Epinephrine
Norepinephrine
Adrenal Medulla
Receptors, Catecholamine
Chromaffin Cells
Chromaffin System
Adrenal Glands
Pheochromocytoma
Normetanephrine
Tyrosine 3-Monooxygenase
Dopamine
Chromaffin Granules
Reserpine
Propranolol
Isoproterenol
Metanephrine
Receptors, Adrenergic
Splanchnic Nerves
Chromogranin A
Phenylethanolamine N-Methyltransferase
Catecholamine Plasma Membrane Transport Proteins
Dihydroxyphenylalanine
Phentolamine
alpha-Methyltyrosine
Chromogranins
Sympathetic Nervous System
Receptors, Adrenergic, beta
Tyramine
Phenoxybenzamine
Cattle
Adrenergic beta-Antagonists
Adrenergic alpha-Antagonists
Paraganglioma, Extra-Adrenal
Exocytosis
Veratridine
Sympathomimetics
Receptors, Adrenergic, alpha
Monoamine Oxidase
Dimethylphenylpiperazinium Iodide
PC12 Cells
Nicotine
Sympathectomy, Chemical
Sympatholytics
Calcium
Digitonin
Catechol O-Methyltransferase
Methoxyhydroxyphenylglycol
Acetylcholine
Hydrocortisone
Hemodynamics
Desipramine
Paraganglioma
Hexamethonium Compounds
Stress, Physiological
Dogs
Cyclic AMP
Potassium
Dopa Decarboxylase
Cats
Electrochemistry
Stimulation, Chemical
Monoamine Oxidase Inhibitors
Norepinephrine Plasma Membrane Transport Proteins
Phenylephrine
Yohimbine
Glycols
Receptors, Adrenergic, beta-2
Adrenergic Uptake Inhibitors
Ganglionic Blockers
Clonidine
Adrenergic Antagonists
Dose-Response Relationship, Drug
Myocardium
Cells, Cultured
Neurotransmitter Agents
Atropine
Trout
Rats, Inbred Strains
Phenethylamines
3-Iodobenzylguanidine
Chromogranin B
Levodopa
Serotonin
Muscarine
Ephedrine
Hypertension
Biogenic Amines
Takotsubo Cardiomyopathy
Metaraminol
Sodium
Receptors, Adrenergic, beta-1
Hexamethonium
Chromatography, High Pressure Liquid
Nadolol
Autonomic Nervous System
Aromatic-L-Amino-Acid Decarboxylases
Rats, Sprague-Dawley
Propanolamines
Hypothalamus
Adrenergic Agents
Alprenolol
Autonomic Agents
Synephrine
Lipolysis
Prazosin
Allyl-containing sulfides in garlic increase uncoupling protein content in brown adipose tissue, and noradrenaline and adrenaline secretion in rats. (1/3332)
The effects of garlic supplementation on triglyceride metabolism were investigated by measurements of the degree of thermogenesis in interscapular brown adipose tissue (IBAT), and noradrenaline and adrenaline secretion in rats fed two types of dietary fat. In Experiment 1, rats were given isoenergetic high-fat diets containing either shortening or lard with or without garlic powder supplementation (8 g/kg of diet). After 28 d feeding, body weight, plasma triglyceride levels and the weights of perirenal adipose tissue and epididymal fat pad were significantly lower in rats fed diets supplemented with garlic powder than in those fed diets without garlic powder. The content of mitochondrial protein and uncoupling protein (UCP) in IBAT, and urinary noradrenaline and adrenaline excretion were significantly greater in rats fed a lard diet with garlic powder than in those fed the same diet without garlic. Other than adrenaline secretion, differences due to garlic were significant in rats fed shortening, also. In Experiment 2, the effects of various allyl-containing sulfides present in garlic on noradrenaline and adrenaline secretion were evaluated. Administration of diallyldisulfide, diallyltrisulfide and alliin, organosulfur compounds present in garlic, significantly increased plasma noradrenaline and adrenaline concentrations, whereas the administration of disulfides without allyl residues, diallylmonosulfide and S-allyl-L-cysteine did not increase adrenaline secretion. These results suggest that in rats, allyl-containing sulfides in garlic enhance thermogenesis by increasing UCP content in IBAT, and noradrenaline and adrenaline secretion. (+info)Viral gene delivery selectively restores feeding and prevents lethality of dopamine-deficient mice. (2/3332)
Dopamine-deficient mice (DA-/- ), lacking tyrosine hydroxylase (TH) in dopaminergic neurons, become hypoactive and aphagic and die by 4 weeks of age. They are rescued by daily treatment with L-3,4-dihydroxyphenylalanine (L-DOPA); each dose restores dopamine (DA) and feeding for less than 24 hr. Recombinant adeno-associated viruses expressing human TH or GTP cyclohydrolase 1 (GTPCH1) were injected into the striatum of DA-/- mice. Bilateral coinjection of both viruses restored feeding behavior for several months. However, locomotor activity and coordination were partially improved. A virus expressing only TH was less effective, and one expressing GTPCH1 alone was ineffective. TH immunoreactivity and DA were detected in the ventral striatum and adjacent posterior regions of rescued mice, suggesting that these regions mediate a critical DA-dependent aspect of feeding behavior. (+info)Adrenoreceptors of the guinea-pig urinary bladder. (3/3332)
1 Adrenaline, noradrenaline and isoprenaline (5 mug/ml) did not affect the resting tone of the isolated urinary bladder of the guinea-pig. 2 The catecholamines (1-2 mug/ml) inhibited neuronally evoked contractions at various stimulation frequencies; the inhibition was maximum at 2 Hz and minimum at 50 Hz. Isoprenaline produced maximum inhibition. 3 Propranolol (0.5 mug/ml) completely blocked the catecholamine-induced inhibition at all the frequencies employed. The concentration-response curves of isoprenaline at 2, 10 and 50 Hz were characteristically shifted by propranolol (50 ng/ml). Phenoxybenzamine (0.2 mug/ml) was totally ineffective. 4 In some experiments adrenaline significantly raised the tone of the bladder exposed to propranolol; this effect could be blocked by phenoxybenzamine. 5 Acetylcholine-induced bladder contractions were inhibited by adrenaline (2 mug/ml); the inhibition was completely blocked by propranolol (0.5 mug/ml). 6 The results indicate the presence of an inhibitory beta-adrenoceptor and suggest the possibility of an excitatory alpha-adrenoceptor in guinea-pig urinary bladder. (+info)In vivo demonstration of H3-histaminergic inhibition of cardiac sympathetic stimulation by R-alpha-methyl-histamine and its prodrug BP 2.94 in the dog. (4/3332)
1. The aim of this study was to investigate whether histamine H3-receptor agonists could inhibit the effects of cardiac sympathetic nerve stimulation in the dog. 2. Catecholamine release by the heart and the associated variation of haemodynamic parameters were measured after electrical stimulation of the right cardiac sympathetic nerves (1-4 Hz, 10 V, 10 ms) in the anaesthetized dog treated with R-alpha-methyl-histamine (R-HA) and its prodrug BP 2.94 (BP). 3. Cardiac sympathetic stimulation induced a noradrenaline release into the coronary sinus along with a tachycardia and an increase in left ventricular pressure and contractility without changes in mean arterial pressure. Intravenous administration of H3-receptor agonists significantly decreased noradrenaline release by the heart (R-HA at 2 micromol kg(-1) h(-1): +77 +/- 25 vs +405 +/- 82; BP 2.94 at 1 mg kg(-1): +12 +/- 11 vs +330 +/- 100 pg ml(-1) in control conditions, P < or = 0.05), and increases in heart rate (R-HA at 2 micromol kg(-1) h(-1): +26 +/- 8 vs +65 +/- 10 and BP 2.94 at 1 mg kg(-1): +30 +/- 8 vs 75 +/- 6 beats min(-1), in control conditions P < or = 0.05), left ventricular pressure, and contractility. Treatment with SC 359 (1 mg kg(-1)) a selective H3-antagonist, reversed the effects of H3-receptor agonists. Treatment with R-HA at 2 micromol kg(-1) h(-1) and BP 2.94 at 1 mg kg(-1) tended to decrease, while that with SC 359 significantly increased basal heart rate (from 111 +/- 3 to 130 +/- 5 beats min(-1), P < or = 0.001). 4. Functional H3-receptors are present on sympathetic nerve endings in the dog heart. Their stimulation by R-alpha-methyl-histamine or BP 2.94 can inhibit noradrenaline release by the heart and its associated haemodynamic effects. (+info)Evaluation of a new method for the analysis of free catecholamines in plasma using automated sample trace enrichment with dialysis and HPLC. (5/3332)
BACKGROUND: Analysis of urinary free catecholamines was automated recently, but analysis of plasma samples posed special difficulties. The present study was undertaken to evaluate a new method for the automated analysis of plasma catecholamines. METHODS: The procedure is based on an improved sample handling system that includes dialysis and sample clean-up on a strong cation trace-enrichment cartridge. The catecholamines norepinephrine, epinephrine, and dopamine are then separated by reversed-phase ion-pair chromatography and quantified by electrochemical detection. RESULTS: Use of a 740- microL sample is required to give the catecholamine detection limit of 0.05 nmol/L and analytical imprecision (CV) between 1.1% and 9.3%. The assay can be run unattended, although >12 h of analysis time is not recommended without cooling of the autosampler rack. Comparison (n = 68) of the automated cation-exchange clean-up with the well-established manual alumina procedure gave excellent agreement (mean, 3.78 +/- 2.76 and 3.8 +/- 2.89 nmol/L for norepinephrine and 0.99 +/- 1.72 and 1.08 +/- 1.78 nmol/L for epinephrine). Hemodialysis had no clear effect on plasma norepinephrine. Epinephrine concentrations were similar (0.05 < P < 0.1) in chronic renal failure patients (0.24 +/- 0.3 nmol/L; n = 15) and healthy controls (0.5 +/- 0.24 nmol/L; n = 31). Dopamine was not quantified, being usually <0.2 nmol/L. CONCLUSION: The availability of such a fully automated procedure should encourage the more widespread use of plasma catecholamine estimation, e.g., after dialysis, exercise, or trauma/surgery and in the investigation of catecholamine-secreting tumors, particularly in the anuric patient. (+info)Expression of the cell adhesion molecules on leukocytes that demarginate during acute maximal exercise. (6/3332)
The pulmonary vascular bed is an important reservoir for the marginated pool of leukocytes that can be mobilized by exercise or catecholamines. This study was designed to determine the phenotypic characteristics of leukocytes that are mobilized into the circulation during exercise. Twenty healthy volunteers performed incremental exercise to exhaustion [maximal O2 consumption (VO2 max)] on a cycle ergometer. Blood was collected at baseline, at 3-min intervals during exercise, at VO2 max, and 30 min after exercise. Total white cell, polymorphonuclear leukocyte (PMN), and lymphocyte counts increased with exercise to VO2 max (P < 0.05). Flow cytometric analysis showed that the mean fluorescence intensity of L-selectin on PMN (from 14.9 +/- 1 at baseline to 9.5 +/- 1.6 at VO2 max, P < 0.05) and lymphocytes (from 11.7 +/- 1.2 at baseline to 8 +/- 0.8 at VO2 max, P < 0.05) decreased with exercise. Mean fluorescence intensity of CD11b on PMN increased with exercise (from 10.2 +/- 0.6 at baseline to 25 +/- 2.5 at VO2 max, P < 0.002) but remained unchanged on lymphocytes. Myeloperoxidase levels in PMN did not change with exercise. In vitro studies showed that neither catecholamines nor plasma collected at VO2 max during exercise changed leukocyte L-selectin or CD11b levels. We conclude that PMN released from the marginated pool during exercise express low levels of L-selectin and high levels of CD11b. (+info)NADPH oxidase inhibition does not interfere with low PO2 transduction in rat and rabbit CB chemoreceptor cells. (7/3332)
The aim of the present work was to elucidate the role of NADPH oxidase in hypoxia sensing and transduction in the carotid body (CB) chemoreceptor cells. We have studied the effects of several inhibitors of NADPH oxidase on the normoxic and hypoxia-induced release of [3H]catecholamines (CA) in an in vitro preparation of intact CB of the rat and rabbit whose CA deposits have been labeled by prior incubation with the natural precursor [3H]tyrosine. It was found that diphenyleneiodonium (DPI; 0.2-25 microM), an inhibitor of NADPH oxidase, caused a dose-dependent release of [3H]CA from normoxic CB chemoreceptor cells. Contrary to hypoxia, DPI-evoked release was only partially Ca2+ dependent. Concentrations of DPI reported to produce full inhibition of NADPH oxidase in the rat CB did not prevent the hypoxic release response in the rat and rabbit CB chemoreceptor cells, as stimulation with hypoxia in the presence of DPI elicited a response equaling the sum of that produced by DPI and hypoxia applied separately. Neopterin (3-300 microM) and phenylarsine oxide (0.5-2 microM), other inhibitors of NADPH oxidase, did not promote release of [3H]CA in normoxic conditions or affect the response elicited by hypoxia. On the basis of effects of neopterin and phenylarsine oxide, it is concluded that NADPH oxidase does not appear to play a role in oxygen sensing or transduction in the rat and rabbit CB chemoreceptor cells in vitro and, in the context of the present study, that DPI effects are not related to NADPH oxidase inhibition. (+info)Mediation of humoral catecholamine secretion by the renin-angiotensin system in hypotensive rainbow trout (Oncorhynchus mykiss). (8/3332)
The individual contributions of, and potential interactions between, the renin-angiotensin system (RAS) and the humoral adrenergic stress response to blood pressure regulation were examined in rainbow trout. Intravenous injection of the smooth muscle relaxant, papaverine (10 mg/kg), elicited a transient decrease in dorsal aortic blood pressure (PDA) and systemic vascular resistance (RS), and significant increases in plasma angiotensin II (Ang II) and catecholamine concentrations. Blockade of alpha-adrenoceptors before papaverine treatment prevented PDA and RS recovery, had no effect on the increase in plasma catecholamines, and resulted in greater plasma Ang II concentrations. Administration of the angiotensin-converting enzyme inhibitor, lisinopril (10(-4) mol/kg), before papaverine treatment attenuated the increases in the plasma concentrations of Ang II, adrenaline, and noradrenaline by 90, 79, and 40%, respectively and also prevented PDA and RS recovery. By itself, lisinopril treatment caused a gradual and sustained decrease in PDA and RS, and reductions in basal plasma Ang II and adrenaline concentrations. Bolus injection of a catecholamine cocktail (4 nmol/kg noradrenaline plus 40 nmol/kg adrenaline) in the lisinopril+papaverine-treated trout, to supplement their circulating catecholamine concentrations and mimic those observed in fish treated only with papaverine, resulted in a temporary recovery in PDA and RS. These results indicate that the RAS and the acute humoral adrenergic response are both recruited during an acute hypotensive stress, and have important roles in the compensatory response to hypotension in rainbow trout. However, whereas the contribution of the RAS to PDA recovery is largely indirect and relies on an Ang II-mediated secretion of catecholamines, the contribution from the adrenergic system is direct and relies at least in part on plasma catecholamines. (+info)Symptoms of pheochromocytoma can include:
* Rapid heartbeat
* High blood pressure
* Sweating
* Weight loss
* Fatigue
* Headaches
* Nausea and vomiting
If left untreated, pheochromocytoma can lead to complications such as heart failure, stroke, and even death. Therefore, it is important that individuals who experience any of the above symptoms seek medical attention as soon as possible.
Treatment options for pheochromocytoma may include surgery to remove the tumor, medication to manage symptoms, and in some cases, radiation therapy. In rare cases, the tumor may recur after treatment, so regular monitoring is necessary to ensure that any new symptoms are detected early on.
Overall, while pheochromocytoma is a rare and potentially life-threatening condition, prompt medical attention and appropriate treatment can help manage symptoms and prevent complications.
Some common types of adrenal gland neoplasms include:
1. Adrenocortical carcinoma: A rare and aggressive malignancy that arises in the outer layer of the adrenal cortex.
2. Adrenocortical adenoma: A benign tumor that arises in the outer layer of the adrenal cortex.
3. Pheochromocytoma: A rare tumor that arises in the inner part of the adrenal medulla and produces excessive amounts of hormones such as epinephrine and norepinephrine.
4. Paraganglioma: A rare tumor that arises in the sympathetic nervous system, often near the adrenal glands.
Symptoms of adrenal gland neoplasms can include:
* Weight gain or weight loss
* High blood pressure
* Fatigue
* Abdominal pain
* Headache
* Nausea and vomiting
* Palpitations
Diagnosis of adrenal gland neoplasms typically involves imaging tests such as computed tomography (CT) scans, magnetic resonance imaging (MRI), and positron emission tomography (PET) scans, as well as hormone level assessments. Treatment options vary depending on the type and size of the tumor, and may include surgery, chemotherapy, and hormone therapy.
Symptoms of an extra-adrenal paraganglioma may include high blood pressure, palpitations, sweating, headaches, and weight loss. The exact cause of this condition is not known, but genetics may play a role in some cases. Treatment options vary depending on the location and size of the tumor, but they often involve surgery to remove the affected tissue.
Paragangliomas are rare, accounting for less than 1% of all tumors diagnosed in adults. They can occur at any age but are more common in young adults and middle-aged individuals. These tumors are more common in males than females, and their incidence is higher in certain families with inherited syndromes, such as neurofibromatosis type 1 (NF1) or familial paraganglioma.
The symptoms of paraganglioma depend on their location and size. Small tumors may not cause any symptoms, while larger tumors can press on nearby organs and structures, causing a variety of symptoms such as:
* Pain in the abdomen or pelvis
* Swelling or lump in the neck or abdomen
* High blood pressure
* Headaches
* Blurred vision
* Confusion or seizures (in cases of malignant paraganglioma)
Paragangliomas are difficult to diagnose, as they can be mistaken for other conditions such as appendicitis or pancreatitis. Imaging studies such as CT or MRI scans are often used to help identify the location and size of the tumor, while laboratory tests may be used to evaluate hormone levels and other factors that can help differentiate paraganglioma from other conditions.
Treatment for paraganglioma depends on the type, size, and location of the tumor, as well as the patient's overall health status. Small, benign tumors may not require treatment, while larger or malignant tumors may be treated with surgery, chemotherapy, or radiation therapy. In some cases, a combination of these treatments may be used.
The prognosis for paraganglioma is generally good if the tumor is diagnosed and treated early, but it can be poor if the tumor is large or has spread to other parts of the body. With surgical removal of the tumor, the 5-year survival rate is approximately 90% for patients with benign paraganglioma and 30-50% for those with malignant paraganglioma. However, the overall prognosis can vary depending on individual factors such as the size and location of the tumor, the effectiveness of treatment, and the patient's underlying health status.
There are two types of hypertension:
1. Primary Hypertension: This type of hypertension has no identifiable cause and is also known as essential hypertension. It accounts for about 90% of all cases of hypertension.
2. Secondary Hypertension: This type of hypertension is caused by an underlying medical condition or medication. It accounts for about 10% of all cases of hypertension.
Some common causes of secondary hypertension include:
* Kidney disease
* Adrenal gland disorders
* Hormonal imbalances
* Certain medications
* Sleep apnea
* Cocaine use
There are also several risk factors for hypertension, including:
* Age (the risk increases with age)
* Family history of hypertension
* Obesity
* Lack of exercise
* High sodium intake
* Low potassium intake
* Stress
Hypertension is often asymptomatic, and it can cause damage to the blood vessels and organs over time. Some potential complications of hypertension include:
* Heart disease (e.g., heart attacks, heart failure)
* Stroke
* Kidney disease (e.g., chronic kidney disease, end-stage renal disease)
* Vision loss (e.g., retinopathy)
* Peripheral artery disease
Hypertension is typically diagnosed through blood pressure readings taken over a period of time. Treatment for hypertension may include lifestyle changes (e.g., diet, exercise, stress management), medications, or a combination of both. The goal of treatment is to reduce the risk of complications and improve quality of life.
The symptoms of Takotsubo cardiomyopathy are similar to those of a heart attack and can include chest pain, shortness of breath, and irregular heartbeat. However, unlike a heart attack, there is no evidence of blockage in the coronary arteries. Instead, the heart muscle becomes stunned and weakened, leading to a decrease in cardiac function.
Takotsubo cardiomyopathy is often brought on by a surge of stress hormones, such as adrenaline and cortisol, which can cause changes in the heart's electrical activity and reduce blood flow to the muscle. The condition is more common in women than men and typically affects individuals between the ages of 58 and 75.
While Takotsubo cardiomyopathy is a serious condition, it is usually reversible with treatment and most patients recover completely within a few weeks. Treatment may include medications to manage symptoms such as high blood pressure and heart failure, as well as therapy to address the underlying stress or emotional trauma that triggered the condition.
In summary, Takotsubo cardiomyopathy is a rare but potentially life-threatening condition that is caused by extreme physical or emotional stress and can mimic the symptoms of a heart attack. It is important to be aware of this condition and seek medical attention immediately if symptoms persist or worsen over time.
Catecholamines up
Catecholamine
History of catecholamine research
Stimulus (physiology)
Labor induction
Norepinephrine (medication)
Michael A. Caligiuri
Self-affirmation
Edith Bülbring
Dopamine
Dromotropic
Deoxyepinephrine
Catecholaminergic
HP-505
Lee Limbird
Epinephrine (medication)
Chromaffin cell
Phenol sulfur transferase deficiency
Non-tropic hormone
Psychoneuroimmunology
Adrenaline
Secondary hypertension
Autoreceptor
Candicine
Norepinephrine
Mahmoud K. Muftić
Branched-chain amino acid
Fjodor Lishajko
Monoamine neurotransmitter
Cysteinyldopa
NIMH » Catecholamines
Catecholamines - urine: MedlinePlus Medical Encyclopedia
DailyMed - Search Results for Catecholamine
Catecholamines - MeSH - NCBI
Catecholamines - Health Library | NewYork-Presbyterian
Catecholamine-induced cardiomyopathy - PubMed
Immunohistochemical and in situ hybridization observations favor a local catecholamine production in the human Achilles tendon
Phosphodiesterase 5 inhibition improves contractile function and restores transverse tubule loss and catecholamine...
JCI -
Effect of Central Catecholamine Depletion on the Osmotic and Nonosmotic Stimulation of Vasopressin (Antidiuretic Hormone)...
Catecholamine autotoxicity. Implications for pharmacology and therapeutics of Parkinson disease and related disorders - PubMed
Nitric oxide synthase inhibitor inhibits catecholamines release caused by hypogastric sympathetic nerve stimulation. | Journal...
Effect of Age on Post-Prandial Blood Pressure, Catecholamine and Insulin Responses | Clinical Science | Portland Press
Catecholamines in Plasma - HPLC
Central cardiovascular effect of α-adrenergic drugs: Differences between catecholamines and imidazolines | CiNii Research
Seven Days of Euglycemic Hyperinsulinemia Induces Insulin Resistance for Glucose Metabolism but Not Hypertension, Elevated...
Apr 10 'Catecholamine-Induced Lipolysis Inhibits Glucose Uptake and Causes mTOR Complex Dissociation in Adipocytes' -...
Partial or complete loss of norepinephrine differentially alters contextual fear and catecholamine release dynamics in...
Subjects: Catecholamines - Digital Collections - National Library of Medicine Search Results
Postmortem Vitreous Analyses: Overview, Vitreous Procurement and Pretreatment, Performable Postmortem Vitreous Analyses
Catecholamines 24h - Diag
Catecholamine Neurotransmitters, Psychoactive Drugs, and Biological Clocks - Digital Collections - National Library of Medicine
Myocardial catecholamines in experimental cholaemia in albino rats.
DailyMed - Search Results for Catecholamine
Urinary catecholamine excretion during gynecological laparoscopy - Fingerprint - Keio University
Biogenic Amines -Catecholamines - Norepinephrine
"Determination of Arterial and Venous Plasma Catecholamines During Hemo" by Leonard F. Rozek
Oxidation of DNA, proteins and lipids by DOPA, protein-bound DOPA, and related catechol(amine)s - Result
Norepinephrine6
- The main types of catecholamines are dopamine, norepinephrine, and epinephrine. (medlineplus.gov)
- The plasma levels of catecholamines norepinephrine, epinephrine and dopamine were measured using a radioenzymatic assay. (aspetjournals.org)
- The catecholamines adrenaline (epinephrine), noradrenaline (norepinephrine) and dopamine are biogenic amines, which play a central role in the body as hormones and neurotransmitters. (chromsystems.com)
- Catecholamine is the name of a group of aromatic amines (noradrenaline or norepinephrine, adrenaline or epinephrine, dopamine, and their derivatives) which act as hormones and neurotransmitters, respectively. (rmdiagnostics.com)
- The catecholamine messengers epinephrine, norepinephrine, and dopamine are synthesized from tyrosine by a common biosynthetic pathway. (ouhsc.edu)
- The catecholamines-primarily epinephrine, but also norepinephrine and dopamine-are secreted by the adrenal medulla and are important for the acute expression of strength and power because the hormones act as central motor stimulators and peripheral vascular dilators to enhance enzyme systems and calcium release in muscle. (nsca.com)
Pheochromocytoma2
- Adrenal medulla, catecholamines, and pheochromocytoma. (medlineplus.gov)
- To review the pathogenesis as well as the clinical and laboratory features of catecholamine-induced cardiomyopathy associated with pheochromocytoma and other disorders and discuss the various treatment options available. (nih.gov)
Receptors3
- Receptors, Catecholamine" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (ouhsc.edu)
- This graph shows the total number of publications written about "Receptors, Catecholamine" by people in this website by year, and whether "Receptors, Catecholamine" was a major or minor topic of these publications. (ouhsc.edu)
- Below are the most recent publications written about "Receptors, Catecholamine" by people in Profiles. (ouhsc.edu)
Examined in c1
- In this study, the role of CNS catecholamines in effecting ADH release was examined in conscious rats 10-14 d after the cerebroventricular injection of 6-hydroxydopamine (6-OHDA). (jci.org)
Sympathetic2
- The observations suggest that the tenocytes, especially those with disfigured appearances in tendinosis, can produce catecholamines and also that they can respond to sympathetic transmitters. (nih.gov)
- Nitric oxide synthase inhibitor inhibits catecholamines release caused by hypogastric sympathetic nerve stimulation. (aspetjournals.org)
Urinary2
Urine8
- A urine test can be done to measure the amount of catecholamines produced by your body. (medlineplus.gov)
- Some foods can increase catecholamines in your urine. (medlineplus.gov)
- Urine catecholamine levels are increased in most people with neuroblastoma. (medlineplus.gov)
- The urine test for catecholamines may also be used to monitor those who are receiving treatment for these conditions. (medlineplus.gov)
- These diseases result in the production of surplus catecholamines, which are then excreted in the urine. (chromsystems.com)
- For the HPLC analysis of catecholamines in urine, there is an additional method available (order no. 6000). (chromsystems.com)
- Determination of catecholamines in plasma and urine. (jchemrev.com)
- After dealing with the fatal circumstances related to the collapse of the hotel and the presence of the snow mass, and the medico-legal estimation of the different agony times, this tragic event allowed a study of the catecholamine levels in the urine of 10 of the cadavers. (unich.it)
Neurotransmitters2
- Neurotransmitters catecholamines and histamine in allelopathy: Plant cells as models in fluorescence microscopy. (jchemrev.com)
- Electrochemical sensors and biosensors for determination of catecholamine neurotransmitters: a review. (jchemrev.com)
Tyrosine hydroxylase1
- In the present study, antibodies against the catecholamine-synthesizing enzyme tyrosine hydroxylase (TH) and alpha1-adrenoreceptors were applied to sections of specimens of normal and tendinosis Achilles tendons. (nih.gov)
Myocardial3
- Catecholamine-mediated myocardial stunning has been implicated in the pathogenesis of stress-induced cardiomyopathy. (nih.gov)
- Myocardial catecholamines in experimental cholaemia in albino rats. (who.int)
- Bilgrami NL, Kumar S, Tariq M. Myocardial catecholamines in experimental cholaemia in albino rats. (who.int)
Metabolites1
- Liquid chromatographic methods for the quantification of catecholamines and their metabolites in several biological samples-a review. (jchemrev.com)
Hormonal2
- Systematic research has yet to elucidate or quantify the extent of the role of the catecholamines or adrenocortical and thyroid axis hormonal influences in the condition. (edu.au)
- Catecholamine and hormonal data were collected sequentially at 4-h intervals or during and between episodes of PSH. (edu.au)
Neurons2
Clinical1
- The determination of catecholamines has clinical significance in the diagnosis of pheochromocytomas and other tumours affecting the nervous system. (chromsystems.com)
Vasopressin3
- Vasopressin injection is indicated to increase blood pressure in adults with vasodilatory shock who remain hypotensive despite fluids and catecholamines. (nih.gov)
- Pressor effects of catecholamines and vasopressin are expected to be additive. (nih.gov)
- After target blood pressure has been maintained for 8 hours without the use of catecholamines, taper vasopressin injection by 0.005 units/minute every hour as tolerated to maintain target blood pressure. (nih.gov)
Synthesis1
- In addition, new animal models are required to probe the effects of altered catecholamine synthesis on release dynamics and contextual learning. (nih.gov)
Mechanisms1
- We wished to determine whether catecholamine (CA) mechanisms are involved in estradiol (E 2 )-induced LH surges and if amplification of such surges by progesterone (P)affects these CA systems. (illinois.edu)
Oxidation4
- Catecholamines and their oxidation products cause a direct toxic effect on the myocardium. (nih.gov)
- Effect of Non- and Low-Caloric Sweeteners on Substrate Oxidation, Energy Expenditure, and Catecholamines in Humans-A Systematic Review. (bvsalud.org)
- This systematic review aimed to assess the impact of NCS and LCS on fasting and postprandial substrate oxidation , energy expenditure , and catecholamines , compared to caloric sweeteners or water , across different doses and types of NCS and LCS, acutely and in the longer-term. (bvsalud.org)
- A total of 20 studies were eligible 16 studies for substrate oxidation and energy expenditure and four studies for catecholamines . (bvsalud.org)
Chemicals1
- Catecholamines are chemicals made by nerve tissue (including the brain) and the adrenal gland. (medlineplus.gov)
Plasma1
- For the HPLC analysis of catecholamines in plasma any isocratic HPLC system with electrochemical detector is suitable. (chromsystems.com)
Behavior3
- Despite evidence that catecholamines contribute to contextual encoding and memory retrieval, the precise temporal dynamics of their release in the hippocampus during behavior is unknown. (nih.gov)
- Cell surface proteins that bind catecholamines with high affinity and trigger intracellular changes which influence the behavior of cells. (ouhsc.edu)
- Studies in: catecholamines and behavior. (nih.gov)
Sensitivity1
- We propose that the molecular switch for the loss of transverse tubules in HF and their restoration following tadalafil treatment involves the BAR domain protein Amphiphysin II (BIN1) and the restoration of catecholamine sensitivity is through reductions in G-protein receptor kinase 2, protein phosphatase 1 and protein phosphatase 2 A abundance following phosphodiesterase 5 inhibition. (nature.com)
Substances1
- It is likely that locally produced catecholamines and the occurrence of autocrine/paracrine effects of these substances are of great relevance during the process of tendinosis. (nih.gov)
Levels3
- Furthermore, the L-NNA-induced attenuation of rises in the resting IASP and catecholamine levels in response to HGNS was reversed stereoselectively by L-arginine. (aspetjournals.org)
- In conclusion, 7 days of euglycemic hyperinsulinemia induces severe insulin resistance with respect to whole-body glucose metabolism but does not increase blood pressure, catecholamine levels, or sodium retention. (diabetesjournals.org)
- Despite this increased awareness, the pathophysiology of the condition remains unknown, and few reports have suggested a specific mechanism, beyond high catecholamine levels, as a trigger for the syndrome. (medscape.com)
Stimulation1
- Parallel studies to determine the effects of hypogastric nerve stimulation (HGNS) on the resting IASP and catecholamine release were performed. (aspetjournals.org)
Results2
- Results of recent studies using immunohistochemistry show evidence of an occurrence of catecholamine production in the cells (tenocytes) of patellar tendons exhibiting tendinopathy (tendinosis). (nih.gov)
- These results therefore suggest that CNS catecholamines may play an important role in mediating ADH release in response to both osmotic and nonosmotic (hypovolemic) stimuli. (jci.org)
Study1
- This study presents an overview on the recent advances in fluorescence methods for detection of catecholamines. (jchemrev.com)
Treatment1
- Using a sheep model of advanced HF, we show that tadalafil treatment improves contractile function, reverses transverse tubule loss, restores calcium transient amplitude and the heart's response to catecholamines. (nature.com)
Production1
- The observations show not only evidence of local catecholamine production at the protein level, which was the case in recent studies for the patellar tendon, but also at the mRNA level. (nih.gov)
Effect1
- Catecholamines also exert a receptor-mediated effect on the myocardium. (nih.gov)
Loss1
- Heart failure (HF) is characterized by poor survival, a loss of catecholamine reserve and cellular structural remodeling in the form of disorganization and loss of the transverse tubule network. (nature.com)
Test2
- Catecholamines can also be measured with a blood test . (medlineplus.gov)
- It is intended as a monitoring test for patients with suspected catecholamine-secreting tumour. (chromsystems.com)