequential oxidation and reduction are used. Other methods of minimizing catecholamine oxidation in acetic acid eluates include refrigerating at 4 degrees C and capping the sample vials to exclude atmospheric oxygen.
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Mpekoulis, George, Vassilina Tsopela, Georgios Panos, Vasileiοs Siozos, Katerina I. Kalliampakou, Efseveia Frakolaki, Constantinos D. Sideris, et al. "Association of Hepatitis C Virus Replication with the Catecholamine Biosynthetic Pathway." Viruses 13, no. 11 (October 23, 2021): 2139. http://dx.doi.org/10.3390/v13112139.
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A bidirectional negative relationship between Hepatitis C virus (HCV) replication and gene expression of the catecholamine biosynthetic enzyme L-Dopa decarboxylase (DDC) was previously shown in the liver and attributed at least to an association of DDC with phosphatidylinositol 3-kinase (PI3K). Here, we report that the biosynthesis and uptake of catecholamines restrict HCV replication in hepatocytes, while HCV has developed ways to reduce catecholamine production. By employing gene silencing, chemical inhibition or induction of the catecholamine biosynthetic and metabolic enzymes and transporters, and by applying the substrates or the products of the respective enzymes, we unravel the role of the different steps of the pathway in viral infection. We also provide evidence that the effect of catecholamines on HCV is strongly related with oxidative stress that is generated by their autoxidation in the cytosol, while antioxidants or treatments that lower cytosolic catecholamine levels positively affect the virus. To counteract the effect of catecholamines, HCV, apart from the already reported effects on DDC, causes the down-regulation of tyrosine hydroxylase that encodes the rate-limiting enzyme of catecholamine biosynthesis and suppresses dopamine beta-hydroxylase mRNA and protein amounts, while increasing the catecholamine degradation enzyme monoamine oxidase. Moreover, the NS4B viral protein is implicated in the effect of HCV on the ratio of the ~50 kDa DDC monomer and a ~120 kDa DDC complex, while the NS5A protein has a negative effect on total DDC protein levels.
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Eisenhofer, G., D. S. Goldstein, R. Stull, H. R. Keiser, T. Sunderland, D. L. Murphy, and I. J. Kopin. "Simultaneous liquid-chromatographic determination of 3,4-dihydroxyphenylglycol, catecholamines, and 3,4-dihydroxyphenylalanine in plasma, and their responses to inhibition of monoamine oxidase." Clinical Chemistry 32, no. 11 (November 1, 1986): 2030–33. http://dx.doi.org/10.1093/clinchem/32.11.2030.
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Abstract This is a reversed-phase liquid-chromatographic method, with electrochemical detection, for simultaneously measuring, in plasma, the concentrations of the catecholamine precursor dihydroxyphenylalanine (DOPA); the endogenous catecholamines norepinephrine, epinephrine, and dopamine; and the deaminated catecholamine metabolites dihydroxyphenylacetic acid (DOPAC) and dihydroxyphenylglycol (DHPG). We used this method to assess effects of monoamine oxidase (EC 1.4.3.4) inhibition in humans. Plasma DHPG concentrations as determined by the present method (mean 826, SEM 61 ng/L) were similar to those found by other methods. Inhibition of monoamine oxidase (by administering deprenyl or tranylcypromine) decreased plasma DHPG by greater than 65%, plasma DOPAC by greater than 50%, and plasma DOPA by about 20%, without consistently affecting norepinephrine or epinephrine. Simultaneous measurement of DOPA, catecholamines, and DHPG may be useful for examining the synthesis, release, and intraneuronal metabolism of norepinephrine. The assay method is rapid, reliable, and simple, and it provides a more comprehensive assessment of noradrenergic nervous function than does measurement only of catecholamines.
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Mahata, Sushil K., Hong Zheng, Sumana Mahata, Xuefei Liu, and Kaushik P. Patel. "Effect of heart failure on catecholamine granule morphology and storage in chromaffin cells." Journal of Endocrinology 230, no. 3 (September 2016): 309–23. http://dx.doi.org/10.1530/joe-16-0146.
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One of the key mechanisms involved in sympathoexcitation in chronic heart failure (HF) is the activation of the adrenal glands. Impact of the elevated catecholamines on the hemodynamic parameters has been previously demonstrated. However, studies linking the structural effects of such overactivation with secretory performance and cell metabolism in the adrenomedullary chromaffin cells in vivo have not been previously reported. In this study, HF was induced in male Sprague-Dawley rats by ligation of the left coronary artery. Five weeks after surgery, cardiac function was assessed by ventricular hemodynamics. HF rats showed increased adrenal weight and adrenal catecholamine levels (norepinephrine, epinephrine and dopamine) compared with sham-operated rats. Rats with HF demonstrated increased small synaptic and dense core vesicle in splanchnic–adrenal synapses indicating trans-synaptic activation of catecholamine biosynthetic enzymes, increased endoplasmic reticulum and Golgi lumen width to meet the demand of increased catecholamine synthesis and release, and more mitochondria with dilated cristae and glycogen to accommodate for the increased energy demand for the increased biogenesis and exocytosis of catecholamines from the adrenal medulla. These findings suggest that increased trans-synaptic activation of the chromaffin cells within the adrenal medulla may lead to increased catecholamines in the circulation which in turn contributes to the enhanced neurohumoral drive, providing a unique mechanistic insight for enhanced catecholamine levels in plasma commonly observed in chronic HF condition.
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Li, Jun, Barbara A. French, Paul Fu, Fawzia Bardag-Gorce, and Samuel W. French. "Mechanism of the alcohol cyclic pattern: role of catecholamines." American Journal of Physiology-Gastrointestinal and Liver Physiology 285, no. 2 (August 2003): G442—G448. http://dx.doi.org/10.1152/ajpgi.00093.2003.
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The cause of the urinary alcohol level (UAL) cycle in rats fed ethanol at a constant rate has been shown to involve the hypothalamic-pituitary thyroid axis. Because the effect of thyroid hormone on the metabolic rate is augmented by catecholamines, the role of catecholamines was investigated by using the intragastric ethanol feeding model of alcoholic liver disease in which the UAL cycles over a 6- to 10-day period. The diet was supplemented with ephedrine and caffeine to test the hypothesis that the UAL cycle involves catecholamines. The UAL was followed to see whether the cycle was ablated by catecholamine supplements. Ethanol fed alone increased the blood levels of catecholamines significantly more than did ephedrine fed alone. However, blood catecholamine levels were significantly higher when ethanol was fed with ephedrine compared with the sum of ethanol and ephedrine fed alone. This indicated that the effect of ethanol and ephedrine were synergistic. The UAL cycle was completely ablated in the ethanol + ephedrine-fed rats. These rats tolerated a much higher dose of ethanol, indicating that they metabolized alcohol faster due to an increase in metabolic rate caused by ephedrine. In the ethanol + ephedrine-fed rats the liver pathology included significantly higher alanine amino transferase (ALT) in the blood and centrilobular ischemic necrosis in the liver. Necrosis was not present in the rats fed ephedrine alone. In conclusion, catecholamine supplements prevented the UAL cycle by increasing the metabolic rate to the point at which fluctuations in the metabolic rate caused by alcohol were prevented.
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Eisenhofer, Graeme, Peter Friberg, Karel Pacak, David S. Goldstein, Dennis L. Murphy, Constantine Tsigos, Arshed A. Quyyumi, Han G. Brunner, and Jacques W. M. Lenders. "Plasma Metadrenalines: Do they Provide Useful Information about Sympatho-Adrenal Function and Catecholamine Metabolism?" Clinical Science 88, no. 5 (May 1, 1995): 533–42. http://dx.doi.org/10.1042/cs0880533.
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1. The clinical utility of plasma metadrenalines for examination of sympatho-adrenal function and catecholamine metabolism was assessed from plasma measurements of these metabolites in a number of clinical conditions (hypertension, cardiac failure, bilateral adrenalectomy and X-chromosomal deletions of the gene for monoamine oxidase), and before and during activation of sympathetic outflow or infusions of noradrenaline and adrenaline. 2. Plasma concentrations of normetadrenaline were less than 25% of those of noradrenaline, concentrations of metadrenaline and adrenaline were similar and those of sulphate-conjugated metadrenalines were 20- to 30-fold higher than free metadrenalines. Hypertensive patients had elevated plasma concentrations of adrenaline, noradrenaline and conjugated but not free metadrenalines. Cardiac failure patients had 2- to 4-fold increases in plasma noradrenaline and free and conjugated normetadrenaline. Adrenalectomy resulted in undetectable plasma concentrations of adrenaline, 91–97% decreases in free and conjugated metadrenaline and a 40% decrease in normetadrenaline relative to noradrenaline. Patients with X-chromosomal deletions of the gene for monoamine oxidase had 6- and 16-fold increases in plasma free and conjugated normetadrenaline and 2- and 4-fold increases in free and conjugated metadrenaline. 3. Infusion of catecholamines increased plasma concentrations of free metadrenalines by less than 6% of increases in precursor amines, indicating that most plasma normetadrenaline (84%) and metadrenaline (90%) is derived from metabolism of catecholamines before their entry into the circulation. Considerable O-methylation of catecholamines within the adrenals explains why sympatho-adrenal activation resulted in smaller proportional increases in plasma metadrenalines than catecholamines. 4. Plasma metadrenalines provide supplementary information about sympatho-adrenal activity to that provided by catecholamines, but are more useful for examination of the extraneuronal inactivation of catecholamines, particularly detection of neurochemical phenotypes in genetic disorders of catecholamine metabolism. Significant formation of metadrenalines within chromaffin tissue explains why measurements of plasma metadrenalines provide an extraordinarily sensitive method for diagnosis of phaeochromocytoma.
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Foucart, Sylvain, Jacques de Champlain та Réginald Nadeau. "In vivo interactions between prejunctional α2- and β2-adrenoceptors at the level of the adrenal medulla". Canadian Journal of Physiology and Pharmacology 66, № 10 (1 жовтня 1988): 1340–43. http://dx.doi.org/10.1139/y88-219.
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The combined effect of a β2-antagonist and an α2-agonist on the release of adrenal catecholamines was studied in the anaesthetized and vagotomized dog. The electrical stimulation of the splanchnic nerve (5-V pulses of 2 ms duration for 3 min at a frequency of 3 Hz) produced a significant rise in adrenal catecholamine release in the adrenal vein. Intravenous injection of a β2-antagonist significantly reduced this response and a subsequent injection of an α2-agonist further reduced the release of catecholamines. However, if the α2-agonist is injected first, the release is not different compared with the control stimulation, and the subsequent injection of the β2-antagonist also did not modify the release in response to electrical stimulation. These results suggest that the blockade of presynaptic β2-receptors reduces the release of adrenal catecholamines without interfering with the activation of the α2-adrenoceptors. In contrast, the pretreatment with the α2-agonist, which does not modify the release of catecholamine at 3 Hz, seems to interfere with the inhibitory effect of the β2-antagonist.
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Aurich, Jörg E., Ina Dobrinski, Annette Petersen, Eberhard Grunert, Wolf-Dieter Rausch, and Wing W. Chan. "Influence of labor and neonatal hypoxia on sympathoadrenal activation and methionine enkephalin release in calves." American Journal of Veterinary Research 54, no. 8 (August 1, 1993): 1333–38. http://dx.doi.org/10.2460/ajvr.1993.54.08.1333.
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Summary Labor and delivery stimulate increased release of catecholamines and endogenous opioid peptides in neonates. Catecholamines promote adaptation to the extrauterine environment after birth. Enkephalins are stored together with catecholamines in the adrenal medulla and have an inhibitory effect on catecholamine release. We investigated the influence of labor and neonatal hypoxia on epinephrine, norepinephrine, and met-enkephalin release in calves. Blood samples were taken from the umbilical artery before rupture of the umbilical cord and from the jugular vein repeatedly after birth. Highest plasma norepinephrine concentration was found in calves delivered at the end of gestation (term calves) before umbilical cord rupture. In calves delivered before the physiologic end of gestation (preterm calves), norepinephrine values increased after cord rupture, but remained lower than values in term calves. Epinephrine release followed a similar pattern, but norepinephrine was clearly predominant. In term calves, met-enkephalin values were significantly higher than values in preterm calves. In calves of both groups, met-enkephalin release increased after cord rupture. During birth, the increase in catecholamine release seems to take place earlier than that of enkephalins. Norepinephrine-dominated stimulation during expulsion of the calf might be followed by increasing enkephalinergic inhibition after cord rupture and onset of respiration. Reduced release of catecholamines and enkephalins in preterm calves may be connected with delayed adaptation to the extrauterine environment.
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Perry, S. F., R. Fritsche, and S. Thomas. "STORAGE AND RELEASE OF CATECHOLAMINES FROM THE CHROMAFFIN TISSUE OF THE ATLANTIC HAGFISH MYXINE GLUTINOSA." Journal of Experimental Biology 183, no. 1 (October 1, 1993): 165–84. http://dx.doi.org/10.1242/jeb.183.1.165.
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A variety of in vivo and in situ experiments were performed on the Atlantic hagfish (Myxine glutinosa) (i) to characterize the levels of circulating catecholamines during acute stresses, including hypoxia, anoxia or physical disturbance (air-exposure), and (ii) to evaluate the potential mechanisms of catecholamine release from the major sites of storage, the systemic heart and posterior cardinal vein (PCV). Adrenaline and noradrenaline were stored at roughly equivalent concentrations (approximately 20 microgram g-1) in cardiac tissue, whereas noradrenaline was the predominant catecholamine stored in the PCV (approximately 50 microgram g-1). The heart stored larger quantities of total catecholamines than did the PCV (approximately three times greater) owing to its larger mass and higher concentration of adrenaline. Exposure of chronically cannulated hagfish to acute hypoxia [mean water PO2 (PwO2)=1.4 kPa; 10.5 mmHg) for 30 min caused a significant decrease in arterial PO2 (from 11.5+/−1.3 kPa to 1.2+/−0.3 kPa) and arterial O2 content (from 3.9+/−0.3 ml 100 ml-1 to 0.9+/−0.2 ml 100 ml-1). The hypoxaemia was associated with a significant increase in plasma noradrenaline levels, whereas plasma adrenaline levels were unaffected. Exposure of uncannulated fish to anoxia (PwO2 approximately 0 kPa) or physical disturbance (15 min of air-exposure) also elicited pronounced increases in plasma noradrenaline levels (6–10 times) and, to a lesser extent, adrenaline levels (2–3 times). An in situ saline-perfused heart preparation was utilized in an attempt to elucidate the mechanism(s) underlying the stress-induced release of catecholamines from the chromaffin tissue of the heart and PCV. Non-specific cell membrane depolarization using 40 or 60 mmol l-1 K+ in the saline elicited a marked release of catecholamines, confirming the suitability of the preparation to assess specific physiological mechanisms of catecholamine release. Lower concentrations of K+ (15–20 mmol l-1) did not evoke catecholamine release, indicating that relatively minor elevation in plasma [K+], as might occur during hypoxia, is not a contributing factor. The cholinergic receptor agonist carbachol (10–5-10-4 mol kg-1) caused a significant release of catecholamines, yet the likelihood of a similar mechanism operating in vivo is doubtful because the hagfish heart is not thought to be innervated. Simulation of (i) internal hypoxaemia by perfusing with anoxic saline or (ii) physical disturbance by perfusing with relatively acidic saline (pH approximately 7.0) failed to elicit catecholamine release. Further, the elevation of perfusion (input) pressure to simulate a rise in venous blood pressure, as might occur during hypoxia or physical disturbance, was also without effect on release. The addition of pituitary extract (from Atlantic cod, Gadus morhua) to the inflowing saline caused a marked release of catecholamines from the chromaffin tissue.
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Owen, N. E. "Effect of catecholamines on Na/H exchange in vascular smooth muscle cells." Journal of Cell Biology 103, no. 5 (November 1, 1986): 2053–60. http://dx.doi.org/10.1083/jcb.103.5.2053.
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Catecholamines were found to activate Na/H exchange in a concentration-dependent manner in primary cultures of vascular smooth muscle cells (VSMC). The potency order was found to be epinephrine greater than norepinephrine greater than isoproterenol. The major pathway for catecholamine effects appeared to be via interaction with an alpha 1 adrenergic receptor. In addition, it was found that alpha 1 receptor-mediated Na/H exchange in VSMC was increased by angiotensin II and inhibited by 12-O-tetradecanoyl phorbol-13-acetate (TPA). Adrenergic receptors have been shown to be coupled to both adenylate cyclase and to inositol phosphate release (Leeb-Lundberg, L. M. F., S. Cotecchia, J. W. Lomasney, J. F. DeBernadis, R. J. Lefkowitz, and M. G. Caron, 1985, Proc. Natl. Acad. Sci. USA, 82:5651-5655.). It was found that catecholamines increased AMP levels in the potency order isoproterenol greater than norepinephrine greater than epinephrine and the receptor involved was a beta adrenergic receptor. Since these findings did not parallel the results obtained for catecholamine stimulation of Na/H exchange, an increase in AMP levels was probably not the mechanism by which major pathway for catecholamine-stimulated Na/H exchange in VSMC (via the alpha 1 receptor) was activated. When the effects of catecholamines were measured on inositol phosphate release, the potency order for catecholamine stimulation was epinephrine greater than norepinephrine greater than isoproterenol, and the receptor involved was an alpha 1 adrenergic receptor. In addition, angiotensin II increased and TPA inhibited catecholamine-stimulated inositol phosphate release. Since these findings paralleled the results obtained for catecholamine stimulation of Na/H exchange, inositol phosphate release may be the mechanism by which the major pathway for catecholamine-stimulated Na/H exchange in VSMC (via the alpha 1 receptor) was activated.
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Smith, Stephanie A., Janette Nason, and Roger P. Croll. "Distribution of catecholamines in the sea scallop, Placopecten magellanicus." Canadian Journal of Zoology 76, no. 7 (July 1, 1998): 1254–62. http://dx.doi.org/10.1139/z98-063.
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Catecholamines have previously been implicated in several important physiological processes in molluscs, including reproduction, respiration, and feeding. Much of the previous research has relied upon high-performance liquid chromatography to identify and quantify the various catecholamines and pharmacological experiments to investigate their actions. In the present report, we expand upon these studies by using histochemical techniques to investigate the distribution of catecholamine-containing cells and fibres in the central nervous system and peripheral tissues of the sea scallop, Placopecten magellanicus. Strong catecholaminergic staining was present in the somata and neuropil of all major central ganglia. Catecholamines were also abundantly stained in peripheral neurones and (or) fibres in several other tissues, including the labial palps, lips, intestine, gill filaments, foot, mantle, tentacles, and gonadal integument. It is concluded that catecholamines are widespread in the tissues of the scallop and could have potential neurotransmission roles in both the central nervous system and peripheral tissues of this species.
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Kolberg, K. J., and V. J. Martin. "Morphological, cytochemical and neuropharmacological evidence for the presence of catecholamines in hydrozoan planulae." Development 103, no. 2 (June 1, 1988): 249–58. http://dx.doi.org/10.1242/dev.103.2.249.
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Planula larvae of Halocordyle disticha were examined for the presence of catecholamines using a multipronged approach. Transmission electron micrographs of planular sensory cells and ganglionic cells demonstrated dense-cored vesicles and electron-dense droplets in both cell types. These vesicles and droplets were similar in morphology to catecholamine-containing granules of vertebrates. Planulae processed with the SPG histofluorescence technique, specific only for catecholamines, exhibited blue-green fluorophores which were most prominent in the anterior ectoderm. Such fluorescence was associated with sensory cells, ganglionic cells and the neural plexus. Pretreatment of planulae with neuropharmacological agents which prevent reuptake (reserpine) or cause release (nicotine, ephedrine) of catecholamines caused a diminution of the fluorophores. Pretreatment of animals with 6-hydroxydopamine, which causes destruction of catecholamine-containing cells, prevented any fluorescent response. Ultrastructural examination of reserpine-treated planulae revealed a dramatic reduction in the populations of dense-cored vesicles and electron-dense droplets. Furthermore, many of the vesicles and droplets remaining in reserpinized animals appeared washed out, i.e. stained faintly. Exposure of planulae to exogenous norepinephrine caused premature, rapid metamorphosis and produced polyps with slightly stunted tentacles and pitted, irregular hypostomes. Exposure of planulae to nicotine caused similar effects. Rearing planulae in sea water containing alpha blockers, phentolamine and tolazoline, had no discernible effect on behaviour (motility, phototactic response) or gross morphology. However, planulae raised in sea water containing propranolol, a beta blocker, ceased all movement, became tack-shaped and died within 72 h. These results meet multiple criteria for the identification of catecholamines in hydrozoan planulae and suggest that such catecholamines may function as neurotransmitters, neurohormones or neuromodulators during larval development.
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Jaillard, S., V. Houfflin-Debarge, Y. Riou, T. Rakza, S. Klosowski, P. Lequien, and L. Storme. "Effects of catecholamines on the pulmonary circulation in the ovine fetus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 281, no. 2 (August 1, 2001): R607—R614. http://dx.doi.org/10.1152/ajpregu.2001.281.2.r607.
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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 μg · 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 μg · kg−1· min−1did not significantly change PVR. Conversely, dopamine infusion at 10 μg · kg−1· min−1increased 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.
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Lenz, T., E. Werle, G. Strobel та H. Weicker. "O-Methylated and sulfoconjugated catecholamines: differential activities at human platelet α2-adrenoceptors". Canadian Journal of Physiology and Pharmacology 69, № 7 (1 липня 1991): 929–37. http://dx.doi.org/10.1139/y91-141.
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The physiological effects of the sulfoconjugates of epinephrine, norepinephrine, and the 3-O-methylated catecholamines, metanephrine, normetanephrine, and methoxytyramine were examined with regard to their α2-adrenoceptor binding properties and aggregation activity in human platelets. Sulfoconjugation of catecholamines resulted in the loss of both their competitive potency for [3H]yohimbine binding and their influence on platelet aggregation. O-Methyl substituted catecholamines showed attenuation of their α2-adrenoceptor binding affinities when compared with those of the corresponding non-etherified amines. Unlike the free amine epinephrine, which stimulated platelet aggregation, the O-methylated catecholamine derivatives inhibited aggregation. Inhibition was dose-dependent and restricted to the α2-adrenoceptor mediated aggregation response stimulated by epinephrine (1 μM) or potentiated by subthreshold concentrations of epinephrine (30–300 nM) in the presence of subaggregatory doses of vasopressin (10–30 nM). Collagen- and ADP-induced platelet aggregation was not affected. The hydrophilic β-antagonist CGP 12177 displayed no effects. However, high concentrations (0.1 mM) of both isomers of the strongly lipophilic β-adrenoceptor antagonist propranolol inhibited the actions of all aggregators by stabilizing the membrane. Such a nonspecific membrane interaction of the methylated catecholamines could be excluded because of their low lipid solubility calculated in a n-octanol–phosphate buffer system at pH 7.4. We suggest therefore that methylated catecholamines are biological α2-adrenoceptor antagonists acting on α2-adrenoceptor stimulated reactions of human platelets. Whether this receptor antagonism is relevant to other human tissues needs clarification. Sulfated catecholamines, however, are wholly ineffective at this receptor site and may constitute a pathway to control the concentration of the active free catecholamines.Key words: sulfoconjugated catecholamines, methylated catecholamines, α2-adrenoceptors, human platelet aggregation, dopamine receptors.
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Quelhas-Santos, Janete, Benedita Sampaio-Maia, Fernando Remião, Paula Serrão, Isabel Soares-Silva, Gary V. Desir, and Manuel Pestana. "Assessment of Renalase Activity on Catecholamines Degradation." Open Hypertension Journal 7, no. 1 (April 29, 2015): 14–18. http://dx.doi.org/10.2174/1876526201507010014.
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Renalase was recently described as a new flavoprotein that functions as FAD/NADH-dependent oxidase and, in contrast to other monoamine oxidases, is secreted into plasma and urine. Recombinant renalase was found to exert powerful and rapid hypotensive effects when administered intravenously on rats and this was suggested to be mediated by circulating catecholamines degradation. However there is no concrete evidence that directly supports the hypothesis that renalase metabolizes catecholamines. In this study we aimed to evaluate the catecholamines-degrading renalase activity by three different technical approaches: 1) Amplex Red Monoamine Oxidase Assay, which evaluates the rate of resaruzin reduction by renalase oxidative activity; 2) assessment of catecholamines consumptions by high-pressure liquid chromatography (HPLC) with electrochemical-detection (ED) and 3) assessment of product formation by HPLC with photodiode array-detection (DAD). Using the Amplex Red MAO Assay, all three catecholamines were degraded by recombinant renalase overtime, being adrenaline the preferred substrate, followed by noradrenaline and dopamine. In addition using HPLC-ED, it was observed the consumption of all three catecholamines by recombinant renalase, which were oxidized to the correspondent aminochromes, as observed by DAD. However the role of renalase as catalyzer of aminochromes production is still undefined. In summary, the data presented in this study propose by different methodologies the involvement of renalase in catecholamine metabolization.
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GAVRILOVIC, LJUBICA, VESNA STOJILJKOVIC, JELENA KASAPOVIC, NATASA POPOVIC, SNEZANA B. PAJOVIC, and SLADJANA DRONJAK. "Treadmill exercise does not change gene expression of adrenal catecholamine biosynthetic enzymes in chronically stressed rats." Anais da Academia Brasileira de Ciências 85, no. 3 (September 2013): 999–1012. http://dx.doi.org/10.1590/s0001-37652013005000041.
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ABSTRACT Chronic isolation of adult animals represents a form of psychological stress that produces sympatho-adrenomedullar activation. Exercise training acts as an important modulator of sympatho-adrenomedullary system. This study aimed to investigate physical exercise-related changes in gene expression of catecholamine biosynthetic enzymes (tyrosine hydroxylase, dopamine-ß-hydroxylase and phenylethanolamine N-methyltransferase) and cyclic adenosine monophosphate response element-binding (CREB) in the adrenal medulla, concentrations of catecholamines and corticosterone (CORT) in the plasma and the weight of adrenal glands of chronically psychosocially stressed adult rats exposed daily to 20 min treadmill running for 12 weeks. Also, we examined how additional acute immobilization stress changes the mentioned parameters. Treadmill running did not result in modulation of gene expression of catecholamine synthesizing enzymes and it decreased the level of CREB mRNA in the adrenal medulla of chronically psychosocially stressed adult rats. The potentially negative physiological adaptations after treadmill running were recorded as increased concentrations of catecholamines and decreased morning CORT concentration in the plasma, as well as the adrenal gland hypertrophy of chronically psychosocially stressed rats. The additional acute immobilization stress increases gene expression of catecholamine biosynthetic enzymes in the adrenal medulla, as well as catecholamines and CORT levels in the plasma. Treadmill exercise does not change the activity of sympatho-adrenomedullary system of chronically psychosocially stressed rats.
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Jiang, Qijiao, Neill A. Gingles, Marc A. Olivier, Lindsey A. Miles, and Robert J. Parmer. "The anti-fibrinolytic SERPIN, plasminogen activator inhibitor 1 (PAI-1), is targeted to and released from catecholamine storage vesicles." Blood 117, no. 26 (June 30, 2011): 7155–63. http://dx.doi.org/10.1182/blood-2010-05-287672.
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Recent studies suggest a crucial role for plasminogen activator inhibitor-1 (PAI-1) in mediating stress-induced hypercoagulability and thrombosis. However, the mechanisms by which PAI-1 is released by stress are not well-delineated. Here, we examined catecholaminergic neurosecretory cells for expression, trafficking, and release of PAI-1. PAI-1 was prominently expressed in PC12 pheochromocytoma cells and bovine adrenomedullary chromaffin cells as detected by Northern blotting, Western blotting, and specific PAI-1 ELISA. Sucrose gradient fractionation studies and immunoelectron microscopy demonstrated localization of PAI-1 to catecholamine storage vesicles. Secretogogue stimulation resulted in corelease of PAI-1 with catecholamines. Parallel increases in plasma PAI-1 and catecholamines were observed in response to acute sympathoadrenal activation by restraint stress in mice in vivo. Reverse fibrin zymography demonstrated free PAI-1 in cellular releasates. Detection of high molecular weight complexes by Western blotting, consistent with PAI-1 complexed with t-PA, as well as bands consistent with cleaved PAI-1, suggested that active PAI-1 was present. Modulation of PAI-1 levels by incubating PC12 cells with anti–PAI-1 IgG caused a marked decrease in nicotine-mediated catecholamine release. In summary, PAI-1 is expressed in chromaffin cells, sorted into the regulated pathway of secretion (into catecholamine storage vesicles), and coreleased, by exocytosis, with catecholamines in response to secretogogues.
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Sakai, Kimiko, Mai Asano, Masahide Hamaguchi, Hidefumi Taniguchi, Osamu Ukimura, and Michiaki Fukui. "A Cortisol-Secreting Adrenal Adenoma Combined With a Micro-Pheochromocytoma: Case Report and Literature Review." Clinical Medicine Insights: Endocrinology and Diabetes 16 (January 2023): 117955142211485. http://dx.doi.org/10.1177/11795514221148556.
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Cushing’s syndrome and pheochromocytomas (PCCs) are associated with endocrine hypertension. Cortisol-producing adrenal adenomas are a major cause of Cushing’s syndrome. Simultaneous occurrence of cortisol-producing adrenal adenomas and PCCs is rare. Additionally, a PCC generally produces catecholamines in proportion to its size; therefore, micro-PCCs are rarely found in clinical practice. It is unknown whether micro-PCCs produce excess catecholamines during the pre-biochemical phase. Herein, we report the case of a 53-year-old woman who was referred to our hospital for further evaluation of left adrenal incidentaloma. She had been suffering from hypertension for 7 years. Endocrine tests indicated autonomous cortisol secretion, and she was diagnosed with cortisol-producing adrenal adenoma. A laparoscopic left adrenalectomy was performed. The final pathological examination revealed an adrenocortical adenoma measuring 26 × 24 mm. In addition, a micro-PCC measuring 3 × 2 mm was incidentally found near the cortisol-secreting adrenal adenoma in the ipsilateral adrenal gland. All catecholamine biosynthetic enzymes, tyrosine hydroxylase, aromatic l-amino acid decarboxylase, dopamine β-hydroxylase, and phenyl ethanolamine N-methyltransferase, were detected in this micro-PCC by immunohistochemical analyses. Although catecholamine levels were not biochemically elevated, the PCC expressed catecholamine biosynthetic enzymes. This is the first immunohistochemical report to show that a micro-PCC produces excess catecholamines in the pre-biochemical phase.
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Strobel, Gɒnther, and HelmuT Weicker. "Catecholamine sulfates as internal standards in HPLC determinations of sulfoconjugated catecholamines in plasma and urine." Clinical Chemistry 37, no. 2 (February 1, 1991): 196–99. http://dx.doi.org/10.1093/clinchem/37.2.196.
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Abstract A method is described to measure catecholamine sulfates from human plasma and urine by isocratic reversed-phase high-performance liquid chromatography with electrochemical detection. For this measurement we use catecholamine 3-sulfate isomers as internal standards and determine the sulfoconjugates only after eliminating the catecholamines. Catecholamines that have previously been used as internal standards are shown to cause a significant overestimation (P less than 0.05) of the catecholamine sulfates--by 10% to 25% and 20% to 42% in human plasma and urine, respectively. The detection limits (signal-to-noise ratio greater than 3) in plasma and urine samples were about 80 pmol/L for each analyte. The intra-assay and interassay CVs were less than 4.0% and 10.6% in human plasma and less than 6.6% and 12.8% in human urine, respectively. The calibration curves for all catecholamine sulfates in human plasma and urine were linear (r greater than 0.96; P less than 0.001) over the respective concentration ranges of 0.1-100 nmol/L and 5-1000 nmol/L.
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Tang, Y., and R. G. Boutilier. "Correlation between catecholamine release and degree of acidotic stress in trout." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 255, no. 3 (September 1, 1988): R395—R399. http://dx.doi.org/10.1152/ajpregu.1988.255.3.r395.
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Exhaustive exercise in freshwater (FW) and seawater (SW) rainbow trout resulted in a marked and acute increase of plasma catecholamines. Immediately after exercise, epinephrine and norepinephrine concentrations in FW trout were 69 and 15 times the resting level, respectively; in SW trout, they were 46 and 11 times the resting value, respectively. Over the 1st h of recovery, the magnitude of the catecholamine surge in FW animals was about twice that of their SW counterparts. Correlated with this was an extracellular pH disturbance in FW trout, which was approximately twice as severe as in SW trout. Indeed, both the magnitudes and time courses of the plasma catecholamine responses were matched to those of the acid-base disturbances. Linear correlations were found to exist between the immediate depression of blood pH and the corresponding increases in plasma epinephrine and norepinephrine. We conclude that catecholamines are released into the plasma in proportion to the magnitude of the acid-base disturbance. The higher postexercise levels of plasma catecholamines in FW trout vs. SW appear to be a response to the greater acid-base disturbance in the FW animals.
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Takiyyuddin, M. A., H. P. Neumann, J. H. Cervenka, B. Kennedy, T. Q. Dinh, M. G. Ziegler, A. D. Baron, and D. T. O'Connor. "Ultradian variations of chromogranin A in humans." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 261, no. 4 (October 1, 1991): R939—R944. http://dx.doi.org/10.1152/ajpregu.1991.261.4.r939.
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Chromogranin A (CgA) is an acidic soluble protein exocytotically released from virtually all neuroendocrine secretory vesicles. Here we examined spontaneous variations in CgA and catecholamine concentrations in humans. In normal subjects, basal CgA showed no day-to-day, week-to-week, or diurnal variability. Plasma CgA had significant ultradian variation in normotensives and hypertensives, and in bilaterally adrenalectomized subjects. Gender, but not age or blood pressure, influenced CgA variations, males having fewer (P less than 0.05) peaks per 8 h. Plasma catecholamines had significant ultradian variations in both controls and bilaterally adrenalectomized subjects. Within individuals, neither basal nor peak plasma CgA correlated with catecholamines, nor was there concordance between plasma CgA and catecholamine peaks. Somatostatin, a widespread inhibitor of nonsympathoadrenal neuroendocrine secretion, diminished both the frequency and amplitude of plasma CgA peaks. Thus spontaneous variations in basal CgA are not directly linked to alterations in sympathoadrenal catecholamine secretion. Furthermore, neuroendocrine secretion at sites other than the sympathoadrenal system contributes to spontaneous variations in CgA concentration.
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Seibold, Jordan, and Ashley Ross. "Sub-second release of Neurotransmitters from CD4+ T lymphocytes." Journal of Immunology 212, no. 1_Supplement (May 1, 2024): 0493_4408. http://dx.doi.org/10.4049/jimmunol.212.supp.0493.4408.
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Abstract The neuroimmune system is complex and is regulated by small chemical messengers released from resident immune and neuronal cells. Catecholamines like dopamine and norepinephrine are important chemical messengers responsible for initiating and propagating messages between neurons and immune cells; however, the mechanism and dynamics of this signaling are relatively unknown. The presence of the intracellular machinery to synthesize and interact with catecholamines in T lymphocytes has been known for over a decade; however, direct measurement of catecholamine secretion in real time from immune cells has not been possible. Here, we have discovered that Naïve CD4+ T cells are capable of releasing catecholamines on a sub-second time scale. We have used a revolutionary technique, often used in the neuroscience field, called fast-scan cyclic voltammetry (FSCV) to measure sub-second fluctuations of catecholamines from isolated CD4+ T cells. This work provides direct evidence that T cells are capable of releasing catecholamines; potentially as a feedback communicator to resident sympathetic neurons in host immune organs. These results also prove that immune cells can signal on the same time scale as neurons. This work will hopefully open the door to enable more sophisticated studies at the neuron-immune synapse in the future and the understanding of neuro-immune based diseases.
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Seibold, Jordan M., and Ashley Ross. "Subsecond release of catecholamines from CD4+ T lymphocytes." Journal of Immunology 210, no. 1_Supplement (May 1, 2023): 83.11. http://dx.doi.org/10.4049/jimmunol.210.supp.83.11.
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Abstract The neuroimmune system is complex and is regulated by small chemical messengers released from resident immune and neuronal cells. Catecholamines like dopamine and norepinephrine are important chemical messengers responsible for initiating and propagating messages between neurons and immune cells; however, the mechanism and dynamics of this signaling is relatively unknown. The presence of the intracellular machinery to synthesize and interact with catecholamines in T lymphocytes has been known for over a decade; however, direct measurement of catecholamine secretion in real time from immune cells has not been possible. Here, we have discovered that CD4+ T cells are capable of releasing catecholamines on a subsecond time scale. We have used a revolutionary technique, often used in the neuroscience field, called fast-scan cyclic voltammetry (FSCV) to measure subsecond fluctuations of catecholamines from isolated CD4+ T cells. This work provides direct evidence that T cells are capable of releasing catecholamines; potentially as a feedback communicator to resident sympathetic neurons in host immune organs. These results also prove that immune cells can signal on the same time scale as neurons . This work will hopefully open the door to enable more sophisticated studies at the neuron-immune synapse in the future. National Institute of Health R01AI151552
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Boone, J. B., T. Sherraden, K. Pierzchala, R. Berger, and G. R. Van Loon. "Plasma Met-enkephalin and catecholamine responses to intense exercise in humans." Journal of Applied Physiology 73, no. 1 (July 1, 1992): 388–92. http://dx.doi.org/10.1152/jappl.1992.73.1.388.
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Native and cryptic Met-enkephalin and catecholamines are coreleased in response to stress. However, it is not known whether Met-enkephalin and catecholamines exhibit concurrent temporal relationships in response to exercise. The purpose of this investigation was to examine the corelease of catecholamines and Met-enkephalin in endurance-trained (n = 6) and untrained (n = 6) male subjects during a 6-min bout of exercise: 4 min at 70% of maximal O2 uptake (VO2max) followed by 2 min at 120% VO2max. Peak catecholamine levels were found at 1 min of recovery. In trained subjects, native Met-enkephalin peaked during exercise at 70% VO2max, declined during exercise at 120% VO2max, and returned to basal levels by 1 min of recovery. In the untrained subjects, native Met-enkephalin peaked at 120% VO2max (6 min) and returned to baseline by 5 min of recovery. In both groups, cryptic Met-enkephalin peaked at 70% VO2max and returned to basal levels during exercise at 120% VO2max. These data demonstrate that during exercise there is a temporal dissociation in plasma levels of Met-enkephalin and catecholamines.
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Ikarugi, Hideo, Tomomi Taka, Shoko Nakajima, Takanori Noguchi, Sadahiro Watanabe, Yasuto Sasaki, Shukoh Haga, Takashi Ueda, Junji Seki, and Junichiro Yamamoto. "Norepinephrine, but not epinephrine, enhances platelet reactivity and coagulation after exercise in humans." Journal of Applied Physiology 86, no. 1 (January 1, 1999): 133–38. http://dx.doi.org/10.1152/jappl.1999.86.1.133.
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The effects of exercise and catecholamines on platelet reactivity or coagulation and fibrinolysis appear to be inconsistent. This may be partly due to the methods employed in previous studies. In the present study, we investigated the effects of acute aerobic exercise and catecholamines on the thrombotic status by a novel in vitro method, shear-induced hemostatic plug formation (hemostatometry), using nonanticoagulated (native) blood. Aerobic exercise (60% maximal O2consumption) was performed by healthy male volunteers for 20 min, and the effect on platelet reactivity and coagulation was assessed by performing hemostatometry before and immediately after exercise. Exercise significantly increased shear-induced platelet reactivity, coagulation, and catecholamine levels. The effect of catecholamines on platelet reactivity and coagulation was assessed in vitro by adding catecholamines to blood collected in the resting state. The main findings of the present study are that elevation of circulating norepinephrine at levels that are attained during exercise causes platelet hyperreactivity and a platelet-mediated enhanced coagulation. This may be a mechanism of an association of aerobic exercise with thrombotic risk.
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Fredj, Zina, and Mohamad Sawan. "Advanced Nanomaterials-Based Electrochemical Biosensors for Catecholamines Detection: Challenges and Trends." Biosensors 13, no. 2 (January 31, 2023): 211. http://dx.doi.org/10.3390/bios13020211.
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Catecholamines, including dopamine, epinephrine, and norepinephrine, are considered one of the most crucial subgroups of neurotransmitters in the central nervous system (CNS), in which they act at the brain’s highest levels of mental function and play key roles in neurological disorders. Accordingly, the analysis of such catecholamines in biological samples has shown a great interest in clinical and pharmaceutical importance toward the early diagnosis of neurological diseases such as Epilepsy, Parkinson, and Alzheimer diseases. As promising routes for the real-time monitoring of catecholamine neurotransmitters, optical and electrochemical biosensors have been widely adopted and perceived as a dramatically accelerating development in the last decade. Therefore, this review aims to provide a comprehensive overview on the recent advances and main challenges in catecholamines biosensors. Particular emphasis is given to electrochemical biosensors, reviewing their sensing mechanism and the unique characteristics brought by the emergence of nanotechnology. Based on specific biosensors’ performance metrics, multiple perspectives on the therapeutic use of nanomaterial for catecholamines analysis and future development trends are also summarized.
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Montpetit, C. J., and S. F. Perry. "Neuronal control of catecholamine secretion from chromaffin cells in the rainbow trout (Oncorhynchus mykiss)." Journal of Experimental Biology 202, no. 15 (August 1, 1999): 2059–69. http://dx.doi.org/10.1242/jeb.202.15.2059.
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The goal of the present investigation was to assess the relative involvement of nicotinic and muscarinic cholinergic receptors in the neuronal control of catecholamine secretion from the chromaffin tissue of rainbow trout (Oncorhynchus mykiss). This was accomplished by first developing and validating a nerve-stimulating technique able specifically to activate the nerve fibres innervating the chromaffin cells in order to elicit secretion of catecholamines. Using an in situ saline-perfused posterior cardinal vein preparation, it was demonstrated that whole-body field stimulation caused specific voltage-dependent neuronal stimulation of adrenaline and noradrenaline secretion. The contribution of non-specific depolarization was negligible. Several experimental results confirmed the specificity of the field stimulation technique. First, pre-treatment with neostigmine (an anticholinesterase) prolonged and more than doubled the amount of adrenaline secreted in response to electrical stimulation. Second, pre-treatment with the nicotinic receptor antagonist hexamethonium inhibited the electrically evoked secretion of adrenaline and noradrenaline. Third, perfusion with Na+-free saline or removal of the spinal cord abolished secretion of both catecholamines in response to the electrical stimulus. By using the field stimulation technique, this study is the first to demonstrate conclusively a role for muscarinic receptors in catecholamine secretion from trout chromaffin cells. Specifically, muscarinic cholinergic stimulation enhances nicotinic-evoked secretion of catecholamines and, under intense stimulation, may directly cause secretion. The results of the present study suggest the presence of muscarinic receptors on rainbow trout chromaffin cells with a functional role in the cholinergic control of catecholamine secretion.
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Kostyn, Kamil, Aleksandra Boba, Anna Kostyn, Bartosz Kozak, Michał Starzycki, Anna Kulma, and Jan Szopa. "Expression of the Tyrosine Hydroxylase Gene from Rat Leads to Oxidative Stress in Potato Plants." Antioxidants 9, no. 8 (August 7, 2020): 717. http://dx.doi.org/10.3390/antiox9080717.
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Catecholamines are biogenic aromatic amines common among both animals and plants. In animals, they are synthesized via tyrosine hydroxylation, while both hydroxylation or decarboxylation of tyrosine are possible in plants, depending on the species, though no tyrosine hydroxylase—a counterpart of the animal enzyme—has been identified yet. It is known that in potato plants, it is the decarboxylation of tyrosine that leads to catecholamine production. In this paper, we present the effects of the induction of an alternative route of catecholamine production by introducing the tyrosine hydroxylase gene from rat. We demonstrate that an animal system can be used by the plant. However, it does not function to synthesize catecholamines. Instead, it leads to elevated reactive oxygen species content and a constant stress condition in the plant, which responds with elevated antioxidant levels and improved resistance to infection.
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Santos, Jenn Rachelle U., Alessandra Brofferio, Bruna Viana, and Karel Pacak. "Catecholamine-Induced Cardiomyopathy in Pheochromocytoma: How to Manage a Rare Complication in a Rare Disease?" Hormone and Metabolic Research 51, no. 07 (September 18, 2018): 458–69. http://dx.doi.org/10.1055/a-0669-9556.
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AbstractPheochromocytomas and paragangliomas (PHEOs) are rare neuroendocrine tumors. Clinical manifestations include different cardiovascular signs and symptoms, which are related to excessive secretion of catecholamines. Catecholamine-induced cardiomyopathy in PHEO (CICMPP) is a rare but dreaded complication of PHEO. Once patient is diagnosed with this condition, the prognosis is worse and a surgical risk is much higher than expected. This article focuses on how catecholamines affect the heart and the pathophysiologic mechanism of CICMPP. The cardiovascular responses to catecholamine depend mostly on which catecholamine is released as well as the amount of catecholamine that is released. The acute release of norepinephrine and epinephrine from PHEO increases heart rate, systemic vascular resistance, myocardial contractility, and reduces venous compliance. The excessive adrenergic stimulation by catecholamine results in severe vasoconstriction and coronary vasospasm, myocardial ischemia, and subsequently damage, and necrosis. Chronically elevated catecholamine levels lead to significant desensitization of cardiac β-adrenoceptors. The increased levels of the enzyme β-adrenoceptors kinase (βARK) in the heart seems to mediate these biochemical and physiological changes that are consistently correlated with attenuated responsiveness to catecholamine stimulation. Through these mechanisms different types of cardiomyopathy (CMP) can be formed. This review discusses extensively the 3 types of cardiomyopathies that can be present in a PHEO patient. It also provides the clinical presentation and diagnostic and therapeutic algorithm in managing patients with CICMPP.
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Aydin, Suna. "Renalase, Catecholamine and Nitric Oxide Changes Before and After Sodium Nitroprusside Administration to Patients who Develop Post-Coronary Artery By-Pass (CABG) Hypertension." Heart Surgery Forum 21, no. 5 (August 7, 2018): E330—E336. http://dx.doi.org/10.1532/hsf.1998.
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Background: Hypertension develops at a rate of 33 to 70% after Coronary artery bypass grafting (CABG) operations. One of the most commonly used drugs to control hypertension is sodium nitroprusside (SNP). Additionally, renalase enzyme destroys catecholamines and mediates the regulation (reduction) of blood pressure. Thus, this clinical study aims to reveal how renalase, catecholamines and nitric oxide (NO) change and how certain hemodynamic parameters are affected in randomly and prospectively selected cases who are administered SNP for the treatment of blood pressure elevation within 6 to 8 hours after CABG surgery.Methods: The study included 26 patients who developed hypertension after CABG, 12 patients who had normal blood pressure after CABG, and 22 healthy individuals. Renalase and catecholamine levels of the patients were measured using ELISA method and NO levels were determined by spectrophotometry.Results: Renalase and NO levels of the patients who developed hypertension after CABG were found statistically significantly lower than those of healthy controls and patients who did not develop hypertension after CABG, while catecholamine levels were significantly higher in the former. After SNP was started, renalase and NO levels increased, and a significant decrease was observed in the catecholamine levels. Additionally, administration of SNP produced a slight increase in the heart rate and a decrease in systolic arterial pressure (SAP), diastolic arterial pressure (DAP) and means arterial pressure (MAP).Conclusion: SNP elevates NO and renalase levels; thus, administration of renalase preparations, which act in the destruction of catecholamines to contain persistent hypertension that develops in association with catecholamine elevation after CABG surgery, along with SNP and other medications used to lower blood pressure can be an effective therapeutic method to control hypertension.
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López García de Lomana, Adrián, Arnar Ingi Vilhjálmsson, Sarah McGarrity, Rósa Sigurðardóttir, Ósk Anuforo, Alexía Rós Viktorsdóttir, Aris Kotronoulas, et al. "Metabolic Response in Endothelial Cells to Catecholamine Stimulation Associated with Increased Vascular Permeability." International Journal of Molecular Sciences 23, no. 6 (March 15, 2022): 3162. http://dx.doi.org/10.3390/ijms23063162.
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Disruption to endothelial cell homeostasis results in an extensive variety of human pathologies that are particularly relevant to major trauma. Circulating catecholamines, such as adrenaline and noradrenaline, activate endothelial adrenergic receptors triggering a potent response in endothelial function. The regulation of the endothelial cell metabolism is distinct and profoundly important to endothelium homeostasis. However, a precise catalogue of the metabolic alterations caused by sustained high catecholamine levels that results in endothelial dysfunction is still underexplored. Here, we uncover a set of up to 46 metabolites that exhibit a dose–response relationship to adrenaline-noradrenaline equimolar treatment. The identified metabolites align with the glutathione-ascorbate cycle and the nitric oxide biosynthesis pathway. Certain key metabolites, such as arginine and reduced glutathione, displayed a differential response to treatment in early (4 h) compared to late (24 h) stages of sustained stimulation, indicative of homeostatic metabolic feedback loops. Furthermore, we quantified an increase in the glucose consumption and aerobic respiration in endothelial cells upon catecholamine stimulation. Our results indicate that oxidative stress and nitric oxide metabolic pathways are downstream consequences of endothelial cell stimulation with sustained high levels of catecholamines. A precise understanding of the metabolic response in endothelial cells to pathological levels of catecholamines will facilitate the identification of more efficient clinical interventions in trauma patients.