Norepinephrine: Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.Norepinephrine Plasma Membrane Transport Proteins: Sodium chloride-dependent neurotransmitter symporters located primarily on the PLASMA MEMBRANE of noradrenergic neurons. They remove NOREPINEPHRINE from the EXTRACELLULAR SPACE by high affinity reuptake into PRESYNAPTIC TERMINALS. It regulates signal amplitude and duration at noradrenergic synapses and is the target of ADRENERGIC UPTAKE INHIBITORS.Epinephrine: The active sympathomimetic hormone from the ADRENAL MEDULLA. It stimulates both the alpha- and beta- adrenergic systems, causes systemic VASOCONSTRICTION and gastrointestinal relaxation, stimulates the HEART, and dilates BRONCHI and cerebral vessels. It is used in ASTHMA and CARDIAC FAILURE and to delay absorption of local ANESTHETICS.Sympathetic Nervous System: The thoracolumbar division of the autonomic nervous system. Sympathetic preganglionic fibers originate in neurons of the intermediolateral column of the spinal cord and project to the paravertebral and prevertebral ganglia, which in turn project to target organs. The sympathetic nervous system mediates the body's response to stressful situations, i.e., the fight or flight reactions. It often acts reciprocally to the parasympathetic system.Catecholamines: A general class of ortho-dihydroxyphenylalkylamines derived from tyrosine.Adrenergic Uptake Inhibitors: Drugs that block the transport of adrenergic transmitters into axon terminals or into storage vesicles within terminals. The tricyclic antidepressants (ANTIDEPRESSIVE AGENTS, TRICYCLIC) and amphetamines are among the therapeutically important drugs that may act via inhibition of adrenergic transport. Many of these drugs also block transport of serotonin.Desipramine: A tricyclic dibenzazepine compound that potentiates neurotransmission. Desipramine selectively blocks reuptake of norepinephrine from the neural synapse, and also appears to impair serotonin transport. This compound also possesses minor anticholinergic activity, through its affinity to muscarinic receptors.Adrenergic alpha-Agonists: Drugs that selectively bind to and activate alpha adrenergic receptors.Dopamine beta-HydroxylaseVasoconstrictor Agents: Drugs used to cause constriction of the blood vessels.Receptors, Adrenergic, alpha: One of the two major pharmacological subdivisions of adrenergic receptors that were originally defined by the relative potencies of various adrenergic compounds. The alpha receptors were initially described as excitatory receptors that post-junctionally stimulate SMOOTH MUSCLE contraction. However, further analysis has revealed a more complex picture involving several alpha receptor subtypes and their involvement in feedback regulation.Adrenergic alpha-Antagonists: Drugs that bind to but do not activate alpha-adrenergic receptors thereby blocking the actions of endogenous or exogenous adrenergic agonists. Adrenergic alpha-antagonists are used in the treatment of hypertension, vasospasm, peripheral vascular disease, shock, and pheochromocytoma.Receptors, Adrenergic: Cell-surface proteins that bind epinephrine and/or norepinephrine with high affinity and trigger intracellular changes. The two major classes of adrenergic receptors, alpha and beta, were originally discriminated based on their cellular actions but now are distinguished by their relative affinity for characteristic synthetic ligands. Adrenergic receptors may also be classified according to the subtypes of G-proteins with which they bind; this scheme does not respect the alpha-beta distinction.Blood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.Dopamine: One of the catecholamine NEUROTRANSMITTERS in the brain. It is derived from TYROSINE and is the precursor to NOREPINEPHRINE and EPINEPHRINE. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of receptors (RECEPTORS, DOPAMINE) mediate its action.Locus Coeruleus: Bluish-colored region in the superior angle of the FOURTH VENTRICLE floor, corresponding to melanin-like pigmented nerve cells which lie lateral to the PERIAQUEDUCTAL GRAY.Receptors, Adrenergic, alpha-2: A subclass of alpha-adrenergic receptors found on both presynaptic and postsynaptic membranes where they signal through Gi-Go G-PROTEINS. While postsynaptic alpha-2 receptors play a traditional role in mediating the effects of ADRENERGIC AGONISTS, the subset of alpha-2 receptors found on presynaptic membranes signal the feedback inhibition of NEUROTRANSMITTER release.Tyramine: An indirect sympathomimetic. Tyramine does not directly activate adrenergic receptors, but it can serve as a substrate for adrenergic uptake systems and monoamine oxidase so it prolongs the actions of adrenergic transmitters. It also provokes transmitter release from adrenergic terminals. Tyramine may be a neurotransmitter in some invertebrate nervous systems.Receptors, Adrenergic, beta: One of two major pharmacologically defined classes of adrenergic receptors. The beta adrenergic receptors play an important role in regulating CARDIAC MUSCLE contraction, SMOOTH MUSCLE relaxation, and GLYCOGENOLYSIS.Methoxyhydroxyphenylglycol: Synthesized from endogenous epinephrine and norepinephrine in vivo. It is found in brain, blood, CSF, and urine, where its concentrations are used to measure catecholamine turnover.Sympathomimetics: Drugs that mimic the effects of stimulating postganglionic adrenergic sympathetic nerves. Included here are drugs that directly stimulate adrenergic receptors and drugs that act indirectly by provoking the release of adrenergic transmitters.Heart Rate: The number of times the HEART VENTRICLES contract per unit of time, usually per minute.Phentolamine: A nonselective alpha-adrenergic antagonist. It is used in the treatment of hypertension and hypertensive emergencies, pheochromocytoma, vasospasm of RAYNAUD DISEASE and frostbite, clonidine withdrawal syndrome, impotence, and peripheral vascular disease.Propranolol: A widely used non-cardioselective beta-adrenergic antagonist. Propranolol has been used for MYOCARDIAL INFARCTION; ARRHYTHMIA; ANGINA PECTORIS; HYPERTENSION; HYPERTHYROIDISM; MIGRAINE; PHEOCHROMOCYTOMA; and ANXIETY but adverse effects instigate replacement by newer drugs.Vasoconstriction: The physiological narrowing of BLOOD VESSELS by contraction of the VASCULAR SMOOTH MUSCLE.Adrenergic Agents: Drugs that act on adrenergic receptors or affect the life cycle of adrenergic transmitters. Included here are adrenergic agonists and antagonists and agents that affect the synthesis, storage, uptake, metabolism, or release of adrenergic transmitters.Biogenic Monoamines: Biogenic amines having only one amine moiety. Included in this group are all natural monoamines formed by the enzymatic decarboxylation of natural amino acids.Yohimbine: A plant alkaloid with alpha-2-adrenergic blocking activity. Yohimbine has been used as a mydriatic and in the treatment of ERECTILE DYSFUNCTION.Dogs: The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)Rats, Sprague-Dawley: A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.Prazosin: A selective adrenergic alpha-1 antagonist used in the treatment of HEART FAILURE; HYPERTENSION; PHEOCHROMOCYTOMA; RAYNAUD DISEASE; PROSTATIC HYPERTROPHY; and URINARY RETENTION.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Receptors, Adrenergic, alpha-1: A subclass of alpha-adrenergic receptors that mediate contraction of SMOOTH MUSCLE in a variety of tissues such as ARTERIOLES; VEINS; and the UTERUS. They are usually found on postsynaptic membranes and signal through GQ-G11 G-PROTEINS.Adrenergic Fibers: Nerve fibers liberating catecholamines at a synapse after an impulse.Adrenergic alpha-2 Receptor Antagonists: Drugs that bind to and block the activation of ADRENERGIC ALPHA-2 RECEPTORS.Normetanephrine: A methylated metabolite of norepinephrine that is excreted in the urine and found in certain tissues. It is a marker for tumors.Neurotransmitter Uptake Inhibitors: Drugs that inhibit the transport of neurotransmitters into axon terminals or into storage vesicles within terminals. For many transmitters, uptake determines the time course of transmitter action so inhibiting uptake prolongs the activity of the transmitter. Blocking uptake may also deplete available transmitter stores. Many clinically important drugs are uptake inhibitors although the indirect reactions of the brain rather than the acute block of uptake itself is often responsible for the therapeutic effects.Serotonin: A biochemical messenger and regulator, synthesized from the essential amino acid L-TRYPTOPHAN. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (RECEPTORS, SEROTONIN) explain the broad physiological actions and distribution of this biochemical mediator.Adrenergic Antagonists: Drugs that bind to but do not activate ADRENERGIC RECEPTORS. Adrenergic antagonists block the actions of the endogenous adrenergic transmitters EPINEPHRINE and NOREPINEPHRINE.Hemodynamics: The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.Clonidine: An imidazoline sympatholytic agent that stimulates ALPHA-2 ADRENERGIC RECEPTORS and central IMIDAZOLINE RECEPTORS. It is commonly used in the management of HYPERTENSION.Vascular Resistance: The force that opposes the flow of BLOOD through a vascular bed. It is equal to the difference in BLOOD PRESSURE across the vascular bed divided by the CARDIAC OUTPUT.PropylaminesAdrenergic Agonists: Drugs that bind to and activate adrenergic receptors.Isoproterenol: Isopropyl analog of EPINEPHRINE; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant.Reserpine: An alkaloid found in the roots of Rauwolfia serpentina and R. vomitoria. Reserpine inhibits the uptake of norepinephrine into storage vesicles resulting in depletion of catecholamines and serotonin from central and peripheral axon terminals. It has been used as an antihypertensive and an antipsychotic as well as a research tool, but its adverse effects limit its clinical use.Hypertension: Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.Neurotransmitter Agents: Substances used for their pharmacological actions on any aspect of neurotransmitter systems. Neurotransmitter agents include agonists, antagonists, degradation inhibitors, uptake inhibitors, depleters, precursors, and modulators of receptor function.Symporters: Membrane transporters that co-transport two or more dissimilar molecules in the same direction across a membrane. Usually the transport of one ion or molecule is against its electrochemical gradient and is "powered" by the movement of another ion or molecule with its electrochemical gradient.Heart: The hollow, muscular organ that maintains the circulation of the blood.Microdialysis: A technique for measuring extracellular concentrations of substances in tissues, usually in vivo, by means of a small probe equipped with a semipermeable membrane. Substances may also be introduced into the extracellular space through the membrane.Electric Stimulation: Use of electric potential or currents to elicit biological responses.Rats, Inbred Strains: Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.Adrenergic beta-Antagonists: Drugs that bind to but do not activate beta-adrenergic receptors thereby blocking the actions of beta-adrenergic agonists. Adrenergic beta-antagonists are used for treatment of hypertension, cardiac arrhythmias, angina pectoris, glaucoma, migraine headaches, and anxiety.Adrenergic alpha-1 Receptor Agonists: Compounds that bind to and activate ADRENERGIC ALPHA-1 RECEPTORS.Droxidopa: A precursor of noradrenaline that is used in the treatment of parkinsonism. The racemic form (DL-threo-3,4-dihydroxyphenylserine) has also been used, and has been investigated in the treatment of orthostatic hypotension. There is a deficit of noradrenaline as well as of dopamine in Parkinson's disease and it has been proposed that this underlies the sudden transient freezing seen usually in advanced disease. Administration of DL-threo-3,4-dihydroxyphenylserine has been claimed to result in an improvement in this phenomenon but controlled studies have failed to demonstrate improvement. (Reynolds JEF(Ed): Martindale: The Extra Pharmacopoeia (electronic version). Micromedex, Inc, Englewood, CO, 1995)Myocardium: The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.Phenylephrine: An alpha-1 adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent.Sympatholytics: Drugs that inhibit the actions of the sympathetic nervous system by any mechanism. The most common of these are the ADRENERGIC ANTAGONISTS and drugs that deplete norepinephrine or reduce the release of transmitters from adrenergic postganglionic terminals (see ADRENERGIC AGENTS). Drugs that act in the central nervous system to reduce sympathetic activity (e.g., centrally acting alpha-2 adrenergic agonists, see ADRENERGIC ALPHA-AGONISTS) are included here.Adrenergic Neurons: Neurons whose primary neurotransmitter is EPINEPHRINE.3-Iodobenzylguanidine: A guanidine analog with specific affinity for tissues of the sympathetic nervous system and related tumors. The radiolabeled forms are used as antineoplastic agents and radioactive imaging agents. (Merck Index, 12th ed) MIBG serves as a neuron-blocking agent which has a strong affinity for, and retention in, the adrenal medulla and also inhibits ADP-ribosyltransferase.Angiotensin II: An octapeptide that is a potent but labile vasoconstrictor. It is produced from angiotensin I after the removal of two amino acids at the C-terminal by ANGIOTENSIN CONVERTING ENZYME. The amino acid in position 5 varies in different species. To block VASOCONSTRICTION and HYPERTENSION effect of angiotensin II, patients are often treated with ACE INHIBITORS or with ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKERS.Adrenergic alpha-2 Receptor Agonists: Compounds that bind to and activate ADRENERGIC ALPHA-2 RECEPTORS.Biogenic Amines: A group of naturally occurring amines derived by enzymatic decarboxylation of the natural amino acids. Many have powerful physiological effects (e.g., histamine, serotonin, epinephrine, tyramine). Those derived from aromatic amino acids, and also their synthetic analogs (e.g., amphetamine), are of use in pharmacology.Adipose Tissue, Brown: A thermogenic form of adipose tissue composed of BROWN ADIPOCYTES. It is found in newborns of many species including humans, and in hibernating mammals. Brown fat is richly vascularized, innervated, and densely packed with MITOCHONDRIA which can generate heat directly from the stored lipids.Mesenteric Arteries: Arteries which arise from the abdominal aorta and distribute to most of the intestines.Hydroxydopamines: Dopamines with a hydroxy group substituted in one or more positions.Synaptosomes: Pinched-off nerve endings and their contents of vesicles and cytoplasm together with the attached subsynaptic area of the membrane of the post-synaptic cell. They are largely artificial structures produced by fractionation after selective centrifugation of nervous tissue homogenates.Tyrosine 3-Monooxygenase: An enzyme that catalyzes the conversion of L-tyrosine, tetrahydrobiopterin, and oxygen to 3,4-dihydroxy-L-phenylalanine, dihydrobiopterin, and water. EC 1.14.16.2.Monoamine Oxidase: An enzyme that catalyzes the oxidative deamination of naturally occurring monoamines. It is a flavin-containing enzyme that is localized in mitochondrial membranes, whether in nerve terminals, the liver, or other organs. Monoamine oxidase is important in regulating the metabolic degradation of catecholamines and serotonin in neural or target tissues. Hepatic monoamine oxidase has a crucial defensive role in inactivating circulating monoamines or those, such as tyramine, that originate in the gut and are absorbed into the portal circulation. (From Goodman and Gilman's, The Pharmacological Basis of Therapeutics, 8th ed, p415) EC 1.4.3.4.Stellate Ganglion: A paravertebral sympathetic ganglion formed by the fusion of the inferior cervical and first thoracic ganglia.Acetylcholine: A neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.Idazoxan: A benzodioxane-linked imidazole that has alpha-2 adrenoceptor antagonist activity.Ephedrine: A phenethylamine found in EPHEDRA SINICA. PSEUDOEPHEDRINE is an isomer. It is an alpha- and beta-adrenergic agonist that may also enhance release of norepinephrine. It has been used for asthma, heart failure, rhinitis, and urinary incontinence, and for its central nervous system stimulatory effects in the treatment of narcolepsy and depression. It has become less extensively used with the advent of more selective agonists.alpha-Methyltyrosine: An inhibitor of the enzyme TYROSINE 3-MONOOXYGENASE, and consequently of the synthesis of catecholamines. It is used to control the symptoms of excessive sympathetic stimulation in patients with PHEOCHROMOCYTOMA. (Martindale, The Extra Pharmacopoeia, 30th ed)Vasomotor System: The neural systems which act on VASCULAR SMOOTH MUSCLE to control blood vessel diameter. The major neural control is through the sympathetic nervous system.Serotonin Plasma Membrane Transport Proteins: Sodium chloride-dependent neurotransmitter symporters located primarily on the PLASMA MEMBRANE of serotonergic neurons. They are different than SEROTONIN RECEPTORS, which signal cellular responses to SEROTONIN. They remove SEROTONIN from the EXTRACELLULAR SPACE by high affinity reuptake into PRESYNAPTIC TERMINALS. Regulates signal amplitude and duration at serotonergic synapses and is the site of action of the SEROTONIN UPTAKE INHIBITORS.Nerve Endings: Branch-like terminations of NERVE FIBERS, sensory or motor NEURONS. Endings of sensory neurons are the beginnings of afferent pathway to the CENTRAL NERVOUS SYSTEM. Endings of motor neurons are the terminals of axons at the muscle cells. Nerve endings which release neurotransmitters are called PRESYNAPTIC TERMINALS.Fluoxetine: The first highly specific serotonin uptake inhibitor. It is used as an antidepressant and often has a more acceptable side-effects profile than traditional antidepressants.Renin: A highly specific (Leu-Leu) endopeptidase that generates ANGIOTENSIN I from its precursor ANGIOTENSINOGEN, leading to a cascade of reactions which elevate BLOOD PRESSURE and increase sodium retention by the kidney in the RENIN-ANGIOTENSIN SYSTEM. The enzyme was formerly listed as EC 3.4.99.19.Sympathectomy, Chemical: Sympathectomy using chemicals (e.g., 6-hydroxydopamine or guanethidine) which selectively and reversibly destroy adrenergic nerve endings while leaving cholinergic nerve endings intact.Rats, Inbred WKY: A strain of Rattus norvegicus used as a normotensive control for the spontaneous hypertensive rats (SHR).Arteries: The vessels carrying blood away from the heart.Sympathetic Fibers, Postganglionic: Nerve fibers which project from sympathetic ganglia to synapses on target organs. Sympathetic postganglionic fibers use norepinephrine as transmitter, except for those innervating eccrine sweat glands (and possibly some blood vessels) which use acetylcholine. They may also release peptide cotransmitters.Methoxamine: An alpha-1 adrenergic agonist that causes prolonged peripheral VASOCONSTRICTION.Vasopressins: Antidiuretic hormones released by the NEUROHYPOPHYSIS of all vertebrates (structure varies with species) to regulate water balance and OSMOLARITY. In general, vasopressin is a nonapeptide consisting of a six-amino-acid ring with a cysteine 1 to cysteine 6 disulfide bridge or an octapeptide containing a CYSTINE. All mammals have arginine vasopressin except the pig with a lysine at position 8. Vasopressin, a vasoconstrictor, acts on the KIDNEY COLLECTING DUCTS to increase water reabsorption, increase blood volume and blood pressure.Trimethaphan: A nicotinic antagonist that has been used as a ganglionic blocker in hypertension, as an adjunct to anesthesia, and to induce hypotension during surgery.Regional Blood Flow: The flow of BLOOD through or around an organ or region of the body.Neuropeptide Y: A 36-amino acid peptide present in many organs and in many sympathetic noradrenergic neurons. It has vasoconstrictor and natriuretic activity and regulates local blood flow, glandular secretion, and smooth muscle activity. The peptide also stimulates feeding and drinking behavior and influences secretion of pituitary hormones.Methyltyrosines: A group of compounds that are methyl derivatives of the amino acid TYROSINE.Forearm: Part of the arm in humans and primates extending from the ELBOW to the WRIST.Adrenergic beta-Agonists: Drugs that selectively bind to and activate beta-adrenergic receptors.Rats, Wistar: A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.Muscle, Smooth, Vascular: The nonstriated involuntary muscle tissue of blood vessels.Dihydroxyphenylalanine: A beta-hydroxylated derivative of phenylalanine. The D-form of dihydroxyphenylalanine has less physiologic activity than the L-form and is commonly used experimentally to determine whether the pharmacological effects of LEVODOPA are stereospecific.3,4-Dihydroxyphenylacetic Acid: A deaminated metabolite of LEVODOPA.Pheochromocytoma: A usually benign, well-encapsulated, lobular, vascular tumor of chromaffin tissue of the ADRENAL MEDULLA or sympathetic paraganglia. The cardinal symptom, reflecting the increased secretion of EPINEPHRINE and NOREPINEPHRINE, is HYPERTENSION, which may be persistent or intermittent. During severe attacks, there may be HEADACHE; SWEATING, palpitation, apprehension, TREMOR; PALLOR or FLUSHING of the face, NAUSEA and VOMITING, pain in the CHEST and ABDOMEN, and paresthesias of the extremities. The incidence of malignancy is as low as 5% but the pathologic distinction between benign and malignant pheochromocytomas is not clear. (Dorland, 27th ed; DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1298)Shock, Septic: Sepsis associated with HYPOTENSION or hypoperfusion despite adequate fluid resuscitation. Perfusion abnormalities may include, but are not limited to LACTIC ACIDOSIS; OLIGURIA; or acute alteration in mental status.Dopamine Plasma Membrane Transport Proteins: Sodium chloride-dependent neurotransmitter symporters located primarily on the PLASMA MEMBRANE of dopaminergic neurons. They remove DOPAMINE from the EXTRACELLULAR SPACE by high affinity reuptake into PRESYNAPTIC TERMINALS and are the target of DOPAMINE UPTAKE INHIBITORS.Adrenal Medulla: The inner portion of the adrenal gland. Derived from ECTODERM, adrenal medulla consists mainly of CHROMAFFIN CELLS that produces and stores a number of NEUROTRANSMITTERS, mainly adrenaline (EPINEPHRINE) and NOREPINEPHRINE. The activity of the adrenal medulla is regulated by the SYMPATHETIC NERVOUS SYSTEM.Chlorisondamine: A nicotinic antagonist used primarily as a ganglionic blocker in animal research. It has been used as an antihypertensive agent but has been supplanted by more specific drugs in most clinical applications.Potassium: An element in the alkali group of metals with an atomic symbol K, atomic number 19, and atomic weight 39.10. It is the chief cation in the intracellular fluid of muscle and other cells. Potassium ion is a strong electrolyte that plays a significant role in the regulation of fluid volume and maintenance of the WATER-ELECTROLYTE BALANCE.Muscle Contraction: A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Cocaine: An alkaloid ester extracted from the leaves of plants including coca. It is a local anesthetic and vasoconstrictor and is clinically used for that purpose, particularly in the eye, ear, nose, and throat. It also has powerful central nervous system effects similar to the amphetamines and is a drug of abuse. Cocaine, like amphetamines, acts by multiple mechanisms on brain catecholaminergic neurons; the mechanism of its reinforcing effects is thought to involve inhibition of dopamine uptake.Rats, Inbred SHR: A strain of Rattus norvegicus with elevated blood pressure used as a model for studying hypertension and stroke.Monoamine Oxidase Inhibitors: A chemically heterogeneous group of drugs that have in common the ability to block oxidative deamination of naturally occurring monoamines. (From Gilman, et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed, p414)Potassium Chloride: A white crystal or crystalline powder used in BUFFERS; FERTILIZERS; and EXPLOSIVES. It can be used to replenish ELECTROLYTES and restore WATER-ELECTROLYTE BALANCE in treating HYPOKALEMIA.Neuroeffector Junction: The synapse between a neuron (presynaptic) and an effector cell other than another neuron (postsynaptic). Neuroeffector junctions include synapses onto muscles and onto secretory cells.Nitroprusside: A powerful vasodilator used in emergencies to lower blood pressure or to improve cardiac function. It is also an indicator for free sulfhydryl groups in proteins.Adrenergic alpha-1 Receptor Antagonists: Drugs that bind to and block the activation of ADRENERGIC ALPHA-1 RECEPTORS.Autonomic Nervous System Diseases: Diseases of the parasympathetic or sympathetic divisions of the AUTONOMIC NERVOUS SYSTEM; which has components located in the CENTRAL NERVOUS SYSTEM and PERIPHERAL NERVOUS SYSTEM. Autonomic dysfunction may be associated with HYPOTHALAMIC DISEASES; BRAIN STEM disorders; SPINAL CORD DISEASES; and PERIPHERAL NERVOUS SYSTEM DISEASES. Manifestations include impairments of vegetative functions including the maintenance of BLOOD PRESSURE; HEART RATE; pupil function; SWEATING; REPRODUCTIVE AND URINARY PHYSIOLOGY; and DIGESTION.Mesenteric Veins: Veins which return blood from the intestines; the inferior mesenteric vein empties into the splenic vein, the superior mesenteric vein joins the splenic vein to form the portal vein.Receptors, Adrenergic, beta-1: A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The adrenergic beta-1 receptors are equally sensitive to EPINEPHRINE and NOREPINEPHRINE and bind the agonist DOBUTAMINE and the antagonist METOPROLOL with high affinity. They are found in the HEART, juxtaglomerular cells, and in the central and peripheral nervous systems.Serotonin Uptake Inhibitors: Compounds that specifically inhibit the reuptake of serotonin in the brain.Brain: The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.Hydrocortisone: The main glucocorticoid secreted by the ADRENAL CORTEX. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions.Cold Temperature: An absence of warmth or heat or a temperature notably below an accustomed norm.Vasodilation: The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.Calcium: A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.Cyclic AMP: An adenine nucleotide containing one phosphate group which is esterified to both the 3'- and 5'-positions of the sugar moiety. It is a second messenger and a key intracellular regulator, functioning as a mediator of activity for a number of hormones, including epinephrine, glucagon, and ACTH.Receptors, Histamine H3: A class of histamine receptors discriminated by their pharmacology and mode of action. Histamine H3 receptors were first recognized as inhibitory autoreceptors on histamine-containing nerve terminals and have since been shown to regulate the release of several neurotransmitters in the central and peripheral nervous systems. (From Biochem Soc Trans 1992 Feb;20(1):122-5)Rabbits: The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.Perfusion: Treatment process involving the injection of fluid into an organ or tissue.Pineal Gland: A light-sensitive neuroendocrine organ attached to the roof of the THIRD VENTRICLE of the brain. The pineal gland secretes MELATONIN, other BIOGENIC AMINES and NEUROPEPTIDES.Lypressin: The porcine antidiuretic hormone (VASOPRESSINS). It is a cyclic nonapeptide that differs from ARG-VASOPRESSIN by one amino acid, containing a LYSINE at residue 8 instead of an ARGININE. Lys-vasopressin is used to treat DIABETES INSIPIDUS or to improve vasomotor tone and BLOOD PRESSURE.TritiumPressoreceptors: Receptors in the vascular system, particularly the aorta and carotid sinus, which are sensitive to stretch of the vessel walls.Shy-Drager Syndrome: A progressive neurodegenerative condition of the central and autonomic nervous systems characterized by atrophy of the preganglionic lateral horn neurons of the thoracic spinal cord. This disease is generally considered a clinical variant of MULTIPLE SYSTEM ATROPHY. Affected individuals present in the fifth or sixth decade with ORTHOSTASIS and bladder dysfunction; and later develop FECAL INCONTINENCE; anhidrosis; ATAXIA; IMPOTENCE; and alterations of tone suggestive of basal ganglia dysfunction. (From Adams et al., Principles of Neurology, 6th ed, p536)Stress, Physiological: The unfavorable effect of environmental factors (stressors) on the physiological functions of an organism. Prolonged unresolved physiological stress can affect HOMEOSTASIS of the organism, and may lead to damaging or pathological conditions.Hypotension, Orthostatic: A significant drop in BLOOD PRESSURE after assuming a standing position. Orthostatic hypotension is a finding, and defined as a 20-mm Hg decrease in systolic pressure or a 10-mm Hg decrease in diastolic pressure 3 minutes after the person has risen from supine to standing. Symptoms generally include DIZZINESS, blurred vision, and SYNCOPE.Oxidopamine: A neurotransmitter analogue that depletes noradrenergic stores in nerve endings and induces a reduction of dopamine levels in the brain. Its mechanism of action is related to the production of cytolytic free-radicals.Neurons: The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.Propanolamines: AMINO ALCOHOLS containing the propanolamine (NH2CH2CHOHCH2) group and its derivatives.Drug Interactions: The action of a drug that may affect the activity, metabolism, or toxicity of another drug.Vasodilator Agents: Drugs used to cause dilation of the blood vessels.Hypothalamus: Ventral part of the DIENCEPHALON extending from the region of the OPTIC CHIASM to the caudal border of the MAMMILLARY BODIES and forming the inferior and lateral walls of the THIRD VENTRICLE.Pure Autonomic Failure: A degenerative disease of the AUTONOMIC NERVOUS SYSTEM that is characterized by idiopathic ORTHOSTATIC HYPOTENSION and a greatly reduced level of CATECHOLAMINES. No other neurological deficits are present.Heart Failure: A heterogeneous condition in which the heart is unable to pump out sufficient blood to meet the metabolic need of the body. Heart failure can be caused by structural defects, functional abnormalities (VENTRICULAR DYSFUNCTION), or a sudden overload beyond its capacity. Chronic heart failure is more common than acute heart failure which results from sudden insult to cardiac function, such as MYOCARDIAL INFARCTION.Hypotension: Abnormally low BLOOD PRESSURE that can result in inadequate blood flow to the brain and other vital organs. Common symptom is DIZZINESS but greater negative impacts on the body occur when there is prolonged depravation of oxygen and nutrients.Brain Chemistry: Changes in the amounts of various chemicals (neurotransmitters, receptors, enzymes, and other metabolites) specific to the area of the central nervous system contained within the head. These are monitored over time, during sensory stimulation, or under different disease states.Arginine Vasopressin: The predominant form of mammalian antidiuretic hormone. It is a nonapeptide containing an ARGININE at residue 8 and two disulfide-linked cysteines at residues of 1 and 6. Arg-vasopressin is used to treat DIABETES INSIPIDUS or to improve vasomotor tone and BLOOD PRESSURE.Ganglionic Blockers: Agents having as their major action the interruption of neural transmission at nicotinic receptors on postganglionic autonomic neurons. Because their actions are so broad, including blocking of sympathetic and parasympathetic systems, their therapeutic use has been largely supplanted by more specific drugs. They may still be used in the control of blood pressure in patients with acute dissecting aortic aneurysm and for the induction of hypotension in surgery.Denervation: The resection or removal of the nerve to an organ or part. (Dorland, 28th ed)Dihydroergotoxine: A mixture of three different hydrogenated derivatives of ERGOTAMINE: DIHYDROERGOCORNINE; DIHYDROERGOCRISTINE; and DIHYDROERGOCRYPTINE. Dihydroergotoxine has been proposed to be a neuroprotective agent and a nootropic agent. The mechanism of its therapeutic actions is not clear, but it can act as an alpha-adrenergic antagonist and a dopamine agonist. The methanesulfonate salts of this mixture of alkaloids are called ERGOLOID MESYLATES.Phenylethanolamine N-Methyltransferase: A methyltransferase that catalyzes the reaction of S-adenosyl-L-methionine and phenylethanolamine to yield S-adenosyl-L-homocysteine and N-methylphenylethanolamine. It can act on various phenylethanolamines and converts norepinephrine into epinephrine. (From Enzyme Nomenclature, 1992) EC 2.1.1.28.Receptors, Adrenergic, beta-2: A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The adrenergic beta-2 receptors are more sensitive to EPINEPHRINE than to NOREPINEPHRINE and have a high affinity for the agonist TERBUTALINE. They are widespread, with clinically important roles in SKELETAL MUSCLE; LIVER; and vascular, bronchial, gastrointestinal, and genitourinary SMOOTH MUSCLE.Cardiac Output: The volume of BLOOD passing through the HEART per unit of time. It is usually expressed as liters (volume) per minute so as not to be confused with STROKE VOLUME (volume per beat).Vanilmandelic AcidSplanchnic Circulation: The circulation of blood through the BLOOD VESSELS supplying the abdominal VISCERA.Dioxanes: 1,4-Diethylene dioxides. Industrial solvents. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), dioxane itself may "reasonably be anticipated to be a carcinogen." (Merck Index, 11th ed)Receptors, Catecholamine: Cell surface proteins that bind catecholamines with high affinity and trigger intracellular changes which influence the behavior of cells. The catecholamine messengers epinephrine, norepinephrine, and dopamine are synthesized from tyrosine by a common biosynthetic pathway.Sympathectomy: The removal or interruption of some part of the sympathetic nervous system for therapeutic or research purposes.Antidepressive Agents: Mood-stimulating drugs used primarily in the treatment of affective disorders and related conditions. Several MONOAMINE OXIDASE INHIBITORS are useful as antidepressants apparently as a long-term consequence of their modulation of catecholamine levels. The tricyclic compounds useful as antidepressive agents (ANTIDEPRESSIVE AGENTS, TRICYCLIC) also appear to act through brain catecholamine systems. A third group (ANTIDEPRESSIVE AGENTS, SECOND-GENERATION) is a diverse group of drugs including some that act specifically on serotonergic systems.Autonomic Nervous System: The ENTERIC NERVOUS SYSTEM; PARASYMPATHETIC NERVOUS SYSTEM; and SYMPATHETIC NERVOUS SYSTEM taken together. Generally speaking, the autonomic nervous system regulates the internal environment during both peaceful activity and physical or emotional stress. Autonomic activity is controlled and integrated by the CENTRAL NERVOUS SYSTEM, especially the HYPOTHALAMUS and the SOLITARY NUCLEUS, which receive information relayed from VISCERAL AFFERENTS.Arterioles: The smallest divisions of the arteries located between the muscular arteries and the capillaries.Desoxycorticosterone: A steroid metabolite that is the 11-deoxy derivative of CORTICOSTERONE and the 21-hydroxy derivative of PROGESTERONE.Synaptic Transmission: The communication from a NEURON to a target (neuron, muscle, or secretory cell) across a SYNAPSE. In chemical synaptic transmission, the presynaptic neuron releases a NEUROTRANSMITTER that diffuses across the synaptic cleft and binds to specific synaptic receptors, activating them. The activated receptors modulate specific ion channels and/or second-messenger systems in the postsynaptic cell. In electrical synaptic transmission, electrical signals are communicated as an ionic current flow across ELECTRICAL SYNAPSES.Stimulation, Chemical: The increase in a measurable parameter of a PHYSIOLOGICAL PROCESS, including cellular, microbial, and plant; immunological, cardiovascular, respiratory, reproductive, urinary, digestive, neural, musculoskeletal, ocular, and skin physiological processes; or METABOLIC PROCESS, including enzymatic and other pharmacological processes, by a drug or other chemical.Kinetics: The rate dynamics in chemical or physical systems.Reference Values: The range or frequency distribution of a measurement in a population (of organisms, organs or things) that has not been selected for the presence of disease or abnormality.Sodium: A member of the alkali group of metals. It has the atomic symbol Na, atomic number 11, and atomic weight 23.Adrenal Gland Neoplasms: Tumors or cancer of the ADRENAL GLANDS.Kidney: Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.Hypothalamus, Anterior: The front portion of the HYPOTHALAMUS separated into the preoptic region and the supraoptic region. The preoptic region is made up of the periventricular GRAY MATTER of the rostral portion of the THIRD VENTRICLE and contains the preoptic ventricular nucleus and the medial preoptic nucleus. The supraoptic region contains the PARAVENTRICULAR HYPOTHALAMIC NUCLEUS, the SUPRAOPTIC NUCLEUS, the ANTERIOR HYPOTHALAMIC NUCLEUS, and the SUPRACHIASMATIC NUCLEUS.Analysis of Variance: A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.Cardiovascular System: The HEART and the BLOOD VESSELS by which BLOOD is pumped and circulated through the body.Antidepressive Agents, Tricyclic: Substances that contain a fused three-ring moiety and are used in the treatment of depression. These drugs block the uptake of norepinephrine and serotonin into axon terminals and may block some subtypes of serotonin, adrenergic, and histamine receptors. However the mechanism of their antidepressant effects is not clear because the therapeutic effects usually take weeks to develop and may reflect compensatory changes in the central nervous system.Adrenergic beta-1 Receptor Agonists: Compounds that bind to and activate ADRENERGIC BETA-1 RECEPTORS.Chromatography, High Pressure Liquid: Liquid chromatographic techniques which feature high inlet pressures, high sensitivity, and high speed.Cells, Cultured: Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.Oxygen Consumption: The rate at which oxygen is used by a tissue; microliters of oxygen STPD used per milligram of tissue per hour; the rate at which oxygen enters the blood from alveolar gas, equal in the steady state to the consumption of oxygen by tissue metabolism throughout the body. (Stedman, 25th ed, p346)Ganglia, Sympathetic: Ganglia of the sympathetic nervous system including the paravertebral and the prevertebral ganglia. Among these are the sympathetic chain ganglia, the superior, middle, and inferior cervical ganglia, and the aorticorenal, celiac, and stellate ganglia.Pentolinium Tartrate: A nicotinic antagonist that has been used as a ganglionic blocking agent in hypertension.Glucagon: A 29-amino acid pancreatic peptide derived from proglucagon which is also the precursor of intestinal GLUCAGON-LIKE PEPTIDES. Glucagon is secreted by PANCREATIC ALPHA CELLS and plays an important role in regulation of BLOOD GLUCOSE concentration, ketone metabolism, and several other biochemical and physiological processes. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1511)Oxymetazoline: A direct acting sympathomimetic used as a vasoconstrictor to relieve nasal congestion. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1251)Vas Deferens: The excretory duct of the testes that carries SPERMATOZOA. It rises from the SCROTUM and joins the SEMINAL VESICLES to form the ejaculatory duct.Chromaffin Granules: Organelles in CHROMAFFIN CELLS located in the adrenal glands and various other organs. These granules are the site of the synthesis, storage, metabolism, and secretion of EPINEPHRINE and NOREPINEPHRINE.Guinea Pigs: A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.Aorta, Thoracic: The portion of the descending aorta proceeding from the arch of the aorta and extending to the DIAPHRAGM, eventually connecting to the ABDOMINAL AORTA.Infusions, Intravenous: The long-term (minutes to hours) administration of a fluid into the vein through venipuncture, either by letting the fluid flow by gravity or by pumping it.Dopamine Uptake Inhibitors: Drugs that block the transport of DOPAMINE into axon terminals or into storage vesicles within terminals. Most of the ADRENERGIC UPTAKE INHIBITORS also inhibit dopamine uptake.Chromaffin System: The cells of the body which stain with chromium salts. They occur along the sympathetic nerves, in the adrenal gland, and in various other organs.Blood Vessels: Any of the tubular vessels conveying the blood (arteries, arterioles, capillaries, venules, and veins).Hydroxyindoleacetic AcidMorpholinesRenal Circulation: The circulation of the BLOOD through the vessels of the KIDNEY.Hypothalamus, Middle: Middle portion of the hypothalamus containing the arcuate, dorsomedial, ventromedial nuclei, the TUBER CINEREUM and the PITUITARY GLAND.Sodium Chloride: A ubiquitous sodium salt that is commonly used to season food.Homovanillic AcidAmphetamine: A powerful central nervous system stimulant and sympathomimetic. Amphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulation of release of monamines, and inhibiting monoamine oxidase. Amphetamine is also a drug of abuse and a psychotomimetic. The l- and the d,l-forms are included here. The l-form has less central nervous system activity but stronger cardiovascular effects. The d-form is DEXTROAMPHETAMINE.Imidazoles: Compounds containing 1,3-diazole, a five membered aromatic ring containing two nitrogen atoms separated by one of the carbons. Chemically reduced ones include IMIDAZOLINES and IMIDAZOLIDINES. Distinguish from 1,2-diazole (PYRAZOLES).Lipid Mobilization: LIPOLYSIS of stored LIPIDS in the ADIPOSE TISSUE to release FREE FATTY ACIDS. Mobilization of stored lipids is under the regulation of lipolytic signals (CATECHOLAMINES) or anti-lipolytic signals (INSULIN) via their actions on the hormone-sensitive LIPASE. This concept does not include lipid transport.Adrenergic beta-2 Receptor Antagonists: Drugs that bind to and block the activation of ADRENERGIC BETA-2 RECEPTORS.Tetralones: A group of TETRAHYDRONAPHTHALENES containing a keto oxygen.Nitric Oxide: A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.Body Weight: The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.Hormones: Chemical substances having a specific regulatory effect on the activity of a certain organ or organs. The term was originally applied to substances secreted by various ENDOCRINE GLANDS and transported in the bloodstream to the target organs. It is sometimes extended to include those substances that are not produced by the endocrine glands but that have similar effects.Posture: The position or attitude of the body.Metanephrine: Product of epinephrine O-methylation. It is a commonly occurring, pharmacologically and physiologically inactive metabolite of epinephrine.Ganglionectomy: Removal of an autonomic or sensory ganglion by any means.

Extra-vesicular binding of noradrenaline and guanethidine in the adrenergic neurones of the rat heart: a proposed site of action of adrenergic neurone blocking agents. (1/10407)

1 The binding and efflux characteristics of [14C]-guanethidine and [3H]-noradrenaline were studied in heart slices from rats which were pretreated with reserpine and nialamide. 2 Binding of both compounds occurred at extra-vesicular sites within the adrenergic neurone. After a brief period of rapid washout, the efflux of [14C]-guanethidine and [3H]-noradrenaline proceeded at a steady rate. The efflux of both compounds appeared to occur from a single intraneuronal compartment. 3 (+)-Amphetamine accelerated the efflux of [14C]-noradrenaline; this effect was inhibited by desipramine. 4 Unlabelled guanethidine and amantadine also increased the efflux of labelled compounds. Cocaine in high concentrations increased slightly the efflux of [14C]-guanethidine but not that of [3H]-noradrenaline. 5 Heart slices labelled with [3H]-noradrenaline became refractory to successive exposures to releasing agents although an appreciable amount of labelled compound was still present in in these slices. 6 It is suggested that [14C]-guanethidine and [3H]-noradrenaline are bound at a common extravesicular site within the adrenergic neurone. Binding of guanethidine to the extra-vesicular site may be relevant to its pharmacological action, i.e., the blockade of adrenergic transmission.  (+info)

Long-term effects of N-2-chlorethyl-N-ethyl-2-bromobenzylamine hydrochloride on noradrenergic neurones in the rat brain and heart. (2/10407)

1 N-2-Chlorethyl-N-ethyl-2-bromobenzylamine hydrochloride (DSP 4) 50 mg/kg intraperitoneally, produced a long-term decrease in the capacity of brain homogenates to accumulate noradrenaline with significant effect 8 months after the injection. It had no effect on the noradrenaline uptake in homogenates from the striatum (dopamine neurones) and on the uptake of 5-hydroxytryptamine (5-HT) in various brain regions. 2 In vitro DSP 4 inhibited the noradrenaline uptake in a cortical homogenate with an IC50 value of 2 muM but was more than ten times less active on the dopamine uptake in a striatal homogenate and the 5-HT uptake in a cortical homogenate. 3 DSP 4 (50 mg/kg i.p.) inhibited the uptake of noradrenaline in the rat heart atrium in vitro but this action was terminated within 2 weeks. 4 DSP 4 (50 mg/kg i.p.) cuased a decrease in the dopamine-beta-hydroxylase (DBH) activity in the rat brain and heart. The onset of this effect was slow; in heart a lag period of 2-4 days was noted. In brain the DBH-activity in cerebral cortex was much more decreased than that in hypothalamus which was only slightly affected. A significant effect was still found 8 months after the injection. The noradrenaline concentration in the brain was greatly decreased for at least two weeks, whereas noradrenaline in heart was only temporarily reduced. 5 The long-term effects of DSP 4 on the noradrenaline accumulation, the DBH activity and noradrenaline concentration in the rat brain were antagonized by desipramine (10 mg/kg i.p.). 6 It is suggested that DSP 4 primarily attacks the membranal noradrenaline uptake sites forming a covalent bond and that the nerve terminals, as a result of this binding, degenerate.  (+info)

Studies on the mechanism of action of amantadine. (3/10407)

1 The effect of amantadine hydrochloride on various aspects of catecholamine metabolism in the rat brain has been investigated. 2 Amantadine failed to have any significant effect on brain concentrations of dopamine or noradrenaline even when administered daily for 9 days. 3 Amantadine had no effect on the rate of decline of noradrenaline and dopamine concentrations after alpha-methyl-p-tyrosine. 4 In vitro amantadine inhibited dopamine uptake into synaptosomes only at high concentrations, and caused little release of dopamine from synaptosomes. 5 There is no evidence from these results to suggest that the anti-Parkinsonian effect of amantadine is related to an action on dopaminergic mechanisms.  (+info)

Further evidence that prostaglandins inhibit the release of noradrenaline from adrenergic nerve terminals by restriction of availability of calcium. (4/10407)

1 Guinea-pig vasa deferentia were continuously superfused after labelling the transmitter stores with [3H](-)-noradrenaline. Release of [3H]-(-)-noradrenaline was induced by transmural nerve stimulation. 2 Prostglandin E2 (14 nM) drastically reduced the release of [3H]-(-)-noradrenaline, while tetraethylammonium (2 mM), rubidium (6 mM), phenoxybenzamine (3 muM) each in the presence or absence of Uptake 1 or 2 blockade, and prolonged pulse duration (from 0.5 to 2.0 ms) all significantly increased the release of [3H]-(-)-noradrenaline per nerve impulse. 3 The inhibitory effect of prostaglandin E2 on evoked release of [3H]-(-)-noradrenaline was significantly reduced by tetraethylammonium, rubidium and prolonged pulse duration, whilst it was actually enhanced by phenoxybenzamine. This indicates that increased release of noradrenaline per nerve impulse does not per se counteract the inhibitory effect of prostaglandin E2. 4 It is concluded that tetraethylammonium, rubidium and prolonged pulse duration counteracted the inhibitory effect of prostaglandin E2 on T3H]-(-)-noradrenaline release by promoting calcium influx during the nerve action potential. The results are consistent with, and add more weight to the view that prostaglandins inhibit the release of noradrenaline by restriction of calcium availability.  (+info)

Modulation of long-term synaptic depression in visual cortex by acetylcholine and norepinephrine. (5/10407)

In a slice preparation of rat visual cortex, we discovered that paired-pulse stimulation (PPS) elicits a form of homosynaptic long-term depression (LTD) in the superficial layers when carbachol (CCh) or norepinephrine (NE) is applied concurrently. PPS by itself, or CCh and NE in the absence of synaptic stimulation, produced no lasting change. The LTD induced by PPS in the presence of NE or CCh is of comparable magnitude with that obtained with prolonged low-frequency stimulation (LFS) but requires far fewer stimulation pulses (40 vs 900). The cholinergic facilitation of LTD was blocked by atropine and pirenzepine, suggesting involvement of M1 receptors. The noradrenergic facilitation of LTD was blocked by urapidil and was mimicked by methoxamine, suggesting involvement of alpha1 receptors. beta receptor agonists and antagonists were without effect. Induction of LTD by PPS was inhibited by NMDA receptor blockers (completely in the case of NE; partially in the case of CCh), suggesting that one action of the modulators is to control the gain of NMDA receptor-dependent homosynaptic LTD in visual cortex. We propose that this is a mechanism by which cholinergic and noradrenergic inputs to the neocortex modulate naturally occurring receptive field plasticity.  (+info)

Allyl-containing sulfides in garlic increase uncoupling protein content in brown adipose tissue, and noradrenaline and adrenaline secretion in rats. (6/10407)

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)

Sympathetic nerve alterations assessed with 123I-MIBG in the failing human heart. (7/10407)

Norepinephrine (NE) reuptake function is impaired in heart failure and this may participate in myocyte hyperstimulation by the neurotransmitter. This alteration can be assessed by 123I-metaiodobenzylguanidine (MIBG) scintigraphy. METHODS: To determine whether the impairment of neuronal NE reuptake was reversible after metoprolol therapy, we studied 18 patients (43+/-7 y) with idiopathic dilated cardiomyopathy who were stabilized at least for 3 mo with captopril and diuretics. Patients underwent, before and after 6 mo of therapy with metoprolol, measurements of radionuclide left ventricular ejection fraction (LVEF), maximal oxygen consumption and plasma NE concentration. The cardiac adrenergic innervation function was scintigraphically assessed with MIBG uptake and release measurements on the planar images obtained 20 min and 4 h after tracer injection. To evaluate whether metoprolol had a direct interaction with cardiac MIBG uptake and release, six normal subjects were studied before and after a 1-mo metoprolol intake. RESULTS: In controls, neither cardiac MIBG uptake and release nor circulating NE concentration changed after the 1-mo metoprolol intake. Conversely, after a 6-mo therapy with metoprolol, patients showed increased cardiac MIBG uptake (129%+/-10% versus 138%+/-17%; P = 0.009), unchanged cardiac MIBG release and decreased plasma NE concentration (0.930+/-412 versus 0.721+/-0.370 ng/mL; P = 0.02). In parallel, patients showed improved New York Heart Association class (2.44+/-0.51 versus 2.05+/-0.23; P = 0.004) and increased LVEF (20%+/-8% versus 27%+/-8%; P = 0.0005), whereas maximal oxygen uptake remained unchanged. CONCLUSION: Thus, a parallel improvement of myocardial NE reuptake and of hemodynamics was observed after a 6-mo metoprolol therapy, suggesting that such agents may be beneficial in heart failure by directly protecting the myocardium against excessive NE stimulation.  (+info)

Influence of vesicular storage and monoamine oxidase activity on [11C]phenylephrine kinetics: studies in isolated rat heart. (8/10407)

[11C]Phenylephrine (PHEN) is a radiolabeled analogue of norepinephrine that is transported into cardiac sympathetic nerve varicosities by the neuronal norepinephrine transporter and taken up into storage vesicles localized within the nerve varicosities by the vesicular monoamine transporter. PHEN is structurally related to two previously developed sympathetic nerve markers: [11C]-meta-hydroxyephedrine and [11C]epinephrine. To better characterize the neuronal handling of PHEN, particularly its sensitivity to neuronal monoamine oxidase (MAO) activity, kinetic studies in an isolated working rat heart system were performed. METHODS: Radiotracer was administered to the isolated working heart as a 10-min constant infusion followed by a 110-min washout period. Two distinctly different approaches were used to assess the sensitivity of the kinetics of PHEN to MAO activity. In the first approach, oxidation of PHEN by MAO was inhibited at the enzymatic level with the MAO inhibitor pargyline. In the second approach, the two hydrogen atoms on the a-carbon of the side chain of PHEN were replaced with deuterium atoms ([11C](-)-alpha-alpha-dideutero-phenylephrine [D2-PHEN]) to inhibit MAO activity at the tracer level. The importance of vesicular uptake on the kinetics of PHEN and D2-PHEN was assessed by inhibiting vesicular monoamine transporter-mediated storage into vesicles with reserpine. RESULTS: Under control conditions, PHEN initially accumulated into the heart at a rate of 0.72+/-0.15 mL/min/g wet. Inhibition of MAO activity with either pargyline or di-deuterium substitution did not significantly alter this rate. However, MAO inhibition did significantly slow the clearance of radioactivity from the heart during the washout phase of the study. Blocking vesicular uptake with reserpine reduced the initial uptake rates of PHEN and D2-PHEN, as well as greatly accelerated the clearance of radioactivity from the heart during washout. CONCLUSION: These studies indicate that PHEN kinetics are sensitive to neuronal MAO activity. Under normal conditions, efficient vesicular storage of PHEN serves to protect the tracer from rapid metabolism by neuronal MAO. However, it is likely that leakage of PHEN from the storage vesicles and subsequent metabolism by MAO lead to an appreciable clearance of radioactivity from the heart.  (+info)

*Norepinephrine transporter

This requires norepinephrine to diffuse from the site it is released to the transporter for reuptake. Norepinephrine ... norepinephrine) transporter and consequently a phenotype of impaired neuronal reuptake of norepinephrine has been implicated in ... norepinephrine-dopamine reuptake inhibitors (NDRIs), norepinephrine reuptake inhibitors (NRIs or NERIs) and the tricyclic ... "Sodium-dependent norepinephrine-induced currents in norepinephrine-transporter-transfected HEK-293 cells blocked by cocaine and ...

*Talopram

... (Lu 3-010), also known as phthalapromine, is a selective norepinephrine reuptake inhibitor (NRI) which was researched ... "From the Selective Serotonin Transporter Inhibitor Citalopram to the Selective Norepinephrine Transporter Inhibitor Talopram: ...

*Norepinephrine

The general function of norepinephrine is to mobilize the brain and body for action. Norepinephrine release is lowest during ... A significant part of the damage is due to the effects of sustained norepinephrine release, because of norepinephrine's general ... A variety of medically important drugs work by altering the actions of norepinephrine systems. Norepinephrine itself is widely ... Once in the synapse, norepinephrine binds to and activates receptors. After an action potential, the norepinephrine molecules ...

*Alpha blocker

Specifically, norepinephrine and epinephrine are secreted by these tumors, either continuously or intermittently. The excess ... This drug blocks the activity of epinephrine and norepinephrine by antagonizing the alpha receptors, thus decreasing vascular ... been efficacious in treating patients with PTSD induced nightmares due to its ability to block the effects of norepinephrine. ...

*Phentolamine

... typically of norepinephrine. Epinephrine infusions are less vasoconstrictive than norepinephrine as they primarily stimulate β ... By abolishing this negative feedback phentolamine leads to even less regulated norepinephrine release, which results in a more ... releasing norepinephrine. In response, the β1 adrenergic receptors on the heart increase its rate, contractility, and ... which function predominantly as presynaptic negative feedback for norepinephrine release. ...

*Norepinephrine (medication)

Norepinephrine acts on beta-1 adrenergic receptors, causing increase in heart rate and cardiac output. Norepinephrine is the ... Norepinephrine works by binding and activating alpha adrenergic receptors. Norepinephrine was discovered in 1946 and was ... Norepinephrine, also known as noradrenaline, is a medication used to treat people with very low blood pressure. It is the ... Norepinephrine is used mainly as a sympathomimetic drug to treat people in vasodilatory shock states such as septic shock and ...

*Norepinephrine releasing agent

A norepinephrine releasing agent (NRA), also known as an adrenergic releasing agent, is a catecholaminergic type of drug which ... A closely related type of drug is a norepinephrine reuptake inhibitor (NRI). Another class of drugs that stimulates adrenergic ... This in turn leads to increased extracellular concentrations of norepinephrine and epinephrine therefore an increase in ... induces the release of norepinephrine (noradrenaline) and epinephrine (adrenaline) from the pre-synaptic neuron into the ...

*Norepinephrine reuptake inhibitor

A norepinephrine reuptake inhibitor (NRI, NERI) or adrenergic reuptake inhibitor (ARI), is a type of drug that acts as a ... However, norepinephrine has been implicated as acting synergistically with dopamine when actions on the two neurotransmitters ... A closely related type of drug is a norepinephrine releasing agent (NRA). Many NRIs exist, including the following: Pure ... A meta analysis published in BMJ in 2011 concluded that the selective norepinephrine reuptake inhibitor reboxetine is ...

*Norepinephrine-dopamine disinhibitor

Norepinephrine and dopamine disinhibitors (NDDIs) are a class of drugs which act at specific sites to disinhibit downstream ... Flibanserin disinhibits norepinephrine and dopamine release in the prefrontal cortex by activating 5-HT1A receptors in this ... Agomelatine, an antidepressant which disinhibits norepinephrine and dopamine release in the frontal cortex by antagonizing 5- ... Stahl SM (October 2007). "Novel mechanism of antidepressant action: norepinephrine and dopamine disinhibition (NDDI) plus ...

*Norepinephrine-dopamine releasing agent

A norepinephrine-dopamine releasing agent (NDRA) is a type of drug which induces the release of norepinephrine (and epinephrine ... A closely related type of drug is a norepinephrine-dopamine reuptake inhibitor (NDRI). Monoamine releasing agent. ...

*Norepinephrine-dopamine reuptake inhibitor

A closely related type of drug is a norepinephrine-dopamine releasing agent (NDRA). Norepinephrine-dopamine reuptake inhibitors ... A norepinephrine-dopamine reuptake inhibitor (NDRI) is a drug that acts as a reuptake inhibitor for the neurotransmitters ... This in turn leads to increased extracellular concentrations of both norepinephrine and dopamine and, therefore, an increase in ... Stahl, S. M. (2004). "A review of the neuropharmacology of bupropion, a dual norepinephrine and dopamine reuptake inhibitor". ...

*Serotonin-norepinephrine reuptake inhibitor

2005). "Discovery and structure-activity relationships of novel selective norepinephrine and dual serotonin/norepinephrine ... normal levels of norepinephrine in the synaptic clefts. Overall, inhibition of norepinephrine reuptake induced by TCAs, leads ... while milnacipran is three times more selective for norepinephrine than serotonin. Elevation of norepinephrine levels is ... Atomoxetine-a norepinephrine-predominant SNRI used in the treatment of ADHD and, off-label, major depression. Was approved by ...

*Serotonin-norepinephrine releasing agent

A serotonin-norepinephrine releasing agent (SNRA) is a type of drug which induces the release of serotonin and norepinephrine ( ... A closely related type of drug is a serotonin-norepinephrine reuptake inhibitor (SNRI). Monoamine releasing agent Serotonin ... releasing agent Norepinephrine releasing agent Serotonin-dopamine releasing agent Serotonin-norepinephrine-dopamine releasing ... a norepinephrine releasing agent, is a functional SNRA that was formerly used as an appetite suppressant for the treatment of ...

*Serotonin-norepinephrine-dopamine releasing agent

Monoamine releasing agent Norepinephrine-dopamine releasing agent Serotonin-dopamine releasing agent Serotonin-norepinephrine ... A serotonin-norepinephrine-dopamine releasing agent (SNDRA), also known as a triple releasing agent (TRA), is a type of drug ... A closely related type of drug is a serotonin-norepinephrine-dopamine reuptake inhibitor (SNDRI). Examples of SNDRAs include ... which induces the release of serotonin, norepinephrine/epinephrine, and dopamine in the brain and body. SNDRAs produce ...

*Serotonin-norepinephrine-dopamine reuptake inhibitor

... norepinephrine, and dopamine. It does this by concomitantly inhibiting the serotonin transporter (SERT), norepinephrine ... A serotonin-norepinephrine-dopamine reuptake inhibitor (SNDRI), also known as a triple reuptake inhibitor (TRI), is a type of ... The mood changes induced by AMPT may be mediated by decreases in norepinephrine, while changes in selective attention and ... They are also very similar to serotonin-norepinephrine-dopamine releasing agents (SNDRAs) like MDMA ("ecstasy") and α- ...

*Atypical antipsychotic

... which is why weight gain occurs with some antipsychotics if the norepinephrine is not inhibited. Inhibition of norepinephrine ... Increased norepinephrine can cause increased glucose levels, which is to say blood sugar levels. Increased blood sugar levels ... "norepinephrine". Cardiosmart.org. 2010-12-15. Retrieved 2016-09-30. Veves A, Malik RA (2008-02-01). Diabetic Neuropathy: ... The atypical antipsychotics integrate with the serotonin (5-HT), norepinephrine (α, β), and dopamine (D) receptors in order to ...

*Antidepressant

Serotonin-norepinephrine reuptake inhibitors (SNRIs) are potent inhibitors of the reuptake of serotonin and norepinephrine. ... serotonin-norepinephrine reuptake inhibitors (SNRIs) and norepinephrine reuptake inhibitors (NRIs). Adverse effects have been ... Norepinephrine reuptake inhibitors (NRIs or NERIs) are a type of drug that acts as a reuptake inhibitor for the ... However, norepinephrine has been implicated as acting synergistically with dopamine when actions on the two neurotransmitters ...

*D-DOPA

Norepinephrine (Noradrenaline; Levophed, etc.) Epinephrine (Adrenaline; Adrenalin, EpiPen, Twinject, etc.). ...

*Neuropeptide

Norepinephrine (noradrenaline). In neurons of the A2 cell group in the nucleus of the solitary tract), norepinephrine co-exists ...

*Methyldopa

Dopamine is a precursor for norepinephrine (noradrenaline) and subsequently epinephrine (adrenaline). This inhibition results ... Norepinephrine (noradrenaline; Levophed, etc.) Epinephrine (adrenaline; Adrenalin, EpiPed, Twinject, etc.) "Methyldopa". The ...

*Adrenal medulla

It is the innermost part of the adrenal gland, consisting of cells that secrete epinephrine (adrenaline), norepinephrine ( ... norepinephrine, and dopamine. Because the ANS, specifically the sympathetic division, exerts direct control over the chromaffin ... the entire body cannot efficiently produce epinephrine and norepinephrine from dopamine, this results in severe dysautonomia ... but most crucially due to autonomous nervous system failure which requires epinephrine and norepinephrine as neurotransmitters ...

*RTI-113

Sofuoglu M, Sewell RA (April 2009). "Norepinephrine and stimulant addiction". Addiction Biology. 14 (2): 119-129. doi:10.1111/j ...

*Etoperidone

... norepinephrine transporter (20,000 nM) > dopamine transporter (52,000 nM). Etoperidone is metabolized in part to meta- ...

*List of phenyltropanes

Hanna, Mona M. (2007). "Synthesis of some tropane derivatives of anticipated activity on the reuptake of norepinephrine and/or ... Norepinephrine transporter selective compounds". Journal of Medicinal Chemistry. 48 (11): 3852-3857. doi:10.1021/jm058164j. ... and norepinephrine transporters". Journal of Medicinal Chemistry. 36 (20): 2886-2890. doi:10.1021/jm00072a007. PMID 8411004. ... 3-Phenyltropane Analogs with High Affinity for the Dopamine and Serotonin Transporters and Low Affinity for the Norepinephrine ...
In the present study, we evaluated the involvement of norepinephrine neurons within the AV3V region in the central action of Ang II and found that norepinephrine turnover was increased by intracerebroventricular Ang II in SHR but not in WKY.. The role of norepinephrine neurons of the central nervous system in the development and maintenance of hypertension has been investigated either by measurement of tissue norepinephrine content or the activity of catecholamine synthesizing enzyme or by evaluation of norepinephrine turnover of the various nuclei. Norepinephrine content is either increased17 or decreased13 18 in the brain stem or hypothalamus of SHR. On the other hand, the activity of the norepinephrine-forming enzyme dopamine β-hydroxylase is decreased in hypothalamic nuclei of SHR. As regards norepinephrine turnover in hypertensive animals, Patel et al19 reported that norepinephrine turnover was decreased in the cortex of young SHR and increased in the hypothalamus of adult SHR. They also ...
BioAssay record AID 179408 submitted by ChEMBL: Concentration that inhibits 50% S-AMPA stimulated (50 uM) [3H]norepinephrine release from rat hippocampal synaptosomes.
Our findings showed a clear association between the orthostatic plasma norepinephrine level and symptom severity in patients with POTS. The orthostatic plasma norepinephrine level of POTS patients also associated with the increment of heat rate from supine position to standing. Especially, we found that the effectiveness of metoprolol in POTS children was related to the level of orthostatic plasma norepinephrine. Our results indicate that plasma level of norepinephrine , 3.59 pg/ml is an indicator of the effectiveness of metoprolol in children and adolescents with POTS.. Children with POTS often have symptoms of OI, such as syncope, dizziness, chest distress, chest pain, headache, palpitation, fatigue, and so on [1]-[4]. Additionally, the recurrent symptoms usually create physical and psychological stresses in childrens daily lives, both at home and school [5],[23],[24]. Therefore, an effective treatment, to improve symptoms, is necessary for the children with POTS.. No definite cause of ...
Ouabain-insensitive salt and water movements in duck red cells. II. Norepinephrine stimulation of sodium plus potassium cotransport ...
Rats were treated with phenylhydrazine. Following the rapid onset of anemia, there was a loss of 60 percent of the stored norepinephrine in the heart within 48 hours of treatment. Associated with the loss of cardiac norepinephrine was an increase in the wet weight of the heart, reaching 40 percent above control 48 hours after treatment. Phenylhydrazine itself probably does not directly mediate this depletion since the vas deferens, brain and spleen have a normal store of norepinephrine at 48 hours. Anemia was also induced by treating rats with antirat red blood cell serum. The hearts of these rats were also depleted of norepinephrine. These experiments show that during two forms of anemia there is a loss of norepinephrine from the sympathetic neurons innervating the heart.
The higher efficacy of MSNA on TPR in elderly blacks than whites suggests that sympathetic vascular transduction at the arterioles and/or other nonadrenergic mechanisms concurrently responsible for vasoconstriction may be enhanced in blacks. The enhanced sympathetic vascular transduction may be attributed to a higher concentration of norepinephrine at the neurovascular junction and/or a greater sensitivity/density of postsynaptic adrenergic receptors. Both supine and upright plasma norepinephrine concentrations were similar between groups despite the lower total MSNA response during tilting in blacks. We recognize that plasma norepinephrine is not a direct index of the synaptic level of norepinephrine; however, the change in plasma norepinephrine concentration has been found to correlate well with the interindividual response in MSNA.32 Therefore, the greater sympathetic vascular transduction in elderly blacks may be attributable to a higher synaptic norepinephrine release per unit increase of ...
Norepinephrine (chemical name C8H11NO3)is a catecholamine present in the human brain, sometimes referred to as noradrenaline. Norepinephrine acts as a hormone when it is released from the adrenal glands into the bloodstream. In concert with epinephrine, norepinephrine influences the fight or flight response by increasing heart rate and muscle readiness, and increasing energy by causing glucose release, thereby heightening readiness to respond (e.g., to fight or flee) to a stressful event. Norepinephrine also acts as a neurotransmitter in the central nervous system and sympathetic nervous system. It influences alertness and arousal, and lower levels are associated with depressed mood. Many antidepressant medications cause increased norepinephrine levels in the brain. Drugs that increase norepinephrine are also used in the treatment of Attention Deficit Hyperactivity Disorder and hypotension (low blood pressure). ...
The release of preloaded radiolabeled norepinephrine ([3H]NE) from slices of rat hippocampus can be stimulated by excitatory amino acids that interact with the N-methyl-D-aspartate (NMDA) receptor. The acidic dipeptide N-acetyl-L-aspartylglutamate (NAAG) is colocalized with NE in the cell bodies of locus coeruleus (the origin of the noradrenergic projections to the hippocampus) and the hippocampus itself. The function of NAAG in these neurons has not been demonstrated, although evidence exists that it may serve as a neuromodulator in other neuronal pathways. NAAG inhibited the release of [3H]NE stimulated by NMDA and L-glutamate in a concentration-related manner. The maximal inhibition produced by NAAG was about 25% of the control release stimulated by 25 microM NMDA. The effects observed were caused by the intact dipeptide and not the degradation artifacts produced by the enzyme N-acetylated-alpha-linked-acidic dipeptidase because N-acetyl-L-aspartate had no significant effect on the release ...
Disappearance rates of intracisternally administered 3H-norepinephrine and activities of tyrosine hydroxylase were examined in the rabbit in five brain regions (telencephalon, hypothalamus, midbrain, medulla-pons, and cerebellum) and in three cord regions (cervical, thoracolumbar, and lumbosacral) 2 weeks after section of the carotid sinus and aortic nerves. Mean blood pressure rose by 29% and heart rate by 17% in the animals with neurogenic hypertension. Endogenous catecholamine concentrations in the eight regions examined were not altered by denervation. In the thoracolumbar region of the spinal cord, 3H-norepinephrine turnover and tyrosine hydroxylase activity were increased approximately twofold in hypertensive rabbits. We suggest that these changes reflect increased physiological activity of bulbospinal noradrenergic neurons and that this increase may mediate the rise in arterial pressure or heart rate that follows sinoaortic denervation. The turnover of 3H-norepinephrine increased in the ...
Amphetamine released 3-H-norepinephrine from rat cerebral cortex tissue which had previously accumulated the 3-H-amine. Destruction of noradrenergic nerve endings by pretreatment of the rats with 6-hydroxydopamine inhibited the accumulation of 3-H-norepinephrine by the tissue and reduced the proportion of the 3-H-amine which was released by amphetamine. Inhibition of storage of 3-H-norepinephrine within nerve endings by pretreatment of the animals with reserpine also reduced accumulation of 3-H-norepinephrine but did not reduce the proportion of the accumulated 3-H-amine which was released by amphetamine. The addition of desipramine (an inhibitor of neuronal uptake) further reduced the accumulation of 3-H-norepinephrine in animals pretreated with reserpine but had no further effect in animals pretreated with 6-hydroxydopamine. A greater proportion of the 3-H-norepinephrine was converted to 3-H-deaminated metabolites in tissues of reserpine-treated animals than in the tissues of control or ...
Feldman, J M.; Blalock, J A.; and Zern, R T., "Elevated hypothalamic norepinephrine content in mice with the hereditary obese-hyperglycemic syndrome." (1979). Subject Strain Bibliography 1979. 2970 ...
Background The sympathetic neurotransmitter Norepinephrine (NE) contributes to tumorigenesis and cancer progression. This study aims to investigate the role of NE in modulating the immune phenotype and allowing pancreatic carcinoma (PC) cells to escape the immune response. Methods Varied concentrations of NE and interferon-gamma (IFN-γ) were administrated to MIA PaCa-2 and BxPC-3 cell lines for 48 hours. Proliferation and invasion were then investigated using an MTT assay and a membrane invasion culture system respectively. MHC-I, B7-1, IDO and B7-H1 expression were measured using real-time quantitative RT-PCR, western blotting and immunocytochemistry. The synergistic and time-dependent effects of NE/IFN-γ were also investigated. Adrenergic antagonists were used to identify the relevant target receptor of NE. Results The results showed that NE had dose-dependent and time-dependent effects on cell biological processes as well as on the expression of MHC-I, B7-1, IDO and B7-H1. These effects
Noradrenergic neurons in the hypothalamus involved in feeding and satiety are activated by gastrointestinal receptors. In the unrestrained rat, sites were first identified at which norepinephrine injected in the medial hypothalamus caused spontaneous feeding, or in the lateral hypothalamus caused no response. The activity of in vivo norepinephrine at these two sites was characterized by localized push-pull perfusion. When a nutrient was infused directly into the rats duodenum, the synaptic release of hypothalamic norepinephrine was enhanced at lateral sites insensitive to norepinephrine, but suppressed at medial sites reactive to norepinephrine. Thus, signals from duodenal receptors are conceivably sent to the rats brain to end feeding by way of noradrenergic inhibitory neurons in the hypothalamus. ...
The ability of normal and transplanted dog hearts to make, bind, store, and metabolize norepinephrine was studied. Transplanted hearts were used in order to assess the effects of adrenergic denervation. Normal hearts bound large quantities of administered C14-dopamine and synthesized considerable quantities of norepinephrine in both the atria and ventricles. Isolated perfused normal hearts steadily removed about 56% of infused dl-H3-norepinephrine; a binding mechanism was the major means of inactivation of the amine. Uptake of radioactive norepinephrine was greater in the ventricles than in the atria because they received more of the amine, and the turnover rate of the labeled amine was also highest in the ventricles. Subcellular fractionation of the bound amine demonstrated that it was localized in particles of microsomal size; radioautographic studies demonstrated the presence of H3-norepinephrine only in association with nerves. About 57% of the H3-norepinephrine released from normal hearts ...
Norepinephrine (NE), also called noradrenaline (NA) or noradrenalin, is an organic chemical in the catecholamine family that functions in the brain and body as a hormone and neurotransmitter. The name "noradrenaline", derived from Latin roots meaning "at/alongside the kidneys", is more commonly used in the United Kingdom; in the United States, "norepinephrine," derived from Greek roots having that same meaning, is usually preferred. "Norepinephrine" is also the international nonproprietary name given to the drug. Regardless of which name is used for the substance itself, parts of the body that produce or are affected by it are referred to as noradrenergic. In the brain, norepinephrine is produced in nuclei that are small yet exert powerful effects on other brain areas. The most important of these nuclei is the locus coeruleus, located in the pons. Outside the brain, norepinephrine is used as a neurotransmitter by sympathetic ganglia located near the spinal cord or in the abdomen, and it is also ...
Monkeys, trained to perform a discrete trial, cued avoidance task, were used to measure the effectiveness of intravenously infused norepinephrine in preventing the hypotension and performance decrement which usually follows 3000- to 30,000-rad doses of radiation. After a 4000-rad dose of mixed gamma- neutron radiation, 10 animals were infused with norepinephrine at a rate designed to maintain mean arterial blood pressure at approximately 100 mm Hg; for comparison 10 control animals were infused with only isotonic saline after similar irradiation. Norepinephrine, although generally adequate for maintaining blood pressure, did not consistently improve performance during the first 30 minutes postirradiation.
1. The sensitivity of isolated tail artery strips from adult spontaneously hypertensive (SH) and normotensive rats to endogenously released and exogenously applied noradrenaline was compared. Release or displacement of endogenous noradrenaline was obtained with electrical stimulation, tyramine, elevated potassium and potassium-free solution. Isometric contractile responses were measured before and after acute denervation with 6-hydroxydopamine or before and after treatment with phentolamine.. 2. The sensitivity to exogenous noradrenaline of innervated arterial strips was similar for SH and normotensive rats. Acute denervation produced a significant shift to the left in the concentration-response curve to noradrenaline only in SH rat arterial strips.. 3. Contractile responses to electrical stimulation and tyramine were similar in both groups before denervation. Contractile responses to potassium-free solution were greater in SH than in normotensive arterial strips. After denervation the SH and ...
Ezrin, radixin, and moesin (ERM) proteins are known to be substrates of Rho kinase (ROCK), a key player in vascular smooth muscle regulation. Their function in arteries remains to be elucidated. The objective of the present study was to investigate E
LOPEZ VERRILLI, María A; RODRIGUEZ FERMEPIN, Martín; FERNANDEZ, Belisario E y GIRONACCI, Mariela M. Role of Angiotensin (1-7) in Neuronal Norepinephrine Reuptake in Hypertension. Rev. argent. cardiol. [online]. 2010, vol.78, n.2, pp. 151-155. ISSN 1850-3748.. We have previously demonstrated that angiotensin (Ang)-(1-7) decreases the release and synthesis of norepinephrine (NE) in spontaneously hypertensive rats (SHR). In the present study, we have investigated the effect of Ang-(1-7) on neuronal NE reuptake and the expression of NE trans-porter (NET), responsible for eliminating NE from the syn-aptic cleft. Although Ang-(1-7) does not have an acute effect on NE neuronal reuptake, it plays a role in stimulating the protein content of the NET in the long-term. Ang-(1-7) activates Mas receptor and stimulates protein synthesis de novo of the transporter. In this way, Ang-(1-7) would contribute to blood pressure control through the regulation of NE levels in the synaptic cleft.. Palabras clave : ...
Norepinephrine is a drug used to increase blood pressure in patients with life-threatening infection. However, norepinephrine may limit the bloodflow to the gut, thereby causing relative lack of oxygen to the cells. This leads to increased formation of lactic acid.. This study examines whether increasing the dose of norepinephrine leads to higher concentrations of lactic acid in the rectum and stomach in patients with life-threatening infection. ...
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Medicine for norepinephrine allergy - What is the definition or description of: Norepinephrine allergy? A drug allergy? Norepinephrine is a hormone related to epinephrine (adrenalin). It is a normal constituent of the body, and a true allergy is unlikely. More likely you are describing a reaction to supplemental norepinephrine as a drug. It is primarily used to raise blood pressure in patients with shock. What type of reaction are you asking about?
Normal subjects were given glucose (300 mg/ min) or tolbutamide (1 g, intravenously), alone and during intravenous infusions of norepi-nephrine (6 lg/ min). Immunoreactive insulin concentration was less than expected during the infusions of norepinephrine, but returned to higher values after the norepinephrine infusions. From these data it is concluded that norepinephrine inhibits the release of insulin from pancreatic beta cells. ...
In myocardial ischemia, nonexocytotic noradrenaline release has been identified as underlying mechanism of ischemia-evoked noradrenaline release. Nonexocytotic noradrenaline release can be suppressed by inhibitors of the neuronal noradrenaline carrie
Inhibition of dopamine β-hydroxylase by U-14,624 results in a specific depletion of norepinephrine (NE) in both mouse brain and rat brain. A single dose of 25 mg/kg significantly reduced brain NE in both species. Maximum depletion of mouse brain NE, to less than 20% of control levels, was detected 18 hours after U-14,624, 200 mg/kg. NE levels returned to control level by 48 hours. Rat brain NE was lowered to approximately 10% of control 18 hours after U-14,624, 200 mg/kg, and brain NE concentrations were not fully restored after 24 hours. Although the initial fall in mouse brain NE was accompanied by a marked increase in brain dopamine (DA), brain DA levels in both species were at control levels or only slightly elevated at times of maximal NE depletion. Pretreatment of rats with U-14,624 slowed the incorporation of tyrosine-C14 into NE. The effectiveness of the block in the synthesis of endogenous NE was also demonstrated by the accumulation of DA resulting from 1) loading rats with L-dopa and ...
AIMS: We examined the effect of norepinephrine (NE) infusion on left ventricular function and apoptotic genes during progression of polymicrobial sepsis. METHODS: Male Sprague-Dawley rats (350-400 g) were made septic by intraperitoneal (i.p.) administration of 200mg/kg cecal inoculum. Sham animals received 5% dextrose water, i.p. Echocardiography was performed at baseline, 3 days and 7 days post-sepsis/sham. NE (0.6 μgkg(-1)h(-1)) was infused for 2h, before the end of day 3 of echocardiography. At the end of day 7, rats were euthanized and heart tissues harvested for isolation of total RNA. PCR was performed using RT(2) profiler™ PCR array PARN-012 (Rat apoptosis array; SuperArray, MD) using RT(2) Real-Time™ SYBR Green PCR master mix PA-012. KEY FINDINGS: NE-infusion resulted in a significant decrease in the left ventricular ejection fraction (EF) (62.56±2.07 from the baseline 71.11±3.23, p SIGNIFICANCE: The data suggest that upregulation of a series of pro-apoptotic molecules could be
Ephedrine has been shown to increase the effectiveness of thermogenesis (fat burning) in the body. It contributes to the release and blocks the re-uptake of the neurotransmitter norepinephrine. This gives norepinephrine the ability to continuously stimulate receptors in your ...
Why Cold Showers Are Amazing for Your Health, Body and Mind! If you could do one thing each morning to improve nearly every aspect of ...
In the present study we have demonstrated that norepinephrine, but not serotonin, activates a stem and precursor cell pool in the adult hippocampus, and have provided evidence for a direct action of norepinephrine on these precursors. Importantly, we have uncovered a novel role for β3-adrenergic receptors in mediating the norepinephrine-dependent activation of the hippocampal precursors both in vitro and in vivo. Consistent with these results, our findings from the slice-sphere assay demonstrate that antidepressants that selectively block the reuptake of norepinephrine but not serotonin enhance hippocampal neurogenesis, primarily by targeting the activity of stem and precursor cells.. The norepinephrine-responsive precursor population appears remarkably similar to the previously identified latent population of stem and precursor cells activated by depolarizing levels of KCl (Walker et al., 2008). The most striking common feature between norepinephrine- and KCl-mediated activation is the ...
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L-phenylalanine is an essential amino acid which can be converted to L-tyrosine by a complex biochemical process which takes place in the liver. L-tyrosine can be converted by neurons in the brain to dopamine and neropinphrine (noradrenaline), hormones which are depleted by stress, overwork and certain drugs. By replenishing norepinephrine in the brain, mental energy levels are enhanced, some forms of depression are alleviated, and a feeling of satiety often occurs. Because of the liver conversion necessary for L-phenylalanine to have these effects, L-tyrosine if often faster acting. In addition, the conversion step from L-tyrosine to norepinephrine may be enhanced if the cofactors (vitamins B6 and C) are included.. Some of the norepinephrine will also be converted to epinephrine (adrenaline) in the brains adrenal medulla by use of S-adenosylmenthionine (SAMe) as a methylaing agent. Since both norepinephrine and epinephrine can cause smooth muscle (arterial) contraction, care with blood ...
In particular surgical conditions, a balanced anesthesia with a high-antinociceptive contribution is required. This may induce cardiovascular impairment and thus compromise tissue oxygenation. In this prospective observational study, we investigated the hemodynamic stability and tissue oxygen saturation (StO2) in 40 patients with a high-antinociceptive general anesthesia, goal-directed fluid therapy, and norepinephrine. In addition, optimal surgical conditions and safe and fast emergence are pivotal parts of anesthetic management. In high-antinociceptive propofol/remifentanil anesthesia with bispectral index (BIS) between 40 and 60, norepinephrine was administered to maintain mean arterial pressure (MAP) above 80% of individual baseline. Fluid was administered if the ∆ plethysmographic waveform amplitude exceeded 10%. Surgical and recovery conditions, hemodynamic responses, and tissue oxygenation were investigated. Mean (SD) StO2 at the left thenar eminence increased from 83 (6)% before to 86 (4)% 20
Although stress in fetal life not only increases fetal catecholamine concentration but also decreases fetal growth, there have been few studies that define the specific role of catecholamines in mediating the fetal response to stress. None, however, have investigated effects on fetal amino acid or protein metabolism, processes that should be affected during aberrant fetal growth. Therefore, hormone concentrations as well as oxygen, glucose, lactate, and amino nitrogen, leucine, and protein metabolism were measured with and without norepinephrine infusion in fetuses of eight pregnant ewes (118-125 days of gestation). Transumbilical uptake of oxygen increased during norepinephrine infusion, whereas uptake of glucose remained constant and that of lactate and amino acids fell. The proportion of fetal oxidative metabolism that could be supported by transplacental uptake of exogenous substrates was , 1, indicating that endogenous substrates were used to maintain fetal oxidative metabolism and ...
Read "The sources of calcium for noradrenaline-induced contraction in the human thoracic internal artery, Pflügers Archiv European Journal of Physiologyl of Physiology" on DeepDyve, the largest online rental service for scholarly research with thousands of academic publications available at your fingertips.
The ability of exercise to reduce depression has long been known, and many supporting studies have been published for the last few decades. Fortunately, you dont have to run to reap the benefits. Not everyone is physically able to run, or even jog. Walking regularly can have a significant effect on depression. I think one of the better studies showed that we should walk 5 days a week, for at least a half hour, for the best benefit. http://www.health.harvard.edu/newswe...rt-excerpt.htm Also noted: Another theory is that exercise stimulates the neurotransmitter norepinephrine, which may directly improve mood. ...
four). Even though the helpful outcome of CB1 receptor antagonism in collagen-induced arthritis in mice was attributed to βtwo-receptor activation on splenocytes, numerous other mechanisms may add for the therapeutic outcomes. CB1 antagonism at sympathetic terminals bordering the synovium may need unique results depending on the magnitude of Restoration of norepinephrine stages in the joint. If βtwo signaling is restored in synovial tissue, nearby concentrations of IFN-γ and TNF may decrease, bringing about an General lower in joint destruction, synovial inflammation and pain [102, 103] (Fig. two). On the other hand, considering the fact that we shown a boost of sympathetic fibers in human synovial adipose tissue, increased norepinephrine release may well even further improve lipolysis and thereby fuel inflammation [91]. Therefore, it truly is very important to maintain norepinephrine concentrations more than a certain βtwo activation threshold in the synovium, which might only be attained ...
Norepinephrine definition is - a monoamine C8H11NO3 that is a neurotransmitter in postganglionic neurons of the sympathetic nervous system and in some parts of the central nervous system, is a vasopressor hormone of the adrenal medulla, and is a precursor of epinephrine in its major biosynthetic pathway.
Nerve cells in the brain send signals to one another by releasing chemicals called neurotransmitters that bind to specific sites on other nerve cells and activate or inhibit a cells activity. One of the neurotransmitters in the brain is called norepinephrine; it is released by specific types of nerve cells located in a region called the locus coeruleus or "LC". Scientists have observed that nerve cells in the LC are especially vulnerable to damage during Alzheimers disease. Specific binding sites for norepinephrine are known as adrenergic receptors. One type of these receptors, known as beta2-adrenergic receptor, are found in parts of the brain that receive signals from the LC, which is important for learning and memory. Decreased beta2-adrenergic signaling, as occurs when norepinephrine cells from the LC are damaged in Alzheimers disease, may contribute to impairments in learning and memory. Researchers working at the Palo Alto Institute for Research and Education, Inc., have been studying ...
Endothelial modulation of norepinephrine (NE)-induced constriction of the isolated rat aorta was studied at normal (PCO2, 41 +/- 0 mmHg) and high CO2 tensions (PCO2, 91 +/- 1 mmHg). In preparations with intact endothelium, increased CO2 tension resulted in rightward shift of the NE dose-response curve with attenuation of maximal contraction. This effect of CO2 was not modified by indomethacin. Treatment with hemoglobin or rubbing of the endothelium meant that increased CO2 tension still resulted in rightward shift of the NE dose-response curve but without altering the maximal contractile response. The basal guanosine 3,5-cyclic monophosphate (cGMP) levels in control and NE-treated aortic preparations were not affected by increasing the CO2 tension. Thus the inhibitory action of CO2 on NE-induced contraction in the presence of endothelium may not be derived from facilitation of endothelium-derived relaxation factor (EDRF)-induced cGMP synthesis. Increasing the CO2 tension attenuated the ...
Noradrenaline ELISA kit is intended for measuring in vitro quantitative levels of norepinephrine (NE) or noradrenaline (NA) in human urine and plasma samples.
Norepinephrine- (0-399) mine is 1089 Catecholamines- (0-699) mine is 1189 Does this indicate that i have neuroblastoma or pheochromocytoma? My endo told me i had a adrenal tumor and ran a 24 u...
Norepinephrine in the context of a glucose intake actually would promote insulin resistance by increasing fat oxidation inappropriately. Norepinephrine is great for food restricted dieting people because it increases fat oxidation of fat tissue, but high norepinephrine/high fat oxidation while eating sucrose and glucose is terrible because it will promote hyperinsulinemia and exaggerated fat storage. Dopamine regulates fat oxidation while norepinephrine just purely increases it; norepinephrine without dopamine = obesity. This may be part of the reason so many become whales on antidepressant meds which usually just increase serotonin and NE, and generally have mild antipsychotic/dopamine suppression effects ...
Norepinephrine: Norepinephrine, substance that is released predominantly from the ends of sympathetic nerve fibers and that acts to increase the force of skeletal muscle contraction and the rate and force of contraction of the heart. The actions of norepinephrine are vital to the fight-or-flight response.
Norepinephrine(Noradrenaline) ELISA kit. This research Norepinephrine ELISA kit enables the ultra-sensitive measurement of Noradrenaline (Norepinephrine) in any biological sample. Intended for research use only, the assay features a lower limit of detection at 1.3 pg/ml and a minimal sample volume as low as 1 µl.. ...
Noradrenaline Mylan is a medicine available in a number of countries worldwide. A list of US medications equivalent to Noradrenaline Mylan is available on the Drugs.com website.
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[Effect of adrenaline and noradrenaline on the electrophysiological properties of ureter muscle cells].by Kochemasova NG, Shuba MF. MiniManuscript.
Deo s medicinskim informacijama na sajtu jw.org namenjen je prvenstveno lekarima specijalistima i drugim zdravstvenim radnicima. On ne sadrži medicinske savete niti preporuke za određeno lečenje i nije zamena za konsultovanje sa stručnim zdravstvenim radnikom. Medicinsku literaturu koja se ovde navodi nisu izdali Jehovini svedoci, ali u njoj se govori o strategijama beskrvnog lečenja koje se mogu uzeti u obzir. Svaki medicinski radnik je odgovoran da bude u toku s novim informacijama, razmotri više načina za pružanje medicinske nege i da pomogne pacijentima da donesu odluku koja je u skladu s njihovim medicinskim stanjem, željama, merilima i verovanjima. Nisu sve ovde navedene strategije primenjive i prihvatljive za sve pacijente.. Za pacijente: Uvek se konsultujte s vašim lekarom ili drugim kvalifikovanim zdravstvenim radnikom u vezi s vašim medicinskim stanjem i lečenjem. Ako smatrate da imate zdravstvenih problema, obratite se lekaru.. Korišćenje ovog veb-sajta propisano je ...
A-77636 je sintetički lek koji deluje kao selektivni agonist D1 receptora.[4] On ispoljava nootropne, anestetičke, i antiparkinsonske efekte u životinjskim studijama,[5][6][7][8][9] ali njegova visoka potentnost i dugotrajno dejstvo uzrokuju umanjenje senzitivnosti D1 receptora i tahifilaksu.[10][11][12] Za razliku od drugih D1 punih agonista kao što je SKF-82,958, on ne proizvodi preferenciju mesta kod životinja.[13] A-77636 parcijalno zamenjuje kokain u životinjskim studijama, te se pretpostavlja da može da nađe primenu kao zamena za drogu u lečenju adikcije.[14] On je bolje poznat po primeni u studijama za ispitivanje uloge D1 receptora u mozgu.[15][16][17] ...
V psihoaktivnih snoveh, kupljenih na črnem trgu pa tudi preko spleta (ne glede na legalnost), se pogosto nahajajo neželene primesi. Nekatere so izredno
In six patients within 12 hours of surgical correction of aortic coarctation there was a 750% increase in plasma noradrenaline concentrations accompanied by an increase in systolic and diastolic blood pressures. The magnitude of the postoperative increase in noradrenaline concentrations was related to the preoperative level of the pressure gradient across the coarctation. Six months after operation plasma noradrenaline concentrations were still significantly elevated. In nine patients who underwent other types of major surgery there was a small increase in plasma noradrenaline concentrations and a return to levels within the normal range within 24 hours. Various explanations for the rise in plasma noradrenaline concentrations are considered. In particular the possibility is raised that after surgical correction of aortic coarctation the increased levels indicate a marked increase in sympathetic nervous system activity; this may be mediated by baroreceptor mechanisms and may persist for up to six ...
Elevation of plasma norepinephrine concentrations to stress levels (1,800 pg/ml) resulted in normal subjects in a significant increase in ketone body production by 155% (determined by use of [14C]acetoacetate infusions), in a decrease of the metabolic clearance rate by 38%, hyperketonemia, and in increased plasma free fatty acid (FFA) levels by 57% after 75 min. Norepinephrine infusion during somatostatin-induced insulin deficiency resulted in an augmented and sustained increase in ketone body concentrations due to increased production and decreased peripheral clearance of ketone bodies. Norepinephrines stimulatory effect on lipolysis waned with time, and its effect on ketogenesis in normal subjects was greater than its influence on plasma FFA levels, and thus presumably on hepatic FFA uptake, suggesting a direct stimulatory effect on hepatic ketogenesis. The data demonstrate that in normal humans the hyperketonemic effect of elevated plasma norepinephrine concentrations results from a ...
Thompson, Caitlin S., Lacy A. Holowatz, and W. Larry Kenney. Cutaneous vasoconstrictor responses to norepinephrine are attenuated in older humans. Am J Physiol Regul Integr Comp Physiol 288: R1108 -R1113, 2005. First published January 20, 2005; doi:10.1152/ajpregu.00839.2004.-Cutaneous vasoconstriction (VC) in response to cooling is impaired with human aging. On the basis of previous findings that older humans rely predominantly on norepinephrine (NE) for reflex VC of skin blood vessels, and that the VC effects of NE are blunted with age in many vascular beds, we tested the hypothesis that cutaneous VC responses to exogenous NE are attenuated in aged skin compared with young skin. In 11 young (18-30 yr) and 11 older (62-76 yr) men and women, skin blood flow was monitored at two forearm sites with laser Doppler (LD) flowmetry, while local skin temperature was clamped at 34°C. At one site, five doses of NE (10 10 to 10 2 M) were sequentially infused via intradermal microdialysis while the other site
1. Stressful sympathetic stimulation (cold pressor test) was applied to 18 patients with essential hypertension and 15 normotensive subjects. Intra-arterial blood pressure, heart rate, plasma adrenaline and noradrenaline concentrations as well as forearm blood flow were measured before and during the cold pressor test; tests were repeated after regional postsynaptic α1-adrenoceptor blockade with prazosin.. 2. Under basal conditions mean blood pressure (P , 0.001), heart rate (P , 0.01), forearm blood flow (P , 0.001) as well as adrenaline concentration (P , 0.01), but not noradrenaline, was higher in patients with essential hypertension.. 3. During the cold pressor test, mean blood pressure, heart rate, plasma adrenaline and noradrenaline concentrations increased and forearm flow decreased (all P , 0.001).. 4. Stress-stimulated plasma adrenaline was higher in essential hypertensive patients than in normotensive subjects (P , 0.01). In the former the stress-induced increase in plasma adrenaline ...
Differences in the norepinephrine system are implicated in depression. Serotonin-norepinephrine reuptake inhibitors are antidepressants that treat depression by increasing the amount of serotonin and norepinephrine available to postsynaptic cells in the brain. There is some recent evidence implying that SNRIs may also increase dopamine transmission.[15] This is because SNRIs work by inhibiting reuptake, i.e. preventing the serotonin and norepinephrine transporters from taking their respective neurotransmitters back to their storage vesicles for later use. If the norepinephrine transporter normally recycles some dopamine too, then SNRIs will also enhance dopaminergic transmission. Therefore, the antidepressant effects associated with increasing norepinephrine levels may also be partly or largely due to the concurrent increase in dopamine (particularly in the prefrontal cortex of the brain). Tricyclic antidepressants (TCAs) increase norepinephrine activity as well. Most of them also increase ...
To identify the mechanisms whereby norepinephrine induces glucose uptake in brown adipose tissue, we used mouse brown adipocytes in culture. Proliferating brown adipocytes had high levels of glucose transporter (GLUT) 1 mRNA and low levels of GLUT4 mRNA. The ratio of GLUT4/GLUT1 mRNA expression increased during differentiation, and mature brown adipocytes had high levels of GLUT4 mRNA. The endogenous adrenergic neurotransmitter norepinephrine induced a potent increase in GLUT1 mRNA and a decrease of GLUT4 mRNA in mature brown adipocytes. The norepinephrine effect was mimicked by isoprenaline and CL 316243 and was thus mediated by beta(3)-adrenergic receptors. The cAMP analog 8-bromoadenosine-cAMP partly mimicked the response on GLUT1 mRNA increase and fully mimicked the GLUT4 mRNA decrease. We found no involvement of alpha(1) or alpha(2)-adrenergic receptors on GLUT1 or GLUT4 mRNA transcription. Norepinephrine treatment led to a large increase of GLUT1 protein amount in brown adipocytes as ...
The aim of this study is to increase norepinephrine levels in a population of young adults where NE levels are very low or undetectable.
The locus coeruleus is responsible for mediating many of the sympathetic effects during stress. The locus coeruleus is activated by stress, and will respond by increasing norepinephrine secretion, which in turn will alter cognitive function (through the prefrontal cortex), increase motivation (through nucleus accumbens), activate the hypothalamic-pituitary-adrenal axis, and increase the sympathetic discharge/inhibit parasympathetic tone (through the brainstem).. Specific to the activation of the hypothalamo-pituitary adrenal axis, norepinephrine will stimulate the secretion of corticotropin-releasing factor from the hypothalamus, that induces adrenocorticotropic hormone release from the anterior pituitary and subsequent cortisol synthesis in the adrenal glands. Norepinephrine released from locus coeruleus will feedback to inhibit its production, and corticotropin-releasing hormone will feedback to inhibit its production, while positively feeding to the locus coeruleus to increase norepinephrine ...
BACKGROUND: Significantly increased plasma and CSF IL-6 levels reflect underlying tissue damage following clinical and experimental traumatic brain injury (TBI). Catecholamines, used under clinical conditions to maintain adequate cerebral perfusion pressure, induce a sustained IL-6 release. Thus an additional elevation in IL-6 could aggravate brain edema in the acute posttraumatic phase. We studied the changes in plasma and cerebrospinal fluid (CSF) IL-6 levels 4 and 24 hours after experimental TBI and assessed possible time-dependent effects of norepinephrine infusion on IL-6 and brain edema. MATERIAL/METHODS: Paired plasma and CSF IL-6 measured at 4 and 24 hours following TBI (n=10) were compared to levels in non-traumatized rats (n=5). In a placebo-controlled trial, 20 brain-injured male Sprague-Dawley rats were randomized to receive norepinephrine or NaCl for 90 minutes at 4 or 24 hours after TBI. Plasma IL-6 was measured before, during, and after the infusion period. One hour after stopping ...
Norepinephrine is currently recommended as the first line vasopressor in septic shocks however early vasopressin use has been proposed as an alternative. This double blind randomised controlled trial at eighteen UK adult ICUs compared the effect of early vasopressin versus norepinephrine on kidney failure in patients with septic shock. Four hundred patients were randomly assigned…
The effect of chronic norepinephrine (NE) administration with increasing dosage from 1-4 mg/kg over a period of 2 weeks was studied on cardiac phospholipids and their fatty acid distribution in rats....
Mladen Boban, John L. Atlee, Martin Vicenzi, John P. Kampine, Zeljko J. Bosnjak; Anesthetics and Automaticity in Latent Pacemaker Fibers: IV. Effects of Isoflurane and Epinephrine or Norepinephrine on Automaticity of Dominant and Subsidiary Atrial Pacemakers in the Canine Heart. Anesthesiology 1993;79(3):555-562. Download citation file:. ...
Low Norepinephrine, unlike High Norepinephrine, is not likely a result of Stress, but rather, a neurophysiological abnormality that relates back to deficit enzymes in certain parts of the Brain. Specifically, we are talking about the enzyme dopamine-beta-hydroxylase" or [DBH]. The condition of low norepinephrine mirrors dysautonomia - a low sympathetic state where blood pressure often falls below normal and many nervous system functions (such as alertness, breathing, reaction time and smell) are disrupted ...
The present study was designed to investigate the influence of aging on noradrenaline content and the density and pattern of prejunctional dopamine D2 receptors in the tail (ventral caudal) artery of male Sprague-Dawley rats. Tail artery is frequently used as a model for investigating mechanisms of sympathetic vascular control and contains prejunctional dopamine receptor belonging to the D2 subtype. Noradrenaline levels were reduced in rats of 12 months of age in comparison with 3-month-old animals. A further reduction in catecholamine concentration was found in 24-month-old rats. The density of prejunctional D2 receptors, which was measured in frozen sections of the tail artery by using both radioligand binding and autoradiographic techniques, was reduced by about 35% in 12-month rats in comparison with 3-month rats. A decrease by about 55% versus 3-month rats and by about 20% versus 12-month rats was observed in 24-month-old rats. Neither the pharmacological profile nor the anatomical ...
1. The aim of the present study was to investigate noradrenaline (NA)-induced regulation of alpha(1) -adrenoceptor (AR) mRNA expression in human embryonic kidney (HEK) 293 cells stably expressing cloned alpha(1) -AR subtypes with similar receptor densities. Stable transfection was performed by calcium phosphate precipitation. Receptor expression was detected by radioligand binding assay. The mRNA expression was measured by RNase protection assay.. 2. alpha(1) -Adrenoceptor subtype mRNA respond in distinct ways following prolonged exposure to NA. The mRNA level of the alpha(1A) -AR subtype was unchanged, the mRNA level of the alpha(1B) -AR subtype was increased and the mRNA level of the alpha(1D) -AR subtype declined time dependently. The protein kinase C (PKC) inhibitor calphostin C or RO 31-8220 abolished the NA-induced downregulation of alpha(1D) -AR mRNA. Phorbol myristate acetate (PMA), a PKC activator, similarly repressed the effects of NA on alpha(1D) -AR. However, calphostin C, RO 31-8220 ...
There is no question that angiotensin II can play its enhancing effects on the sympathetic nervous system at various levels and that not only a presynaptic potentiation of norepinephrine secretion but also an amplification of the responsiveness of adrenergic receptors to neural stimuli is involved as indicated by the data of Lyons et al.R1 In a study we performed several years ago in humans,R2 we also suggested this to be the case because in hypertensive patients both acute and long-term ACE inhibition attenuated the reflex increase in forearm vascular resistance due to unloading of cardiac receptors without any concomitant alteration of the reflex increase in plasma norepinephrine.. There is also no question that the enhancing effect of angiotensin II on sympathetic cardiovascular influences is reciprocated because sympathetic nerve activity is an important determinant of renal secretion of reninR3 R4 and thus of the activity of the renin-angiotensin system. It is certainly possible, on the ...
Results IL-7 stimulated IL-7R+ mature B cells act proinflammatory (increased clinical score, increased anticollagen type II antibodies) after cell transfer in CIA. The sympathetic neurotransmitter norepinephrine abrogates this effect. Expression of IL-7Rα is increased when B cells are activated (anti-CD40 or lipopolysaccharide) in vitro and stimulating the IL-7R induces intracellular accumulation of pSTAT5. α- And β-adrenergic agonists show no influence on expression levels of IL-7R on activated B cells; however, intracellular IL-7R downstream signalling is abrogated via the β2-adreonceptor (β2AR) agonist terbutaline. IL-7R and β2AR are also expressed on B cells in synovial tissue from RA and OA patients.. ...
Norepinephrine uptake into a crude preparation of rat brain synaptic vesicles showed a marked dependence on Mg2+ concentration. Mn2+ or Co+ could substitute for Mg2+, but displayed lower affinities. Zn2+, Ni2+ and Ca2+ stimulated uptake only slightly and other divalent cations were ineffective. ATP, GTP and UTP produced stimulation of norepinephrine uptake, but only ATP was fully effective. ADP and AMP inhibited the ATP-induced stimulation. The irreversible inhibitor of ATPases, N-ethylmaleimide (NEM), blocked norepinephrine uptake; the effect was enhanced by pre-incubation of the vesicle preparation with NEM prior to addition of the cofactors and the enhancement was partially prevented by addition of ATP-Mg2+ during the pre-incubation. Replacement of K+ by Na+ in the medium did not alter norepinephrine uptake, but Li+ inhibited uptake by competing with Mg2+. The use of hypertonic medium inhibited uptake, while hypotonic medium markedly enhanced only the nonspecific uptake component (not ATP or ...
The objective of the present study was to analyze the anatomical basis of the A5 depressor response and to test if the putative neurotransmitter noradrenaline is involved in the response. Two approaches were used; one was neuroanatomical and the other was pharmacological. First, the retrograde transport method in which two fluorescent markers (Fast blue and rhodamine microspheres) was used in combination with the indirect immunofluorescence technique to establish that A5 catecholamine neurons project to both the spinal cord and the region of the nucleus tractus solitarii (NTS). Second, we analyzed the effects of 6-hydroxydopamine (6-OHDA) lesions of the spinal cord and/or NTS area on the A5 depressor response. This response was elicited by a 80-nl microinjection of L-glutamate (500 mM) into the A5 region in pentobarbital anesthetized rats; it was characterized by a decrease in blood pressure and heart rate. After destruction of various noradrenergic terminal fields we have found that intraspinal
Nine subjects were randomized to the subcutaneous epinephrine group (epinephrine solution) and 8 to the intramuscular injection group (EpiPen Auto-Injector). The mean peak plasma epinephrine concentration in the subcutaneous group was 1802 ± 214 pg/mL. The mean time to reach maximum plasma concentrations was 34 ± 14 minutes in this group, with only 2 subjects achieving maximum concentration by 5 minutes. In contrast, the mean peak maximum plasma epinephrine concentration in the intramuscular group was 2136 ± 351 pg/mL. The mean time to reach maximum plasma concentration was 8 ± 2 minutes (P , .05, compared to subcutaneous group), with 6 achieving the peak concentration by 5 minutes. No serious adverse effects were reported in either group. ...
Introduction: We aimed to investigate the role of α- and β-receptors in control of contractile activity in circular jejunal muscle in rat and to delineate changes in adrenergic neurotransmission during postoperative ileus.. Materials and methods: Muscle strips (n=8/rat) of 6 naive (NC) and 8 Sprague Dawley rats after small bowel manipulation (POI) were studied. Ileus was confirmed by delayed small bowel transit. Dose-response curves were generated for phenylephrine (α-agonist; 10-8-3x10-6M) and isoprenaline (β-agonist; 3x10-10-10-7M) and effects of bethanechol-precontraction (3x10-6M), L-NIL and nimesulide (inhibiting inducible NO-synthase (10-4M) and cyclooxygenase-2 (10-5M)), L-NNA (non-specific NO-synsthase inhibitor; 10-4M), tetrodotoxin (TTX; blocking enteric nervous system; 10-6M), phentolamine (α-antagonist; 10-5M) or propranolol (β-antagonist; 5x10-6M) on response to agonists were studied. Release of excitatory neurotransmitters was investigated by electrical field stimulation ...
Despite extensive clinical study, there is no distinct consensus on the optimal management of fibromyalgia. The cause of fibromyalgia has not been clearly defined, but several mechanisms may be involved. Abnormalities in sleep patterns, muscle structure, and cerebral blood flow have been associated with the syndrome, but it is unclear whether a causal relation exists between these abnormalities and fibromyalgia. Recent evidence suggests that alterations in the metabolism and function of the neurotransmitters serotonin, norepinephrine, and substance P may contribute to the development of fibromyalgia. No pharmacologic agents are indicated specifically for the treatment of fibromyalgia in the United States, and most pharmacologic therapies show only limited success, although drugs that affect serotonin or norepinephrine at the receptor site (such as antidepressants or tramadol) seem to generate the most consistent results. Tricyclic antidepressants may diminish the sleep disturbance and pain ...
During the follow-up, BNP, NT-proBNP, and norepinephrine progressively decreased in group T (F = 7.49, p , 0.01; F = 4.84, p , 0.01; and F = 9.88, p , 0.001, respectively) but not in group C (Fig. 1). No changes were found in either group with respect to plasma renin activity and aldosterone. At the end of the program, peak Vo2in group T inversely correlated to BNP (R = 0.52, p , 0.001), NT-proBNP (R = 0.51, p , 0.001), and norepinephrine levels (R = 0.49, p , 0.001) at a similar extent, as compared with baseline. A similar correlation was found between Ve/Vco2slope and the levels of BNP (R = 0.61, p , 0.001), NT-proBNP (R = 0.60, p , 0.001), and norepinephrine (R = 0.59, p , 0.001). The change in peak Vo2at the end of the program was correlated with BNP and NT-proBNP changes (R = 0.42, p , 0.001 and R = 0.31, p , 0.01, respectively), but not with norepinephrine changes (Fig. 2).Conversely, no correlation was found between the decrease in BNP, NT-proBNP, and norepinephrine values and the ...
Du, XJ, Bobik, A, Little, PJ, Esler, MD and Dart, AM (1997) Role of Ca2+ in metabolic inhibition-induced norepinephrine release in rat brain synaptosomes. Circulation Research, 80 2: 179-188. ...
Experiments were designed to study the potential mechanisms underlying the vasodilator effect of celiprolol. Rings of canine left circumflex coronary artery and rat mesenteric artery, with and without endothelium, were suspended in organ chambers for isometric tension recording. In both blood vessels, celiprolol (10-9-10-4 M) failed to produce relaxation in rings with and without endothelium; these same tissues relaxed in an endothelium-dependent manner to acetylcholine (10-6 M). All tissues relaxed completely in the presence of papaverine (10-4 M). In the coronary artery, isoproterenol (10-9-10-4 M) produced endothelium-independent relaxations which were inhibited in a competitive fashion by celiprolol (pA2 = 7.52 + 0.14; slope = 0.98, 95% confidence limits = 0.80-1.15). In other experiments, strips of canine saphenous veins were incubated with [3H]norepinephrine ([3H]NE) and suspended for superfusion. Electrical stimulation (2 Hz, 4 V, 2 ms for 6 min) produced an increase in [3H]NE overflow. ...
The 12th International Congress of Pharmacology, Montreal, Canada, 24-29 July 1994. In Canadian Journal of Physiology and Pharmacology, v. 72 n. 424, p. 1 ...
TY - JOUR. T1 - Az ATP-fuggo K+-csatorna-(K+(ATP))-aktivalo pinacidil pre- es poszt- szinaptikus hatasa nyul pulmonaris arterian. AU - Rácz, Dániel. AU - Zillkens, Stefán. AU - Forstreuter, Péter. AU - Nagykáldi, Zsolt. AU - Magyar, K.. AU - Torök, Tamás. PY - 1999/6. Y1 - 1999/6. N2 - Low frequency (2 Hz) of electrical depolarisation induced [3H]noradrenaline ([3H]NA) release has been measured from the isolated main pulmonary artery of the rabbit in the presence of uptake blockers (cocaine, 3x10-5M and corticosterone, 5x10-5M), with parallel measurements of post- junctional contractile responses. The K+(ATP)-channel opener pinacidil (10- 6-10-4M), slightly potentiated the nerve-evoked release of [3H]NA which failed to show close concentration-dependency. Large concentration of pinacidil (10-4M) increased the ratio of [3H]NA release from 0.99±0.02 to 1.28±0.05 (P-4M caused nearly 70% inhibition of contractile response. The pre- and post-junctional effects of pinacidil were studied under ...
The effect of the α1, α2-antagonist phentolamine (PTA) on neuromuscular transmission and exogenous norepinephrine (NE) was assessed in arteries of diminishing diameter posessing a substantial adventitiomedial junction adrenergic innervation in the rabbit ear, i/.e., central ear artery (CEA), unstretched lumen diameter (ULD) ≃ 300 μm; main side branch (MSB) off the CEA (ULD ≃ 150 μm); and terminal branch (TB) off the MSB (ULD ≃ 75 μm). With increasing PTA concentrations, contractile response to transmural nerve stimulation (TNS) were decreased proportionately less in TB than in MSB and CEA. PTA (4 x 10-6 M, a competitive antagonist concentration) blocked the tetrodotoxin-sensitive TNS-induced contractions of CEA segments at 2, 4, and 8 Hz. The response at 8 Hz was reduced at least 98% in MSB and 86% in TB. However, responses to 8 Hz were not abolished in MSB and TB until 2 x 10-5 and 3 x 10-5 M PTA, respectively. PTA (3 x 10-5 M) possessed nonspecific depressant
Definition of norepinephrine in US English - a hormone that is released by the adrenal medulla and by the sympathetic nerves and functions as a neurotransmitter. It
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Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic ...
Adrenaline and noradrenaline will remain as the approved names in Australia. There is no intent to move to using epinephrine and norepinephrine as the new ingredient names.. Instead, medicines containing adrenaline and noradrenaline will start to include the international names epinephrine and norepinephrine on labels and information leaflets. By including this information on labels indefinitely, we hope to reduce confusion for health professionals and consumers.. ...
The ability of adrenergic agents to promote the differentiation and especially the mitochondriogenesis of brown fat precursor cells, grown in culture, was investigated. These cells begin to differentiate during the days preceding confluence. We found here that, already during the early growth phase, the cultures (essentially precursor cells and preadipocytes at this stage) show increased cyclic AMP (cAMP) levels when acutely stimulated with norepinephrine (NE). The cultured cells were therefore chronically treated with NE up to the time of confluence, and their cytochrome-c oxidase activity was measured as an index of mitochondriogenesis. Chronic NE treatment resulted in an increased cytochrome-c oxidase activity of the cells at confluence. This effect was reproduced by selective activation of adenylate cyclase with cholera toxin, suggesting that the NE effect was exerted through an increase in cAMP. Ascorbate (added with NE as an antioxidant) had in itself a positive effect, both on final cell ...
Wednesday my Endo said i have an adrenal tumor. Norepinephrine,Pl- (0-399) mine was 1042 Catecholamine,TOT,PL- (0-699) mine was 1189 My thyroid was still out of whack- TSH- 0.179 Hyper...
Epinephrine/Norepinephrine ELISA Kit Catalog Number KA assays Version: 01 Intended for research use only Table of Contents Introduction... 3 Intended Use... 3 Principle of the Assay...
LEVOPHED (Norepinephrine) drug information & product resources from MPR including dosage information, educational materials, & patient assistance.
I am not an expert either, but there are post-synaptic receptors (the ones that exert the main effect of the neurotransmitter) and there are pre-synaptic autoreceptors and heteroreceptors which affect the release of the neurotransmitter.. So, for example, if you take a reuptake inhibitor, you immediately increase the amount of neurotransmitter in the synapse. However, this activates the post-synaptic receptors and the autoreceptors. When the autoreceptors are activated, this slows the firing / release of the neurotransmitter from the presynaptic neuron.. Over time, the autoreceptors can desensitize which can result in increased firing.. Take, for example clonidine. It is a blood pressure medication which slows the release of norepinephrine. It does this by activating a specific norepinephrine autoreceptor (alpha-2). This receptor can also be activated by norepinephrine itself to slow the release of more neurotransmitter.. Mirtazapine and yohimbine block this same adrenaline receptor, which ...
I am not an expert either, but there are post-synaptic receptors (the ones that exert the main effect of the neurotransmitter) and there are pre-synaptic autoreceptors and heteroreceptors which affect the release of the neurotransmitter.. So, for example, if you take a reuptake inhibitor, you immediately increase the amount of neurotransmitter in the synapse. However, this activates the post-synaptic receptors and the autoreceptors. When the autoreceptors are activated, this slows the firing / release of the neurotransmitter from the presynaptic neuron.. Over time, the autoreceptors can desensitize which can result in increased firing.. Take, for example clonidine. It is a blood pressure medication which slows the release of norepinephrine. It does this by activating a specific norepinephrine autoreceptor (alpha-2). This receptor can also be activated by norepinephrine itself to slow the release of more neurotransmitter.. Mirtazapine and yohimbine block this same adrenaline receptor, which ...
The increases in MAP and HR recorded via telemetry during the first week after CBU are very similar to results published previously based on daily recordings with the dog resting quietly in a sling under laboratory conditions (28). The effects of CBU on PRA were also replicated; PRA was elevated on some days during the week following CBU but never suppressed below control levels. Furthermore, we also observed a significant increase in plasma NE in response to CBU. All of these responses are compatible with the hypothesis that CBU caused an increase in sympathetic outflow. However, contrary to our expectations, the initial increases in MAP, HR, and plasma NE were not sustained. Plasma NE and HR declined to control levels by the third week after CBU (Figs. 4 and 7). There was also a decline in MAP over the same time period, but MAP stabilized at a level that averaged 10 ± 3 mmHg above control during the third to fifth weeks after CBU (Fig. 2). There are a number of possibilities that could ...
In our latest paper, we report that the sensitivity of fat cells to signals that increase the breakdown of fat is linked to the receptor ALK7. The discovery, which is published today in eLife, suggests that ALK7 is an interesting target for future strategies to treat obesity.. The ALK7 receptor is predominantly found in fat cells and tissues involved in controlling the metabolism. Intriguingly, mice with a mutation in ALK7 accumulate less fat than mice with a functional version of the protein. Until now, it has not been known why.. We created mice whose fat cells lack ALK7, but whose other cells all produce ALK7 as normal. We found that fat cells lacking the ALK7 receptor are more sensitive to adrenaline and noradrenaline signals, a finding that can explain why they accumulate less fat even though the mice were on a high-fat diet. Adrenaline and noradrenaline are central players in metabolism. These hormones trigger the burst of energy and increase in heart rate and blood pressure that are ...
(R)-noradrenaline 51-41-2 MSDS report, (R)-noradrenaline MSDS safety technical specifications search, (R)-noradrenaline safety information specifications ect.
2-4 h nach Hypophysektomie erhöht Noradrenalin den Sauerstoffverbrauch wie bei Kontrollratten, 7 Tage nach der Entfernung der Hypophyse ist jedoch diese Wirkung des Noradrenalin aufgehoben. Die CO2-Ab...
... - Noradrenaline Sintetica® - Noradrenaline Bitartrate - Noradrenaline Sintetica® is the natural transmitter of postganglionic adrenergic nerves and, by means of general vasoconstriction, increases systolic and diastolic blood pressure (with the exception of the coronary arteries). It is particularly used as an emergency (life-saving) drug against hypotonicity and in intensive care unit. Patented premixed ready to use formulations of Noradrenaline Sintetica are under development.
Levophed is a common drug used in critical care medicine. When do you use this? What effect does it have? Learn the simple facts from an ICU RN.
Noradrenaline and adrenaline are catecholamines that play major roles in regulation of the inner world of the body by the brain
What is ADRA2A? ADRA2A, located on chromosome 10, encodes the α-2A adrenergic receptor, a norepinephrine receptor that is the primary site of action for α-2A agonists. The α-2A adrenergic receptor…. ...
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Stress is a feeling of strain and pressure. When stressed, the body releases a complex mix of hormones and chemicals such as adrenaline, cortisol and norepinephrine to prepare the body for physical activity.
Date: Sat, 28 Sep 2019 02:34:28 +0200 From: Heiko Schlittermann ,[email protected], To: oss-security ,[email protected], Cc: [email protected], [email protected] Subject: Exim CVE-2019-16928 RCE using a heap-based buffer overflow CVE ID: CVE-2019-16928 Date: 2019-09-27 (CVE assigned) Version(s): from 4.92 up to and including 4.92.2 Reporter: [email protected] Reference: https://bugs.exim.org/show_bug.cgi?id=2449 Issue: Heap-based buffer overflow in string_vformat, remote code execution seems to be possible Conditions to be vulnerable =========================== All versions from (and including) 4.92 up to (and including) 4.92.2 are vulnerable. Details ======= There is a heap-based buffer overflow in string_vformat (string.c). The currently known exploit uses a extraordinary long EHLO string to crash the Exim process that is receiving the message. While at this mode of operation Exim already dropped its privileges, other paths to reach the vulnerable code may ...
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Looking for online definition of noradrenergic nerve in the Medical Dictionary? noradrenergic nerve explanation free. What is noradrenergic nerve? Meaning of noradrenergic nerve medical term. What does noradrenergic nerve mean?
After bilateral olfactory bulbectomy in rats a significant increase of norepinephrine (NE) level in the hypothalamus was found. However, no difference was observed between hypothalamic NE turnover of bulbectomized and sham operated animals. In the amygdaloid cortex the NE level was not affected by bulbectomy. In this area, however, the ... read more NE turnover appeared to be decreased after bulbectomy. The latter finding may be related to the deficits in passive avoidance behaviour as found in bulbectomized rats. show less ...
A norepinephrine releasing agent (NRA), also known as an adrenergic releasing agent, is a catecholaminergic type of drug which induces the release of norepinephrine (noradrenaline) and epinephrine (adrenaline) from the pre-synaptic neuron into the synapse. This in turn leads to increased extracellular concentrations of norepinephrine and epinephrine therefore an increase in adrenergic neurotransmission. A closely related type of drug is a norepinephrine reuptake inhibitor (NRI). Another class of drugs that stimulates adrenergic activity is the adrenergic receptor agonist class. NRAs are used for a variety of clinical indications including the following: For the treatment of attention deficit hyperactivity disorder (ADHD) - e.g., amphetamine, methamphetamine, pemoline As anorectics in the treatment of obesity - e.g., amphetamine, phentermine, benzphetamine, phenmetrazine, aminorex As wakefulness-promoting agents in the treatment of narcolepsy - e.g., amphetamine, methamphetamine As nasal ...
The effect of chronic, unilateral superior cervical ganglionectomy on cerebral blood flow and blood flow autoregulation to changes in perfusion pressure was examined in seven phencyclidine anesthetized monkeys. Ten to 14 days prior to the experiments Doppler ultrasonic flow transducers were placed on both carotid arteries after ligation of the external carotid branches and removal of one superior cervical ganglion. Autoregulation was tested by exsanguination and metaraminol infusion with the monkeys inspiring room air, 9% and 12% carbon dioxide in air. Immediately following experimentation the cerebral vessels were examined for the presence of noradrenergic fibers. The results of the study demonstrate that: (1) superior cervical ganglionectomy produces a significant reduction in the noradrenergic innervation of ipsilateral extraparenchymal arteries; (2) the peripheral sympathetic nervous system contributes to overall cerebral vascular resistance primarily by affecting resistance in ...
TCAs were the first medications that had dual mechanism of action. The mechanism of action of tricyclic secondary amine antidepressants is only partly understood. TCAs have dual inhibition effects on norepinephrine reuptake transporters and serotonin reuptake transporters. Increased norepinephrine and serotonin concentrations are obtained by inhibiting both of these transporter proteins. TCAs have substantially more affinity for norepinephrine reuptake proteins than the SSRIs. This is because of a formation of secondary amine TCA metabolites.[24][25]. In addition, the TCAs interact with adrenergic receptors. This interaction seems to be critical for increased availability of norepinephrine in or near the synaptic clefts. Actions of imipramine-like tricyclic antidepressants have complex, secondary adaptions to their initial and sustained actions as inhibitors of norepinephrine transport and variable blockade of serotonin transport. Norepinephrine interacts with postsynaptic α and β adrenergic ...
The importance of counterregulatory mechanisms triggered by arterial vasodilation for the antihypertensive response to the calcium entry blocking agent nifedipine was investigated in 13 men with mild to moderate essential hypertension. Blood pressure and systemic vascular resistance were significantly reduced 30 minutes after sublingual administration of 10 mg of nifedipine while heart rate, cardiac index and plasma norepinephrine concentrations increased (all p , 0.01). Also, changes in mean blood pressure correlated inversely with arterial baroreflex sensitivity (r = -0.74, p , 0.01), suggesting that arterial baroreflex mechanisms by means of sympathetic activation tend to limit the acute antihypertensive response. Blood pressure, but not systemic vascular resistance, decreased further (p , 0.01) after 6 weeks of therapy with nifedipine 20 mg three times daily, while average heart rate, cardiac index and plasma norepinephrine concentrations had returned toward pretreatment values.. Thus, a ...
Hypertension is associated with enhanced cardiac sympathetic transmission, although the exact mechanisms underlying this are still unknown. We hypothesized that defective function of the norepinephrine uptake transporter (NET) may contribute to the sympathetic phenotype of the spontaneously hypertensive rat, and that this may occur before the development of hypertension itself. The dynamic kinetics of NET were monitored temporally using a novel fluorescent assay of the transporter in cultured postganglionic sympathetic neurons from the cardiac stellate ganglion, the superior cervical ganglion, the celiac ganglia/superior mesenteric ganglia, and the renal sympathetic chain. All NET activity was blocked by desipramine. NET rate was significantly impaired in cardiac stellate sympathetic neurons from the prehypertensive spontaneously hypertensive rat compared with age-matched normotensive Wistar-Kyoto rats. A similar response was seen in hypertensive spontaneously hypertensive rats stellate sympathetic
Objective: To determine the effect of renal denervation (RDN) on the severity of atherosclerosis and aortic aneurysm in hypertensive mice. Methods: Hypertension, atherosclerosis and aortic aneurysm were induced by subcutaneous infusion of angiotensin II (1 µg/kg/min) for 28 days in apolipoprotein E-deficient mice. RDN was conducted using combined surgical and local chemical denervation. The norepinephrine concentration in the kidney was measured by high-performance liquid chromatography. Blood pressure was measured by the tail-cuff method. Atherosclerosis was assessed by Sudan IV staining of the aortic arch. The aortic diameter was measured by the morphometric method. The mRNA expression of genes associated with atherosclerosis and aortic aneurysm were analyzed by quantitative PCR. Results: RDN decreased the median norepinephrine content in the kidney by 93.4% (n=5-7, P=0.003) five days after the procedure, indicating that the RDN procedure was successful. RDN decreased systolic blood pressure in

2017 AACC2017 AACC

VMA is an end-stage metabolite of the catecholamines: epinephrine, and norepinephrine. Catecholamines are secreted by ...
more infohttp://events.jspargo.com/aacc17/Public/eBooth.aspx?BoothID=474782&Task=PressReleases&SSID=1130

EC 2.1.1.28EC 2.1.1.28

Other name(s): noradrenaline N-methyltransferase; noradrenalin N-methyltransferase; norepinephrine methyltransferase; ... norepinephrine N-methyltransferase; phenethanolamine methyltransferase; phenethanolamine N-methyltransferase. Systematic name: ...
more infohttp://www.sbcs.qmul.ac.uk/iubmb/enzyme/EC2/1/1/28.html

Ronald T. Borchardt | School of PharmacyRonald T. Borchardt | School of Pharmacy

Comparison with Norepinephrine Uptake", Mol. Pharmacol., 21, 362-367 (1982).. 93. J. A. Yoffe and R. T. Borchardt, " ... M. F. Rafferty, D. S. Wilson, J. A. Monn, P. Krass, R. T. Borchardt and G. L. Grunewald, "Comparisons of Norepinephrine N- ... G. L. Grunewald, J. Monn, M. F. Rafferty, P. Krass and R. T. Borchardt, "Probes of the Active Site of Norepinephrine N- ... M. F. Rafferty, G. L. Grunewald and R. T. Borchardt, "Probes of the Active Site of Norepinephrine N-Methyltransferase: ...
more infohttp://pharmacy.drupal.ku.edu/ronald-t-borchardt

Norepinephrine - WikipediaNorepinephrine - Wikipedia

The general function of norepinephrine is to mobilize the brain and body for action. Norepinephrine release is lowest during ... A significant part of the damage is due to the effects of sustained norepinephrine release, because of norepinephrines general ... A variety of medically important drugs work by altering the actions of norepinephrine systems. Norepinephrine itself is widely ... Once in the synapse, norepinephrine binds to and activates receptors. After an action potential, the norepinephrine molecules ...
more infohttps://en.wikipedia.org/wiki/Norepinephrine

Norepinephrine (medication) - WikipediaNorepinephrine (medication) - Wikipedia

Norepinephrine acts on beta-1 adrenergic receptors, causing increase in heart rate and cardiac output. Norepinephrine is the ... Norepinephrine works by binding and activating alpha adrenergic receptors. Norepinephrine was discovered in 1946 and was ... Norepinephrine, also known as noradrenaline, is a medication used to treat people with very low blood pressure. It is the ... Norepinephrine is used mainly as a sympathomimetic drug to treat people in vasodilatory shock states such as septic shock and ...
more infohttps://en.wikipedia.org/wiki/Norepinephrine_(medication)

Norepinephrine | Encyclopedia.comNorepinephrine | Encyclopedia.com

Norepinephrine Norepinephrine (noradrenaline) belongs to a family of biological compounds called catecholamines. These ... Norepinephrine Chemistry: Foundations and Applications COPYRIGHT 2004 The Gale Group, Inc.. Norepinephrine. Norepinephrine ( ... norepinephrine (nor-epi-nef-rin) n. see noradrenaline. Cite this article Pick a style below, and copy the text for your ... Norepinephrine is produced from the catecholamine dopamine by the action of the enzyme dopamine β -hydroxylase. This enzyme is ...
more infohttps://www.encyclopedia.com/science-and-technology/biochemistry/biochemistry/norepinephrine

Serotonin-norepinephrine reuptake inhibitor - WikipediaSerotonin-norepinephrine reuptake inhibitor - Wikipedia

Dual serotonin and norepinephrine reuptake inhibitors[edit]. Agents with dual serotonin and norepinephrine reuptake inhibition ... Serotonin-norepinephrine reuptake inhibitor. From Wikipedia, the free encyclopedia. (Redirected from Serotonin-norepinephrine ... normal levels of norepinephrine in the synaptic clefts. Overall, inhibition of norepinephrine reuptake induced by TCAs, leads ... Serotonin-norepinephrine reuptake inhibitors (SNRIs) are a class of antidepressant drugs that treat major depressive disorder ( ...
more infohttps://en.wikipedia.org/wiki/Serotonin-norepinephrine_reuptake_inhibitor

Norepinephrine News, ResearchNorepinephrine News, Research

Early use of norepinephrine could benefit patients with sepsis and low blood pressure Patients with septic shock who were ... treated with norepinephrine earlier than patients receiving standard care were more likely to have their blood pressure and ...
more infohttps://www.news-medical.net/?tag=/Norepinephrine

Norepinephrine and Mental HealthNorepinephrine and Mental Health

What is Norepinephrine?. Norepinephrine is another term for noradrenaline. It is a stress hormone released into the blood that ... Do Norepinephrine levels affect mental health?. Depression and norepinephrine. Despite the presence of numerous explanations as ... Norepinephrine in treatments for mental health disorders. Norepinephrine release may have a pronounced effect on large areas of ... ADHD and Norepinephrine. Low levels of norepinephrine and another neurotransmitter, dopamine, can affect a persons ability to ...
more infohttps://www.news-medical.net/health/Norepinephrine-and-Mental-Health.aspx

Norepinephrine - Trip DatabaseNorepinephrine - Trip Database

Helping you find trustworthy answers on Norepinephrine , Latest evidence made easy ... Find all the evidence you need on Norepinephrine via the Trip Database. ... Norepinephrine vs Norepinephrine and Dobutamine in Cardiogenic Shock Norepinephrine vs Norepinephrine and Dobutamine in ... 1. Early Norepinephrine Administration in Septic Shock Early Norepinephrine Administration in Septic Shock Early Norepinephrine ...
more infohttps://www.tripdatabase.com/search?criteria=Norepinephrine

Serotonin-norepinephrine-dopamine reuptake inhibitor - WikipediaSerotonin-norepinephrine-dopamine reuptake inhibitor - Wikipedia

... norepinephrine, and dopamine. It does this by concomitantly inhibiting the serotonin transporter (SERT), norepinephrine ... A serotonin-norepinephrine-dopamine reuptake inhibitor (SNDRI), also known as a triple reuptake inhibitor (TRI), is a type of ... The mood changes induced by AMPT may be mediated by decreases in norepinephrine, while changes in selective attention and ... They are also very similar to serotonin-norepinephrine-dopamine releasing agents (SNDRAs) like MDMA ("ecstasy") and α- ...
more infohttps://en.wikipedia.org/wiki/Serotonin%E2%80%93norepinephrine%E2%80%93dopamine_reuptake_inhibitor

norepinephrinenorepinephrine

... is used to treat life-threatening low blood pressure (hypotension) that can occur with certain medical ... Norepinephrine is similar to adrenaline. It works by constricting (narrowing) the blood vessels and increasing blood pressure ... How is norepinephrine given?. Norepinephrine is given as an injection through a needle placed into a large vein. ... What is norepinephrine?. Norepinephrine is similar to adrenaline. It works by constricting (narrowing) the blood vessels and ...
more infohttps://www.cardiosmart.org/Healthwise/d003/23/d00323

Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs)Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs)

Serotonin-norepinephrine reuptake inhibitors work by inhibiting the reabsorption of not one but two important brain chemicals. ... Norepinephrine is related to alertness and energy. It is thought that SNRIs help treat depression by keeping up the levels of ... About Serotonin-Norepinephrine Reuptake Inhibitors. Medically reviewed by Lindsay Slowiczek, PharmD on. December 6, 2016. - ... Serotonin-norepinephrine reuptake inhibitors (SNRIs) were first introduced in the mid-1990s as a class of antidepressant drugs ...
more infohttps://www.healthline.com/health/depression/serotonin-norepinephrine-reuptake-inhibitors-snris

Noradrenaline (Norepinephrine)Noradrenaline (Norepinephrine)

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norepinephrine | Definition, Function, Effects, & Facts | Britannica.comnorepinephrine | Definition, Function, Effects, & Facts | Britannica.com

The actions of norepinephrine are vital to the fight-or-flight response. ... Norepinephrine, substance that is released predominantly from the ends of sympathetic nerve fibers and that acts to increase ... Norepinephrine, similar to other catecholamines, is generated from the amino acid tyrosine. Norepinephrine exerts its effects ... The actions of norepinephrine are vital to the fight-or-flight response, whereby the body prepares to react to or retreat from ...
more infohttps://www.britannica.com/science/norepinephrine

Norepinephrine (Professional Patient Advice) - Drugs.comNorepinephrine (Professional Patient Advice) - Drugs.com

Professional guide for Norepinephrine. Includes: pharmacology, pharmacokinetics, contraindications, interactions, adverse ... Note: Dose is stated in terms of norepinephrine base.. Hypotension/shock (off-label use): Infants, Children, and Adolescents: ... Droxidopa: Norepinephrine may enhance the hypertensive effect of Droxidopa. Monitor therapy. Ergot Derivatives: May enhance the ... Serotonin/Norepinephrine Reuptake Inhibitors may enhance the vasopressor effect of Alpha-/Beta-Agonists. Consider therapy ...
more infohttps://www.drugs.com/ppa/norepinephrine.html

Norepinephrine dictionary definition | norepinephrine definedNorepinephrine dictionary definition | norepinephrine defined

norepinephrine definition: a hormone or neurotransmitter, CHNO, related to epinephrine, that is used medically to constrict ... norepinephrine. nor·ep·i·neph·rine. a hormone or neurotransmitter, CHNO, related to epinephrine, that is used medically to ... norepinephrine. noun. A substance, C8H11NO3, both a hormone and neurotransmitter, that is secreted by the adrenal medulla and ... "norepinephrine." YourDictionary, n.d. Web. 17 August 2018. ,http://www.yourdictionary.com/norepinephrine,. ...
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Norepinephrine, (+)- | C8H11NO3 - PubChemNorepinephrine, (+)- | C8H11NO3 - PubChem

Norepinephrine, (+)- , C8H11NO3 , CID 5814 - structure, chemical names, physical and chemical properties, classification, ...
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NorepinephrineNorepinephrine

Posts Tagged Norepinephrine. Chemical Reasons for SAD. Alaska Northern Lights February 21, 2012 Sometimes known as the " ... Tags: Bright light therapy, Depression, Dopamine, Light box, Light Therapy, Melatonin, Norepinephrine, SAD, SAD light, SAD ...
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Norepinephrine - encyclopedia article - CitizendiumNorepinephrine - encyclopedia article - Citizendium

Norepinephrine [r]: Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic ... Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in ...
more infohttp://en.citizendium.org/wiki/Norepinephrine

High Norepinephrine,High Catecholamines - Cancer - MedHelpHigh Norepinephrine,High Catecholamines - Cancer - MedHelp

Norepinephrine,Pl- (0-399) mine was 1042 Catecholamine,TOT,PL- (0-699) mine was 1189 My thyroid was still out of whack- TSH- ... Norepinephrine,Pl- (0-399) mine was 1042 Catecholamine,TOT,PL- (0-699) mine was 1189 My thyroid was still out of whack- TSH- ... Norepinephrine- 1042 High (0-399 PG/ML) Epinephrine,PL- 10 (0-99 PG/ML) Dopamine,PL- 137 (0-142 PG/ML) Catecholamines,TOT,PL- ... The adrenal tumor was a presumption on my Endos part because the norepinephrine and the Catecholamines were high. No imaging ...
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High Norepinephrine,High Catecholamines - Genetics - MedHelpHigh Norepinephrine,High Catecholamines - Genetics - MedHelp

Norepinephrine- (0-399) mine is 1089 Catecholamines- (0-699) mine is 1189 Does this indicate that i have neuroblastoma or ... High Norepinephrine,High Catecholamines. Norepinephrine- (0-399) mine is 1089 Catecholamines- (0-699) mine is 1189 Does this ... Norepinephrine- (0-399) mine is 1089 Catecholamines- (0-699) mine is 1189 Does this indicate that i have neuroblastoma or ...
more infohttp://www.medhelp.org/posts/Genetics/High-Norepinephrine-High-Catecholamines/show/984726

Norepinephrine - Substance Information - ECHANorepinephrine - Substance Information - ECHA

Harmonised classification and labelling is a legally binding classification and labelling for a substance, agreed at European Community level. Harmonisation is based on the substances physical, toxicological and eco-toxicological hazard assessment. The Hazard classification and labelling section uses the signal word, pictogram(s) and hazard statements of the substance under the harmonised classification and labelling (CLH) as its primary source of information.. If the substance is covered by more than one CLH entry (e.g. disodium tetraborate EC no. 215-540-4, is covered by three harmonisations: 005-011-00-4; 005-011-01-1 and 005-011-02-9), CLH information cannot be displayed in the InfoCard as the difference between the CLH classifications requires manual interpretation or verification. If a substance is classified under multiple CLH entries, a link to the C&L Inventory is provided to allow users to view CLH information associated with the substance, instead of having the information ...
more infohttps://echa.europa.eu/substance-information/-/substanceinfo/100.000.088

Norepinephrine Side Effects in Detail - Drugs.comNorepinephrine Side Effects in Detail - Drugs.com

Learn about the potential side effects of norepinephrine. Includes common and rare side effects information for consumers and ... Applies to norepinephrine: injectable solution, intravenous solution. General. If plasma volumes are not corrected, hypotension ... Hypotension midodrine, phenylephrine, norepinephrine, ephedrine, Levophed, Northera, ProAmatine, droxidopa, Akovaz, Orvaten, ... Norepinephrine Side Effects. Medically reviewed by Drugs.com. Last updated on Aug 7, 2017. ...
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Selective noradrenaline/norepinephrine agentsSelective noradrenaline/norepinephrine agents

Bupropion, which is thought to act on both the dopamine and norepinephrine (NE) systems, has not been widely used as an ...
more infohttps://www.biopsychiatry.com/noradrenergic.htm
  • Regardless of how and where it is released, norepinephrine acts on target cells by binding to and activating noradrenergic receptors located on the cell surface. (wikipedia.org)
  • Guanfacine also lowers both the systolic blood pressure, or top reading, and the diastolic blood pressure, or bottom reading, by stimulating norepinephrine receptors in the prefrontal cortex. (livestrong.com)
  • A stimulation of the norepinephrine receptors leads to a decrease in nerve signals from the vasomotor center to blood vessels and heart. (livestrong.com)
  • With this in mind, pharmaceutical companies have worked to hard to develop new types of antidepressants that act on norepinephrine and dopamine receptors. (wisegeek.com)
  • Atomoxetine -a norepinephrine-predominant SNRI used in the treatment of ADHD and, off-label, major depression. (wikipedia.org)
  • High blood concentrations of norepinephrine can cause insomnia and anxiety. (livestrong.com)
  • High concentrations of norepinephrine in the blood often correlates with insomnia and anxiety. (livestrong.com)
  • The newest class of anti-depressants, which selectively inhibits the reuptake of both serotonin and norepinephrine, may be even more successful in treating depression and anxiety and lowering blood concentrations of stress chemicals, according to a study in the October 2009 issue of "Journal of Medicinal Chemistry. (livestrong.com)
  • Medications that inhibit the re-uptake of norepinephrine can sometimes cause anxiety and elevated blood pressure. (treatment4addiction.com)
  • Low levels of dopamine tend to suggest low levels of norepinephrine, and the absence or near absence of these chemicals in concert could result in very serious depression or anxiety. (wisegeek.com)
  • If dopamine increases in supply it might stimulate greater production of norepinephrine, and this could result in shaking, anxiety, mania , paranoia or other extremely undesirable features. (wisegeek.com)
  • After release from a neuron, norepinephrine diffuses through the tiny space between the cells (the synapse), where it can bind to a receptor protein on the surface of a nearby cell. (encyclopedia.com)
  • When physiological changes are triggered by a stressful situation, the locus ceruleus in the brain is activated, in turn causing the release of norepinephrine. (news-medical.net)
  • Norepinephrine is released when a host of physiological changes are activated by a stressful event. (wikidoc.org)
  • while your attending instructs you to wait and see how she responds to the fluid bolus, you remember reading an article in one of the "throw away" journals you receive suggesting that there was a benefit to early norepinephrine administration in sepsis, initiated concomitant with fluid resuscitation. (tripdatabase.com)
  • Norepinephrine may also be used for purposes other than those listed in this medication guide. (cardiosmart.org)
  • Norepinephrine is usually given for as long as needed until your body responds to the medication. (cardiosmart.org)
  • To be sure norepinephrine is not causing harmful effects, your blood pressure and breathing will be checked during the entire time you are receiving this medication. (cardiosmart.org)
  • Norepinephrine can damage the skin or tissues around the injection site if the medication accidentally leaks out of the vein. (cardiosmart.org)
  • Norepinephrine levels may be elevated through means other than medication, as remembering stressful events has been shown to drive up norepinephrine activity. (britannica.com)
  • The attention deficit hyperactivity disorder medication guanfacine is a potentially effective medication for lowering blood concentrations of norepinephrine. (livestrong.com)
  • Dopamine specifically creates norepinephrine with use of other chemicals like beta-hydroxylase. (wisegeek.com)
  • Bupropion, which is thought to act on both the dopamine and norepinephrine (NE) systems, has not been widely used as an antidepressant and has more recently been licensed as adjunctive therapy for smoking cessation. (biopsychiatry.com)
  • Norepinephrine release is lowest during sleep, rises during wakefulness, and reaches much higher levels during situations of stress or danger, in the so-called fight-or-flight response. (wikipedia.org)
  • Norepinephrine plays a role in a number of functions including memory, attention, stress reactions, energy levels, and the regulation of emotions. (news-medical.net)
  • Do Norepinephrine levels affect mental health? (news-medical.net)
  • When a person experiences chronic stress, the levels of norepinephrine may fall below normal due to the development of underactivity of the stress response system following prolonged exposure. (news-medical.net)
  • Norepinephrine also acts to increase blood glucose levels and levels of circulating free fatty acids . (britannica.com)
  • High levels of norepinephrine can refer to high levels of the chemical either in the blood or in the central nervous system. (livestrong.com)
  • Though both levels can be measured, it is considerably simpler and more common to measure norepinephrine in the blood than in the central nervous system. (livestrong.com)