Methyldopa: An alpha-2 adrenergic agonist that has both central and peripheral nervous system effects. Its primary clinical use is as an antihypertensive agent.Guanabenz: An alpha-2 selective adrenergic agonist used as an antihypertensive agent.Adrenergic Agonists: Drugs that bind to and activate adrenergic receptors.Adrenergic alpha-Agonists: Drugs that selectively bind to and activate alpha adrenergic receptors.Adrenergic alpha-2 Receptor Agonists: Compounds that bind to and activate ADRENERGIC ALPHA-2 RECEPTORS.Clonidine: An imidazoline sympatholytic agent that stimulates ALPHA-2 ADRENERGIC RECEPTORS and central IMIDAZOLINE RECEPTORS. It is commonly used in the management of HYPERTENSION.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.Dopamine Agonists: Drugs that bind to and activate dopamine receptors.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.Adrenergic beta-Agonists: Drugs that selectively bind to and activate beta-adrenergic receptors.Blood Platelets: Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.Platelet Membrane Glycoproteins: Surface glycoproteins on platelets which have a key role in hemostasis and thrombosis such as platelet adhesion and aggregation. Many of these are receptors.Platelet Aggregation: The attachment of PLATELETS to one another. This clumping together can be induced by a number of agents (e.g., THROMBIN; COLLAGEN) and is part of the mechanism leading to the formation of a THROMBUS.Drug Partial Agonism: Drug agonism involving selective binding but reduced effect. This can result in some degree of DRUG ANTAGONISM.Cell Membrane: The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.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.Kinetics: The rate dynamics in chemical or physical systems.Radioligand Assay: Quantitative determination of receptor (binding) proteins in body fluids or tissue using radioactively labeled binding reagents (e.g., antibodies, intracellular receptors, plasma binders).Cycloserine: Antibiotic substance produced by Streptomyces garyphalus.Low Back Pain: Acute or chronic pain in the lumbar or sacral regions, which may be associated with musculo-ligamentous SPRAINS AND STRAINS; INTERVERTEBRAL DISK DISPLACEMENT; and other conditions.Back Pain: Acute or chronic pain located in the posterior regions of the THORAX; LUMBOSACRAL REGION; or the adjacent regions.Pain: An unpleasant sensation induced by noxious stimuli which are detected by NERVE ENDINGS of NOCICEPTIVE NEURONS.Medetomidine: An agonist of RECEPTORS, ADRENERGIC ALPHA-2 that is used in veterinary medicine for its analgesic and sedative properties. It is the racemate of DEXMEDETOMIDINE.Chronic Pain: Aching sensation that persists for more than a few months. It may or may not be associated with trauma or disease, and may persist after the initial injury has healed. Its localization, character, and timing are more vague than with acute pain.Guanfacine: A centrally acting antihypertensive agent with specificity towards ADRENERGIC ALPHA-2 RECEPTORS.Attention Deficit Disorder with Hyperactivity: A behavior disorder originating in childhood in which the essential features are signs of developmentally inappropriate inattention, impulsivity, and hyperactivity. Although most individuals have symptoms of both inattention and hyperactivity-impulsivity, one or the other pattern may be predominant. The disorder is more frequent in males than females. Onset is in childhood. Symptoms often attenuate during late adolescence although a minority experience the full complement of symptoms into mid-adulthood. (From DSM-V)Impulsive Behavior: An act performed without delay, reflection, voluntary direction or obvious control in response to a stimulus.Hyperkinesis: Excessive movement of muscles of the body as a whole, which may be associated with organic or psychological disorders.Questionnaires: Predetermined sets of questions used to collect data - clinical data, social status, occupational group, etc. The term is often applied to a self-completed survey instrument.Delayed-Action Preparations: Dosage forms of a drug that act over a period of time by controlled-release processes or technology.Prospective Studies: Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group.Phenylacetates: Derivatives of phenylacetic acid. Included under this heading are a variety of acid forms, salts, esters, and amides that contain the benzeneacetic acid structure. Note that this class of compounds should not be confused with derivatives of phenyl acetate, which contain the PHENOL ester of ACETIC ACID.Reproducibility of Results: The statistical reproducibility of measurements (often in a clinical context), including the testing of instrumentation or techniques to obtain reproducible results. The concept includes reproducibility of physiological measurements, which may be used to develop rules to assess probability or prognosis, or response to a stimulus; reproducibility of occurrence of a condition; and reproducibility of experimental results.Severity of Illness Index: Levels within a diagnostic group which are established by various measurement criteria applied to the seriousness of a patient's disorder.Patents as Topic: Exclusive legal rights or privileges applied to inventions, plants, etc.Names: Personal names, given or surname, as cultural characteristics, as ethnological or religious patterns, as indications of the geographic distribution of families and inbreeding, etc. Analysis of isonymy, the quality of having the same or similar names, is useful in the study of population genetics. NAMES is used also for the history of names or name changes of corporate bodies, such as medical societies, universities, hospitals, government agencies, etc.Terminology as Topic: The terms, expressions, designations, or symbols used in a particular science, discipline, or specialized subject area.Foramen Ovale, Patent: A condition in which the FORAMEN OVALE in the ATRIAL SEPTUM fails to close shortly after birth. This results in abnormal communications between the two upper chambers of the heart. An isolated patent ovale foramen without other structural heart defects is usually of no hemodynamic significance.United StatesProfessional Autonomy: The quality or state of being independent and self-directing, especially in making decisions, enabling professionals to exercise judgment as they see fit during the performance of their jobs.Carcinoma, Lewis Lung: A carcinoma discovered by Dr. Margaret R. Lewis of the Wistar Institute in 1951. This tumor originated spontaneously as a carcinoma of the lung of a C57BL mouse. The tumor does not appear to be grossly hemorrhagic and the majority of the tumor tissue is a semifirm homogeneous mass. (From Cancer Chemother Rep 2 1972 Nov;(3)1:325) It is also called 3LL and LLC and is used as a transplantable malignancy.Health Services Accessibility: The degree to which individuals are inhibited or facilitated in their ability to gain entry to and to receive care and services from the health care system. Factors influencing this ability include geographic, architectural, transportational, and financial considerations, among others.Health Services: Services for the diagnosis and treatment of disease and the maintenance of health.Guaifenesin: An expectorant that also has some muscle relaxing action. It is used in many cough preparations.Pseudoephedrine: A phenethylamine that is an isomer of EPHEDRINE which has less central nervous system effects and usage is mainly for respiratory tract decongestion.Investigational New Drug Application: An application that must be submitted to a regulatory agency (the FDA in the United States) before a drug can be studied in humans. This application includes results of previous experiments; how, where, and by whom the new studies will be conducted; the chemical structure of the compound; how it is thought to work in the body; any toxic effects found in animal studies; and how the compound is manufactured. (From the "New Medicines in Development" Series produced by the Pharmaceutical Manufacturers Association and published irregularly.)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.Drug Approval: Process that is gone through in order for a drug to receive approval by a government regulatory agency. This includes any required pre-clinical or clinical testing, review, submission, and evaluation of the applications and test results, and post-marketing surveillance of the drug.Nasal Decongestants: Drugs designed to treat inflammation of the nasal passages, generally the result of an infection (more often than not the common cold) or an allergy related condition, e.g., hay fever. The inflammation involves swelling of the mucous membrane that lines the nasal passages and results in inordinate mucus production. The primary class of nasal decongestants are vasoconstrictor agents. (From PharmAssist, The Family Guide to Health and Medicine, 1993)United States Food and Drug Administration: An agency of the PUBLIC HEALTH SERVICE concerned with the overall planning, promoting, and administering of programs pertaining to maintaining standards of quality of foods, drugs, therapeutic devices, etc.Loratadine: A second-generation histamine H1 receptor antagonist used in the treatment of allergic rhinitis and urticaria. Unlike most classical antihistamines (HISTAMINE H1 ANTAGONISTS) it lacks central nervous system depressing effects such as drowsiness.Drugs, Investigational: Drugs which have received FDA approval for human testing but have yet to be approved for commercial marketing. This includes drugs used for treatment while they still are undergoing clinical trials (Treatment IND). The main heading includes drugs under investigation in foreign countries.

Modulation of long-term synaptic depression in visual cortex by acetylcholine and norepinephrine. (1/2158)

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)

Modulation of basal intracellular calcium by inverse agonists and phorbol myristate acetate in rat-1 fibroblasts stably expressing alpha1d-adrenoceptors. (2/2158)

In rat-1 fibroblasts stably expressing alpha1d-adrenoceptors BMY 7378, phentolamine, chloroethylclonidine and 5-methyl urapidil decreased basal [Ca2+]i. WB 4101 induced a very small effect on this parameter but when added before the other antagonists it blocked their effect. All these agents inhibited the action of norepinephrine. Phorbol myristate acetate also blocked the effect of norepinephrine and decreased basal [Ca2+]i. Staurosporine inhibited these effects of the phorbol ester. Our results suggest that: (1) alpha1d-adrenoceptors exhibit spontaneous ligand-independent activity, (2) BMY 7378, phentolamine, chloroethylclonidine and 5-methyl urapidil act as inverse agonists and (3) protein kinase C activation blocks spontaneous and agonist-stimulated alpha1d-adrenoceptor activity.  (+info)

Uninjured C-fiber nociceptors develop spontaneous activity and alpha-adrenergic sensitivity following L6 spinal nerve ligation in monkey. (3/2158)

We investigated whether uninjured cutaneous C-fiber nociceptors in primates develop abnormal responses after partial denervation of the skin. Partial denervation was induced by tightly ligating spinal nerve L6 that innervates the dorsum of the foot. Using an in vitro skin-nerve preparation, we recorded from uninjured single afferent nerve fibers in the superficial peroneal nerve. Recordings were made from 32 C-fiber nociceptors 2-3 wk after ligation and from 29 C-fiber nociceptors in control animals. Phenylephrine, a selective alpha1-adrenergic agonist, and UK14304 (UK), a selective alpha2-adrenergic agonist, were applied to the receptive field for 5 min in increasing concentrations from 0.1 to 100 microM. Nociceptors from in vitro control experiments were not significantly different from nociceptors recorded by us previously in in vivo experiments. In comparison to in vitro control animals, the afferents found in lesioned animals had 1) a significantly higher incidence of spontaneous activity, 2) a significantly higher incidence of response to phenylephrine, and 3) a higher incidence of response to UK. In lesioned animals, the peak response to phenylephrine was significantly greater than to UK, and the mechanical threshold of phenylephrine-sensitive afferents was significantly lower than for phenylephrine-insensitive afferents. Staining with protein gene product 9.5 revealed an approximately 55% reduction in the number of unmyelinated terminals in the epidermis of the lesioned limb compared with the contralateral limb. Thus uninjured cutaneous C-fiber nociceptors that innervate skin partially denervated by ligation of a spinal nerve acquire two abnormal properties: spontaneous activity and alpha-adrenergic sensitivity. These abnormalities in nociceptor function may contribute to neuropathic pain.  (+info)

Homologous regulation of the alpha2C-adrenoceptor subtype in human hepatocarcinoma, HepG2. (4/2158)

1. Previous studies of the regulation of the alpha2C-adrenoceptor in OK and in transfected cells have led to discrepant conclusions. In the present work, we examined the homologous regulation of the human alpha2C-adrenoceptor in the hepatocarcinoma cell-line, HepG2; a model which expresses this subtype spontaneously. 2. Short-period treatment of the cells with UK14304 provoked neither a diminution of the potency of the alpha2-agonist to inhibit forskolin-induced cyclic AMP-accumulation nor a change in the degree of receptor coupling to G-proteins. 3. Long-period exposure to UK14304 resulted in a large reduction of [3H]MK912 binding sites (55% decrease). The action of UK14304 was dose-dependent (EC50 = 190 +/- 45 nM), rapid (t1/2 = 4.2 h) and reversible. Receptor down-regulation was also observed with clonidine or (-)adrenaline (38 and 36% decrease, respectively) and was blocked by the addition of alpha2-antagonists. 4. Conversely to that observed with alpha2-agonists, treatment of the cells with RX821002 or yohimbine alone, but not with phentolamine, promoted a significant increase of the receptor expression. 5. The observed alterations of receptor density are not the reflection of changes at the alpha2C4 mRNA level. Estimation of the receptor protein turnover and measurement of its half-life demonstrated that down-regulation by alpha2-agonists and up-regulation by alpha2-antagonists, with inverse-agonist efficacy, are respectively the consequence of increased and decreased rate of receptor degradation. 6. In conclusion, our data show that alpha2C-adrenoceptor does not undergo desensitization but is down-regulated in HepG2. The lack of desensitization agrees with previous results obtained in cells transfected with the alpha2C4 gene, but not with observations made in OK cells. Inversely, down-regulation fits with results obtained in OK but not in transfected cells. The reasons for these discrepancies are discussed. Our results also demonstrated that certain alpha2-antagonists behave as inverse agonist on the HepG2 model and thus provide for the first time evidence of inverse efficacy of antagonists on a cellular model expressing physiological level of a wild-type alpha2-adrenoceptor.  (+info)

Effects of heptanol on the neurogenic and myogenic contractions of the guinea-pig vas deferens. (5/2158)

1. The effects of the putative gap junction uncoupler, 1-heptanol, on the neurogenic and myogenic contractile responses of guinea-pig vas deferens were studied in vitro. 2. Superfusion of 2.0 mM heptanol for 20-30 min produced the following reversible changes in the biphasic neurogenic contractile response (8 trials): (i) suppression of both phases; (ii) delayed development of both the first as well as the second phase, accompanied by complete temporal separation of the two phases; (iii) prominent oscillations of force during the second (noradrenergic) phase only. 3. To eliminate prejunctional effects of heptanol, myogenic contractions were evoked by field stimulation of the vas in the presence of suramin (200 microM) and prazosin (1 microM). Heptanol (2.0 mM) abolished these contractions reversibly. 4. These results show that (i) heptanol inhibits both excitatory junction potential (EJP)-dependent and non EJP-dependent contractions of the vas; (ii) a postjunctional site of action of heptanol, probably intercellular uncoupling of smooth muscle cells, contributes to the inhibition of contraction.  (+info)

alpha1-Adrenergic stimulation of FGF-2 promoter in cardiac myocytes and in adult transgenic mouse hearts. (6/2158)

Fibroblast growth factor (FGF-2), a mitogenic, angiogenic, and cardioprotective agent, is reported to be released from the postnatal heart by a mechanism of transient remodeling of the sarcolemma during contraction. This release can be increased with adrenergic stimulation. RNA blotting was used to assess whether FGF-2 synthesis in neonatal rat cardiomyocytes might also be regulated by adrenergic stimulation. FGF-2 RNA levels were increased after treatment with norepinephrine for 6 h or with the alpha-adrenergic agonist phenylephrine for 48 h. To assess an effect on transcription, neonatal rat cardiomyocytes were transfected with a hybrid rat FGF-2 promoter/luciferase gene (-1058FGFp.luc) and treated with norepinephrine or phenylephrine for 6 or 48 h, respectively. FGF-2 promoter activity was increased two- to sevenfold in an alpha1-specific manner. Putative phenylephrine-responsive elements (PEREs) were identified at positions -780 and -761 relative to a major transcription initiation site. However, deletion analysis of -1058FGFp.luc showed that the phenylephrine response was independent of the putative PEREs, cell contraction, and Ca2+ influx. In transgenic mice expressing -1058FGFp.luc, a significant three- to sevenfold stimulation of FGF-2 promoter activity was detected in the hearts of two independent lines 6 h after intraperitoneal administration of phenylephrine (50 mg/kg). This increase was still apparent at 24 h but was not detected at 48 h posttreatment. Analysis of FGF-2 mRNA in normal mouse hearts revealed accumulation of the 6.1-kb transcript at 24 h. Control of local FGF-2 synthesis at the transcriptional level through adrenergic stimulation may be important in the response to injury as well as in the maintenance of a healthy myocardium.  (+info)

Endothelin antagonists block alpha1-adrenergic constriction of coronary arterioles. (7/2158)

We have previously observed that intracoronary administration of the alpha1-adrenergic agonist phenylephrine (PE) over a period of minutes induced both an immediate and long-lasting (2 h) vasoconstriction of epicardial coronary arterioles. Because it is unlikely that alpha1-adrenergic constriction would persist for hours after removal of the agonist, this observation supports the view that another constrictor(s) is released during alpha1-adrenergic activation and induces the prolonged vasoconstriction. Therefore, we hypothesized that the prolonged microvascular constriction after PE is due to the production of endothelin (ET). We focused on ET not only because this peptide produces potent vasoconstriction but also because its vasoconstrictor action is characterized by a long duration. To test this hypothesis, the diameters of coronary arterioles (<222 micrometers) in the beating heart of pentobarbital-anesthetized dogs with stroboscopic intravital microscopy were measured during a 15-min intracoronary infusion of PE (1 microgram. kg-1 . min-1) and at 15-min intervals for a total of 120 min. All experiments were performed in the presence of beta-adrenergic blockade with propranolol. At 120 min, arterioles in the PE group were constricted (-23 +/- 9% change in diameter vs. baseline). Pretreatment with the ET-converting enzyme inhibitor phosphoramidon or the ETA-receptor antagonist FR-139317 prevented the PE-induced constriction at 120 min (-1 +/- 3 and -6 +/- 3%, respectively, P < 0.01 vs. PE). Pretreatment with the selective alpha1-adrenergic antagonist prazosin (Prz) also prevented the sustained constriction (0 +/- 2%, P < 0.01 vs. PE) but Prz given 60 min after PE infusion did not (-13 +/- 3%). In the aggregate, these results show that vasoconstriction of epicardial coronary arterioles via alpha1-adrenergic activation is blocked by an ET antagonist and an inhibitor of its production. From these data, we conclude that alpha1-adrenergic activation promotes the production and/or release of ET, which produces or facilitates microvascular constriction of epicardial canine coronary arterioles.  (+info)

Effect of bolus epinephrine on systemic hemodynamics in canine anaphylactic shock. (8/2158)

OBJECTIVE: Epinephrine (Epi) is considered to be the drug of choice for anaphylactic shock (AS). However, the benefit of this drug on improving systemic hemodynamics in AS has never been shown. We used a canine ragweed model of AS to determine if an intravenous bolus of Epi hastened the recovery of hemodynamics and modified mediator release (Med) compared with no treatment (NT). METHODS: In one protocol (n = 8), the effects on hemodynamics of two intravenous doses of Epi (0.01 and 0.025 mg/kg) were examined for 3 h postshock in respective studies approximately three weeks apart under pentobarbital anesthesia in the same animal. In five other dogs, left ventricular (LV) mechanics were additionally determined by sonomicrometric techniques to determine changes in contractility as defined by the preload recruitable stroke-work (SW) relationship. RESULTS: Compared with NT values, Epi treatments produced only transient increases in mean arterial pressure (MAP) and cardiac output (CO) post-challenge. By 20 min postshock, CO in the Epi studies were generally lower (p < 0.05) and BP was not different from NT values. With Epi treatment, SW was reduced for a given LV end-diastolic volume compared with the control study. Epi treatments also caused relatively higher plasma thromboxane B2 concentrations postshock. CONCLUSION: Our findings indicate that, when given immediately postshock, bolus-Epi did not hasten recovery and caused impairment in LV mechanics in canine AS.  (+info)

*Alpha-1A adrenergic receptor

... a potent alpha 1-adrenergic receptor agonist, selective for the alpha 1A receptor subtype". J. Pharmacol. Exp. Ther. 274 (1): ... 1994). "Cloning, expression and characterization of human alpha adrenergic receptors alpha 1a, alpha 1b and alpha 1c". Biochem ... The alpha-1A adrenergic receptor (α1A adrenoreceptor), also known as ADRA1A, formerly known also as the alpha-1C adrenergic ... There are 3 alpha-1 adrenergic receptor subtypes: alpha-1A, -1B and -1D, all of which signal through the Gq/11 family of G- ...

*Alpha-adrenergic agonist

An adrenergic alpha-agonist (or alpha-adrenergic agonists) are a class of sympathomimetic agents that selectively stimulates ... Alpha blocker Adrenergic agonist Beta-adrenergic agonist Declerck I, Himpens B, Droogmans G, Casteels R (September 1990). "The ... α Adrenergic agonists have the opposite function of alpha blockers. Alpha adrenoreceptor ligands mimic the action of ... alpha adrenergic receptors. The alpha-adrenergic receptor has two subclasses α1 and α2. Alpha 2 receptors are associated with ...

*Mivazerol

... is an alpha-adrenergic agonist. Fox K, Dargie HJ, de Bono DP, Oliver MF, Wülfert E, Kharkevitch T (September 1999). " ... "Effect of an alpha(2) agonist (mivazerol) on limiting myocardial ischaemia in stable angina". Heart. 82 (3): 383-5. doi:10.1136 ...

*Allergic rhinitis

For nocturnal symptoms, intranasal corticosteroids can be combined with nightly oxymetazoline, an adrenergic alpha-agonist, or ...

*Nasal congestion

Alpha-adrenergic agonists are the first treatment of choice. They relieve congestion by constricting the blood vessels in the ...

*Vasoactivity

Important vasoactive substances are angiotensin-11, endothelin-1, and alpha-adrenergic agonists. Various vasoactive agents, ...

*Ciliary body

Alpha-adrenergic agonists work by decreasing production of fluid and increasing drainage. Brimonidine and Apraclonidine are two ... less selective alpha agonists such as [epinephrine] may decrease the production of aqueous humor through vasoconstriction of ... commonly prescribes alpha agonists for glaucoma treatment. Alphagan P uses a purite preservative, which is better tolerated ...

*Amitraz

Adverse effects in mammals are caused by amitraz' alpha-adrenergic agonist activity. Symptoms can include low blood pressure ... Its effectiveness is traced back on alpha-adrenergic agonist activity, interaction with octopamine receptors of the central ...

*Xylometazoline

... is in the decongestant and alpha-adrenergic agonist families of medication. Xylometazoline was patented in 1956 ... It binds to α1 and α2 adrenergic receptors in the nasal mucosa. Due to its sympathomimetic effects, it should not be used by ... The drug works by stimulating adrenergic receptors on the lamina propria of blood vessels in the nose. The decongestant effect ... Haenisch, B.; Walstab, J.; Herberhold, S.; Bootz, F.; Tschaikin, M.; Ramseger, R.; Bönisch, H. (2009). "Alpha-adrenoceptor ...

*List of MeSH codes (D16)

... adrenergic agents MeSH D27.505.519.625.050.100 --- adrenergic agonists MeSH D27.505.519.625.050.100.100 --- adrenergic alpha- ... adrenergic agents MeSH D27.505.696.577.050.100 --- adrenergic agonists MeSH D27.505.696.577.050.100.100 --- adrenergic alpha- ... agonists MeSH D27.505.519.625.050.100.200 --- adrenergic beta-agonists MeSH D27.505.519.625.050.200 --- adrenergic antagonists ... agonists MeSH D27.505.696.577.050.100.200 --- adrenergic beta-agonists MeSH D27.505.696.577.050.200 --- adrenergic antagonists ...

*Overflow incontinence

Alpha-adrenergic agonists may cause urinary retention by stimulating the contraction of the urethral sphincter. Calcium channel ...

*Benign prostatic hyperplasia

Alpha-adrenergic agonist medications, such as decongestants with pseudoephedrine can increase bladder outlet resistance. In ... Effects may take longer to appear than alpha blockers, but they persist for many years. When used together with alpha blockers ... As men age, the enzymes aromatase and 5-alpha reductase increase in activity. Aromatase and 5-alpha reductase are responsible ... Alpha blockers relax smooth muscle in the prostate and the bladder neck, thus decreasing the blockage of urine flow. Common ...

*Beta blocker

... s must not be used in the treatment of selective alpha-adrenergic agonist overdose. The blockade of only beta ... β1-adrenergic receptors are located mainly in the heart and in the kidneys. β2-adrenergic receptors are located mainly in the ... Newer, third-generation beta blockers can cause vasodilation through blockade of alpha-adrenergic receptors. Accordingly, ... These agents are capable of exerting low-level agonist activity at the β-adrenergic receptor while simultaneously acting as a ...

*Alpha-2 adrenergic receptor

"Inhibition of the lipolytic action of beta-adrenergic agonists in human adipocytes by alpha-adrenergic agonists". J. Lipid Res ... Agonists 4-NEMD 7-Me-marsanidine (also I1 agonist) Agmatine (also I agonist, NMDA, 5-HT3, nicotinic antagonist and NOS ... The alpha-2 (α2) adrenergic receptor (or adrenoceptor) is a G protein-coupled receptor (GPCR) associated with the Gi ... Agonists (activators) of the α2-adrenergic receptor are frequently used in veterinary anaesthesia where they affect sedation, ...

*Hydromorphone

"Simultaneous treatment of hypertension and opiate withdrawal using an alpha 2 adrenergic agonist" (PDF). J Natl Med Assoc. 75: ... Hydromorphone is a semi-synthetic μ-opioid agonist. As a hydrogenated ketone of morphine, it shares the pharmacologic ...

*Micro-g environment

Another countermeasure includes administration of Midodrine, which is a selective alpha-1 adrenergic agonist. Midodrine ... The use of beta-2 adrenergic agonists to increase muscle mass, and the use of essential amino acids in conjunction with ...

*Methyldopa

... is in the alpha-2 adrenergic receptor agonist family of medication. It works by stimulating the brain to decrease ... α-methylnorepinephrine is an agonist of presynaptic central nervous system α2 adrenergic receptors. Activation of these ... with increased use of other safer and more tolerable agents such as alpha blockers, beta blockers, and calcium channel blockers ... This inhibition results in reduced dopaminergic and adrenergic neurotransmission in the peripheral nervous system. This effect ...

*4-NEMD

... is a potent sedative drug which acts as a selective alpha-2 adrenergic agonist. It is closely related to dexmedetomidine ... ethyl-1H-imidazoles on alpha 1- and alpha 2-adrenergic receptors". Journal of Medicinal Chemistry. 37 (15): 2328-33. doi: ... Like other alpha-2 agonists, it produces sedative and muscle relaxant effects but without producing respiratory depression. It ... "Medetomidine analogs as alpha 2-adrenergic ligands. 3. Synthesis and biological evaluation of a new series of medetomidine ...

*Attention deficit hyperactivity disorder

Medications used include stimulants, atomoxetine, alpha-2 adrenergic receptor agonists, and sometimes antidepressants. In those ...

*TEAD3

... is a transcriptional activator in alpha 1-adrenergic agonist-stimulated cardiac myocytes". The Journal of Biological Chemistry ...

*C10H16N2O3S

The molecular formula C10H16N2O3S (molar mass : 244.31 g/mol) may refer to : Amidephrine, an alpha-adrenergic agonist Biotin, a ...

*Beta-adrenergic agonist

Alpha-adrenergic agonist "WHAT ARE BETA-AGONISTS?". Thoracic.org. American Thoracic Society. Retrieved 17 October 2014. ... Beta adrenergic agonists or beta agonists are medications that relax muscles of the airways, which widen the airways and result ... In general, pure beta-adrenergic agonists have the opposite function of beta blockers. Beta adrenoreceptor agonist ligands ... Adrenergic beta-Agonists at the US National Library of Medicine Medical Subject Headings (MeSH) Delbruck, Max. "The beta- ...

*Urinary retention

... alpha-adrenergic agonists, opiates, nonsteroidal anti-inflammatories (NSAIDs), calcium-channel blockers and beta-adrenergic ... BPH may respond to alpha blocker and 5-alpha-reductase inhibitor therapy, or surgically with prostatectomy or transurethral ... 2010-02-10 Fisher, Euan; Subramonian, Kesavapillai; Omar, Muhammad Imran (2014-06-10). "The role of alpha blockers prior to ... agonists, may increase the risk. Anesthesia: General anesthetics during surgery may cause bladder atony by acting as a smooth ...

*2C-H

It was found to be an active Alpha-1 adrenergic receptor agonist in rabbit ear arteries. It has binding affinity towards 5-HT2C ... Very little data exists about the pharmacological properties, metabolism, and toxicity of 2C-H. It exhibits agonist activity at ...

*Alpha agonist

... may refer to: Alpha-adrenergic agonist, drugs that selectively stimulate alpha adrenergic receptors PPAR ... modulator, drugs which act upon the Peroxisome proliferator-activated receptor alpha. ...

*Cannabigerol

CBG has been found to act as a high affinity α2-adrenergic receptor agonist, moderate affinity 5-HT1A receptor antagonist, and ... "Evidence that the plant cannabinoid cannabigerol is a highly potent alpha(2)-adrenoceptor agonist and moderately potent 5HT ... Evidence that the plant cannabinoid cannabigerol is a highly potent α2-adrenoceptor agonist and moderately potent 5HT1A ...

*Prazosin

It is an α1-blocker which acts as an inverse agonist at alpha-1 adrenergic receptors. These receptors are found on vascular ... Day, H. E.; Campeau, S.; Watson Jr, S. J.; Akil, H. (1997). "Distribution of alpha 1a-, alpha 1b- and alpha 1d-adrenergic ... A larger controlled Phase II "Clinical Trial of the Adrenergic Alpha-1 Antagonist Prazosin for Alcohol Dependence" is currently ... "A pilot trial of the alpha-1 adrenergic antagonist, prazosin, for alcohol dependence". Alcoholism: Clinical and Experimental ...
Removal of endothelial cells on rings of rat aorta increased the sensitivity to the selective alpha-1 adrenoceptor agonist phenylephrine, to the nonselective alpha adrenoceptor agonist norepinephrine and to the selective alpha-2 adrenoceptor agonist clonidine. In the case of the first two, which are strong agonists for the alpha-1 adrenoceptor-mediating contraction, removal of endothelium increased sensitivity 4- and 6-fold at the EC30 level, but produced little or no increase in maximum. In the case of clonidine, a partial agonist for the alpha-1 adrenoceptor, which gave only about 15% of the maximum given by phenylephrine on endothelium-containing rings, removal of the endothelium not only shifted the curve to the left but also increased the maximum to about 50% of that given by phenylephrine. The depression of sensitivity to these agonists in rings with endothelium appeared to be due to the vasodepressor action of endothelium-derived relaxing factor (EDRF), as hemoglobin, a specific blocking ...
Ample experimental evidence supports the existence of two distinct types of vasoconstrictor α-adrenoceptors in vascular smooth muscle at postjunctional sites, showing similarities with α1 and α2-adrenoceptors. Especially in vivo, the characterization of an α2-adrenoceptor mediating an increase in diastolic pressure has been most successful. In this respect the model of the pithed rat has been employed most frequently (for reviews see [1, 2]).. At present, the agents cirazoline, (−) phenylephrine, (±)-erythro-methoxamine, (−)-amidephrine, SKF89748, St587 and Sgd 101/75 fulfil the criteria for selective α1-adrenoceptor agonists; their log dose-vasopressor effect curves are virtually unaffected by previous treatment with yohimbine or rauwolscine (selective dose in pithed rats: 1 mg/kg), whereas prazosin (selective dose in pithed rats: 0.1 mg/kg) causes an appreciable parallel rightward displacement. The reverse holds true for the stimulants B-HT 920, B-HT 933, B-HT 958, UK-14304, ...
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The invention relates to combinations of an aminosugar and a beta-2-adrenoceptor agonist, such as salbutamol, for the treatment of diseases associated with hypersensivity and inflamation, in particula
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MK 912 is a potent antagonist at central α2 adrenoceptors. MK 912 is reported to almost completely inhibit the effects of clonidine, a central α2 agonist. MK
Physostigmine (P) was used as a model in anesthetized rats for the development of hypertension by a central cholinergic mechanism. P (25-100 micrograms/kg i.v.) produced a dose-related increase in mean arterial pressure which was inhibited 30 to 90% by preinjection of clonidine (100 micrograms/kg i.v.). This dose of clonidine was without effect on the pressor response to ganglionic stimulation produced by 1,1-dimethyl-4-phenylpipera-zinium iodine. To examine further the central inhibitory effect of clonidine on the pressor response to P, regional brain acetylcholine turnover rate was measured in control and clonidine-pretreated rats. Clonidine significantly reduced turnover in hypothalamus (69%), pons-medulla (43%) and midbrain (39%) but not in striatum or hippocampus. These observations are consistent with an inhibitory effect of clonidine on central cholinergic neurons involved in cardiovascular regulation. ...
1. Earlier studies have shown that exposure of fat-cells to insulin results in the rapid increased phosphorylation of an acid-soluble 22 kDa protein and that increases in phosphorylation were also evident in cells exposed to adrenaline [Belsham & Denton (1980) Biochem. Soc. Trans. 8, 382-383; Belsham, Brownsey, Hughes & Denton (1980) Diabetologia 18, 307-312]. 2. The effects of adrenaline are shown to be brought about through beta-adrenergic receptors and to be mimicked by other agents which increase cell cyclic AMP concentrations. The maximum extent of phosphorylation is about 60% of that observed with insulin. Increased phosphorylation is also observed in fat-cells exposed to vasopressin, oxytocin and phorbol esters, but not to alpha-adrenergic agonists. 3. No changes in the phosphorylation of the protein are evident in epididymal fat-pads from fat-fed, starved or starved/refed animals, despite the large changes in protein composition of fat-cells which accompany these nutritional alterations. ...
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The invention provides compounds useful as β 3 -adrenorecptor agonists and pharmaceutical compositions comprising such compounds. The invention further includes a method for stimulating, regulating, and modulating metabolism in fats of adipose tissue in mammals by administering an effective amount of a compound of the invention.
The present study examined the effect of structural analogs of clonidine on feeding in both rabbits and monkeys. In rabbits, lofexidine and tizanidine either did not influence or decreased food intake in contrast to clonidine, which stimulated food i
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This study investigated the participation of median raphe nucleus (MnR) α1-adrenergic receptors in the control of feeding behaviour. The α1-adrenergic agonist phenylephrine (PHE) and α2-adrenergic agonist clonidine (CLON) (at equimolar doses of 0, 6 and 20 nmol) were injected into the MnR of: a) rats submitted to overnight fasting (18 h); or b) rats maintained with 15 g of lab chow/day for 7 days. Immediately after the drug injections, the animals were placed in the feeding chamber and feeding and non-ingestive behaviours such as grooming, rearing, resting, sniffing and locomotion were recorded for 30 min. The results showed that both doses of PHE injected into the MnR of overnight fasted animals decreased food intake accompanied by an increase in the latency to start feeding. A reduction in feeding duration was observed only after treatment of the MnR with the 20 nmol dose of PHE. Both locomotion duration and sniffing frequency increased after injection with the highest dose PHE into the MnR.
1.Impaired vasoconstriction in animals with cirrhosis is maintained in isolated vessels in vitro, indicating an intrinsic alteration in function or structure of the cells in the vascular wall. This may be due to receptor down-regulation, a defect in post-receptor signal transduction or overproduction of vasodilator compounds. This investigation examined the role of these mechanisms in modulating α-adrenoceptor-mediated contraction in hepatic arteries from patients with advanced cirrhosis.. 2.Hepatic arteries were obtained from subjects with and without cirrhosis for functional investigation in vitro. Endothelial cell function was assessed using endothelium-dependent (acetylcholine) and independent (3′-morpholinosydnonimine) vasodilators. α-Adrenoceptor-mediated contraction was assessed by constructing cumulative concentration-response curves to the α1-selective agonist phenylephrine, the non-selective adrenoceptor agonist noradrenaline and the receptor-independent vasoconstrictor potassium ...
Objectives: 1) To describe electroencephalogram (EEG) appearance in the awake dog and compare these results with EEG recordings after low dose medetomidine (2 μg/kg IV) followed by atipamezole (10 μg/kg, IM); 2) To institute EEG recordings after low dose medetomidine or dexmedetomidine as a standard of practice if focal abnormalities and amplitudes were not significantly altered by pharmaceuticals in Phase 1 of this study. Methods: Electroencephalograms were performed on eight clinical canine patients with suspected intracranial disease involving the prosencephalon. A five lead montage was used to record the EEGs. Each dog had an awake, baseline recording followed by an EEG performed after administration of low dose medetomidine (2 μg/kg IV) then atipamezole (10 μg/kg, IM). In the second phase of this study, the same dose of medetomidine or dexmedetomidine at 1 μg/kg IV and atipamezole (10 μg/kg, IM) were used in the evaluation of 20 clinical patients with suspected neurologic disease
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BACKGROUND AND PURPOSE: In mouse tail arteries, selective alpha(2)-adrenoceptor antagonism with rauwolscine caused powerful dilation during constriction to the alpha(1)-adrenoceptor agonist phenylephrine. This study therefore assessed phenylephrines selectivity at vascular alpha-adrenoceptors and the mechanism(s) underlying dilation to rauwolscine. EXPERIMENTAL APPROACH: Mouse isolated tail arter
Background. Though buprenorphine effectively treats opioid dependence, some abstinent patients relapse to maladaptive use of opioids during treatment. Relapse may be triggered by stress. Rodent studies have demonstrated that stress can induce relapse to heroin and cocaine use (Erb, et al., 1996; Shaham, et al., 1996; Shaham and Stewart, 1995). In a rodent model, stress-induced relapse to heroin and cocaine seeking is blocked by the alpha-2 adrenergic agonist clonidine. In this study, clonidine will be compared to placebo in preventing relapse to opioid abuse in opioid maintained patients who have achieved abstinence while on buprenorphine and contingency management.. Scientific goals. To determine whether clonidine, given to abstinent patients maintained on buprenorphine, prevents relapse to opioid use more effectively than placebo.. Participant population. 300 opioid-dependent outpatients (120 evaluable). Target enrollment will include 40 persent women and 60 percent minorities (mostly ...
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Initially, we observed strong labeling when sections were examined with the light microscope; but when examined with the electron microscope, we observed only a few profiles containing DAB in the neuropil of the BNST. Instead, we observed what appeared to be DAB reaction product in the extracellular space outlining neuropil elements that themselves contained no clear label (Fig. 3A2). We reasoned that this was because the HA tag was attached to the N terminus of the receptor, a region predicted to be on the extracellular surface when the receptor is on the plasma membrane. Accordingly, we pretreated animals with the α2-AR agonist clonidine before death to induce internalization of the receptor (Lu et al., 2009). We found that, with clonidine pretreatment, the extracellular label was greatly decreased and neuropil elements containing DAB label were more common. Dendritic shafts and preterminal axons appeared most commonly labeled in this clonidine-treated material, but dendritic spines and axon ...
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Dexmedetomidine is a new selective and potent alpha-2 agonist. It has centrally acting anesthetic properties. It has been known that intrathecal addition of alpha-2 adrenergic agents result in prolongation of the duration of the sensory and motor blockade induced by hyperbaric bupivacaine. But the effects of intravenous dexmedetomidine on the spinal block was not evaluated. The aim of study is to assess the effect of intravenous dexmedetomidine on the low-dose spinal anesthesia for the transurethral surgery ...
SINGH, Gyan D. et al. Clinicophysiological and haemodynamic effects of fentanyl with xylazine, medetomidine and dexmedetomidine in isoflurane-anaesthetised water buffaloes (Bubalus bubalis). J. S. Afr. Vet. Assoc. [online]. 2013, vol.84, n.1, pp.1-11. ISSN 2224-9435.. The present study was undertaken to investigate the sedative, analgesic and clinical effects of xylazine, medetomidine and dexmedetomidine with fentanyl as pre-anaesthetics in water buffaloes and to compare the dose-sparing effect of xylazine, medetomidine and dexmedetomidine on thiopental for induction and isoflurane for maintenance of anaesthesia in water buffaloes. Six male water buffaloes randomly received intravenous fentanyl (5.0 pg/kg body weight) and xylazine (0.05 mg/kg body weight), fentanyl (5.0 pg/kg body weight) and medetomidine (2.5 pg/kg body weight), fentanyl (5.0 pg/kg body weight) and dexmedetomidine (5.0 pg/kg body weight) at weekly intervals in groups I1, I2 and I3, respectively. After 15 min, the animals were ...
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The principal mechanism by which bronchodilator β-adrenoceptor agonists act is to relax airways smooth muscle although they may also be anti-inflammatory. However, the extent of anti-inflammatory activity and the cell types affected by these agonists are uncertain. The purpose of this study was to evaluate whether β-adrenoceptor agonists prevent pro-inflammatory cytokine generation from activated human lung macrophages. Macrophages were isolated and purified from human lung. The cells were pre-treated with both short-acting (isoprenaline, salbutamol, terbutaline) and long-acting (formoterol, salmeterol, indacaterol) β-agonists before activation with lipopolysaccharide (LPS) to induce cytokine (TNFα, IL-6, IL-8 and IL-10) generation. The experiments showed that short-acting β-agonists were poor inhibitors of cytokine generation. Of the long-acting β-agonists studied, formoterol was also a weak inhibitor of cytokine generation whereas only indacaterol and salmeterol showed moderate ...
Recent studies have shown that dexmedetomidine exerts an anti-inflammatory effect by reducing serum levels of inflammatory factors, however, the up-stream mechanism is still unknown. The transcription factor NF-κB enters the nucleus and promotes the transcription of its target genes, including those encoding the pro-inflammatory cytokines IL-6 and TNF-α. In this study, we established a rat model that simulates a clinical surgical procedure to investigate the anti-inflammatory effect of perineural administration of dexmedetomidine and the underlying mechanism. Dexmedetomidine reduced the sciatic nerve levels of IL-6 and TNF-α at both the mRNA and protein level. Dexmedetomidine also inhibited the translocation of activated NF-κB to the nucleus and the binding activity of NF-κB. The anti-inflammatory effect is confirmed to be dose-dependent. Finally, pyrrolidine dithiocarbamate also reduced the levels of IL-6 and TNF-α and the activation of NF-κB. In conclusion, dexmedetomidine inhibited the nuclear
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3.0.CO;2-3 Hoehe MR, Berrettini WH, Schwinn DA, Hsieh WT (1993). «A two-allele PstI RFLP for the alpha-1C adrenergic receptor gene (ADRA1C).». Hum. Mol. Genet. 1 (5). 349 páginas. PMID 1363873. doi:10.1093/hmg/1.5.349-a !CS1 manut: Nomes múltiplos: lista de autores (link) Schwinn DA, Lomasney JW, Lorenz W; et al. (1990). «Molecular cloning and expression of the cDNA for a novel alpha 1-adrenergic receptor subtype.». J. Biol. Chem. 265 (14): 8183-9. PMID 1970822 !CS1 manut: Uso explícito de et al. (link) !CS1 manut: Nomes múltiplos: lista de autores (link) Hirasawa A, Shibata K, Horie K; et al. (1995). «Cloning, functional expression and tissue distribution of human alpha 1c-adrenoceptor splice variants.». FEBS Lett. 363 (3): 256-60. PMID 7737411. doi:10.1016/0014-5793(95)00330-C !CS1 manut: Uso explícito de et al. (link) !CS1 manut: Nomes múltiplos: lista de autores (link) Diehl NL, Shreeve SM (1995). «Identification of the alpha 1c-adrenoceptor in rabbit arteries and the human ...
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Researchers from the Johns Hopkins University School of Medicine have been looking into the effects of drugs called beta 2 adrenergic agonists on unborn children. The drugs are used to treat asthma and to inhibit or slow down labour but the study found that they may also increase the incidence of autism, mental-health problems, cognitive problems and poor school performance. The drugs are thought to have an adverse effect by disrupting the balance between the sympathetic and parasympathetic nervous systems but it is important to remember that early labour and asthma in pregnancy can also have adverse effects on mothers and children. You should always see your doctor before stopping taking medicine. ...
Woohoo! My favorite receptors! Adrenergic receptors activate the sympathetic branch of the autonomic nervous system. So, adrenergic agonists are known as sympathomimetics, that is, they mimic a sympathetic, or fight or flight, response. Adrenergic antagonists are called sympatholytics. Some highlights: 1. There are FIVE very important subtypes of adrenergic receptor (these will be addressed in…
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Synonyms for alpha-adrenergic receptor in Free Thesaurus. Antonyms for alpha-adrenergic receptor. 2 synonyms for alpha-adrenergic receptor: alpha receptor, alpha-adrenoceptor. What are synonyms for alpha-adrenergic receptor?
Background: Dysmenorrhoea is a common gynaecological complaint that can affect as many as 50% of premenopausal women, 10% of whom suffer severely enough to be rendered incapacitated for one to three days during each menstrual cycle. Primary dysmenorrhoea is where women suffer from menstrual pain but lack any pathology in their pelvic anatomy. Beta2-adrenoceptor agonists have been used in the treatment of women with primary dysmenorrhoea but their effects are unclear. Objectives: To determine the effectiveness and safety of beta2-adrenoceptor agonists in the treatment of primary dysmenorrhoea. Search methods: We searched the Cochrane Menstrual Disorders and Subfertility Group Specialised Register, CENTRAL (The Cochrane Library 2011, Issue 8), MEDLINE, EMBASE, PsycINFO and the EBM Reviews databases. The last search was on 22 August 2011.Selection criteriaRandomised controlled trials comparing beta2-adrenoceptor agonists with placebo or no treatment, each other or any other conventional treatment in women
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TY - JOUR. T1 - Alpha1-adrenoceptor-mediated excitation of substantia nigra pars reticulata neurons. AU - Berretta, N.. AU - Bernardi, G.. AU - Mercuri, N. B.. PY - 2000/6. Y1 - 2000/6. N2 - The effect of noradrenaline was studied in principal neurons of the substantia nigra pars reticulata in rat brain slices using patch clamp recordings. Perfusion of noradrenaline or the α1-adrenoceptor agonist phenylephrine increased the spontaneous firing activity of reticulata cells. The α1-adrenoceptor antagonist prazosin counteracted the effects of noradrenaline. In contrast, the β-adrenoceptor agonist isoproterenol did not affect the activity of reticulata cells and the β-adrenoceptor antagonist pindolol did not prevent noradrenalines effect. In whole-cell recordings, at -60 mV holding potential, noradrenaline caused a tetrodotoxin-resistant inward current with a time-course similar to the increase in firing activity. Analysis of the reversal potential of this current did not give homogeneous ...
Cerebral (BIS, NIRS, CBFV) and cardiorespiratory parameters (mean arterial pressure, arterial oxygen saturation, ETco2, respiratory rate, heart rate) were observed continuously throughout the study period. In addition, at six predetermined intervals, simultaneous samples of arterial and jugular venous blood were obtained for blood gas determination. The six intervals were presedation, presedation with hyperventilation (presedation-HV), steady state dexmedetomidine plasma level 0.6 ng/ml (0.6 ng/ml), steady state dexmedetomidine plasma level 1.2 ng/ml (1.2 ng/ml), steady state dexmedetomidine plasma level 1.2 ng/ml with hyperventilation (1.2 ng/ml-HV), and 30 min after discontinuation of dexmedetomidine infusion (recovery). After placement of the right internal jugular catheter, the room lighting was lowered, and 10 min of undisturbed stabilization ensued. Thereafter, the presedation arterial and venous samples and physiologic data were obtained. The subject was then asked to hyperventilate ...

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The alpha 2 adrenergic agonists clonidine and guanfacine were developed 30 years ago to treat hypertension, but have been used ... Alpha-2 adrenergic receptor inhibition of hippocampal epileptiform activity: comparisons of ligand efficacy and potency ... alpha]-methyl-NE , 6-FNE , (-)NE , Deoxy EPI , Dopamine (deoxyNE) , Xylazine , (+)-NE , (-)-Phenylephrine , Isoproterenol.. ...
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DailyMed - Search Results for Adrenergic alpha-AgonistsDailyMed - Search Results for Adrenergic alpha-Agonists

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Familial Dysautonomia Medication: Benzodiazepines, H2 receptor antagonists, Alpha-adrenergic agonists, CorticosteroidsFamilial Dysautonomia Medication: Benzodiazepines, H2 receptor antagonists, Alpha-adrenergic agonists, Corticosteroids

Alpha-adrenergic agonists. Class Summary. These agents stimulate alpha-adrenoreceptors in brain stem, activating an inhibitory ... A central alpha-adrenergic agonist that suppresses peripheral release of norepinephrine, resulting in lower blood pressure; ... A pure peripheral alpha-adrenergic agonist, which causes peripheral vasoconstriction and raises blood pressure without ...
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An adrenergic alpha-agonist (or alpha-adrenergic agonists) are a class of sympathomimetic agents that selectively stimulates ... Alpha blocker Adrenergic agonist Beta-adrenergic agonist Declerck I, Himpens B, Droogmans G, Casteels R (September 1990). "The ... α Adrenergic agonists have the opposite function of alpha blockers. Alpha adrenoreceptor ligands mimic the action of ... alpha adrenergic receptors. The alpha-adrenergic receptor has two subclasses α1 and α2. Alpha 2 receptors are associated with ...
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Midodrine is a prodrug, i.e., the therapeutic effect of orally administered midodrine is due to the major metabolite desglymidodrine formed by deglycination of midodrine. Desglymidodrine diffuses poorly across the blood-brain barrier, and is therefore not associated with effects on the central nervous system. Administration of midodrine results in a rise in standing, sitting, and supine systolic and diastolic blood pressure in patients with orthostatic hypotension of various etiologies. Standing systolic blood pressure is elevated by approximately 15 to 30 mmHg at 1 hour after a 10-mg dose of midodrine, with some effect persisting for 2 to 3 hours. Midodrine has no clinically significant effect on standing or supine pulse rates in patients with autonomic failure ...
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Alpha-adrenergic Agonists for the Management of Opioid Withdrawal - Medicine by the Numbers - American Family PhysicianAlpha-adrenergic Agonists for the Management of Opioid Withdrawal - Medicine by the Numbers - American Family Physician

Alpha-adrenergic agonists were more efficacious than placebo in the management of opioid withdrawal, but are best reserved as ... ALPHA-ADRENERGIC AGONISTS FOR THE MANAGEMENT OF OPIOID WITHDRAWAL. Benefits. Harms. NNT = 3 to prevent one episode of severe ... ALPHA-ADRENERGIC AGONISTS FOR THE MANAGEMENT OF OPIOID WITHDRAWAL. Benefits. Harms. NNT = 3 to prevent one episode of severe ... Alpha2-adrenergic agonists for the management of opioid withdrawal. Cochrane Database Syst Rev. 2016;(5):CD002024. ...
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Dexmedetomidine activates 2-adrenoceptors, and causes the decrease of sympathetic tone, with attenuation of the neuroendocrine and hemodynamic responses to anesthesia and surgery; it reduces anesthetic and opioid requirements; and causes sedation and analgesia ...
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Alpha2 adrenergic agonists for the management. of opioid withdrawal (Cochrane Review) by. Gowing L, Farrell M, Ali R, White J. ... Ten studies compared a treatment regime based on an alpha2 adrenergic agonist with one based on reducing doses of methadone. ... From the comparison of alpha2 adrenergic agonist regimes with reducing doses of methadone, withdrawal intensity is similar to, ... REVIEWERS CONCLUSIONS: Treatment regimes based on the alpha2 adrenergic agonists clonidine and lofexidine, and those based on ...
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Cyanide Toxicity Medication: Antidotes, Anticonvulsants, Other, Alpha/Beta Adrenergic AgonistsCyanide Toxicity Medication: Antidotes, Anticonvulsants, Other, Alpha/Beta Adrenergic Agonists

Alpha/Beta Adrenergic Agonists. Class Summary. These agents augment coronary and cerebral blood flow during the low-flow states ... It has alpha-agonist effects that include increased peripheral vascular resistance, reversed peripheral vasodilatation, ... Jorge A Martinez, MD, JD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency ... Suzanne White, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Clinical Toxicology, ...
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Clonidine is classified as a centrally acting alpha adrenergic agonist.Clonidine acts centrally as an imidazoline receptor ... Clonidine hydrochloride Alpha adrenergic agonist Clonidine is classified as a centrally acting alpha adrenergic agonist. ... Clonidine is classified as a centrally acting alpha adrenergic agonist.Clonidine acts centrally as an imidazoline receptor ... Clonidine is classified as a centrally acting alpha adrenergic agonist.Clonidine acts centrally as an imidazoline receptor ...
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Selective aortic arch perfusion using perfluorochemical and alpha adrenergic agonist to treat cardiac arrest ... 5. A method according to claim 1, wherein said alpha adrenergic receptor agonist is selected from the group consisting of ... administering said subject an alpha adrenergic receptor agonist in an amount effective to enhance coronary perfusion with said ... and other alpha adrenergic receptor agonists. Epinephrine is currently preferred. Vasoconstrictors may be administered by any ...
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Mivazerol, a new alpha 2-adrenergic agonist, blunts cardiovascular effects following surgical stress in pentobarbital...Mivazerol, a new alpha 2-adrenergic agonist, blunts cardiovascular effects following surgical stress in pentobarbital...

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US5216032A - Selective aortic arch perfusion using perfluorochemical and alpha adrenergic agonist to treat cardiac arrest 
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p-[125I]iodoclonidine is a partial agonist at the alpha 2-adrenergic receptor.p-[125I]iodoclonidine is a partial agonist at the alpha 2-adrenergic receptor.

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Faculty Collaboration Database - Recurrent laryngeal nerve activation by alpha 2 adrenergic agonists in goats.  Respir Physiol...Faculty Collaboration Database - Recurrent laryngeal nerve activation by alpha 2 adrenergic agonists in goats. Respir Physiol...

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The effect of clonidine premedication on hemodynamic responses to microlaryngoscopy and rigid bronchoscopy.The effect of clonidine premedication on hemodynamic responses to microlaryngoscopy and rigid bronchoscopy.

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  • These agents stimulate alpha-adrenoreceptors in brain stem, activating an inhibitory neuron, which in turn results in reduced sympathetic outflow. (medscape.com)
  • Injection of either alpha 2 agonist resulted in respiratory arrhythmias with a greater than seven-fold increase in TE and a 30% reduction in TI. (mcw.edu)
  • The results indicate that central apneas and respiratory arrhythmias may be associated with alpha 2-adrenoceptor modulation of laryngeal expiratory-related activity. (mcw.edu)
  • PIC had minimal agonist activity in inhibiting adenylate cyclase in platelet membranes, but it potentiated platelet aggregation induced by ADP with an EC50 of 1.5 microM. (biomedsearch.com)
  • The purpose of this study was to test the hypothesis that respiratory and apneas induced by alpha 2 agonists in anesthetized goats are associated with an increase of upper airway expiratory-related activity, rather than a general depression of breathing. (mcw.edu)
  • SELECTION CRITERIA: Randomised or quasi-randomised controlled trials that compared alpha2 adrenergic agonists with another form of treatment (or placebo) to modify the signs and symptoms of withdrawal in participants who were primarily opioid dependent. (opioids.com)
  • Ten studies compared a treatment regime based on an alpha2 adrenergic agonist with one based on reducing doses of methadone. (opioids.com)
  • 125I]PIC should prove useful in binding assays involving tissues with a low receptor density or in small tissue samples and in studies of cloned and expressed alpha 2-AR. (biomedsearch.com)