Adrenergic alpha-2 Receptor Agonists
Clonidine
Medetomidine
Adrenergic alpha-1 Receptor Agonists
Phenylephrine
Clenbuterol
Receptors, Adrenergic, alpha
Isoproterenol
Adrenergic alpha-Antagonists
Receptors, Adrenergic
Receptors, Adrenergic, alpha-2
Epinephrine
Yohimbine
Norepinephrine
Dexmedetomidine
Receptors, Adrenergic, beta
Prazosin
Receptors, Adrenergic, beta-3
Receptors, Adrenergic, alpha-1
Propranolol
Dose-Response Relationship, Drug
Receptors, Adrenergic, beta-2
Sympathomimetics
Imidazoles
Guanfacine
Albuterol
Phenoxypropanolamines
Xylazine
Rats, Sprague-Dawley
Dioxanes
Adipose Tissue, Brown
Cyclic AMP
Adrenergic beta-Antagonists
Autonomic Agents
Midodrine
Cyclic CMP
Hypnotics and Sedatives
Propanolamines
Injections, Spinal
Sympatholytics
GABA Agonists
Phentolamine
Rats, Wistar
Dihydroalprenolol
Cells, Cultured
Carbachol
Fluocinolone Acetonide
Alprenolol
Lacrimal Apparatus
Adrenergic Agents
Muscarinic Agonists
Pertussis Toxin
Adrenergic Antagonists
Nicotinic Agonists
Rats, Inbred Strains
Calcium
Drug Interactions
Parasympathomimetics
Colforsin
Serotonin 5-HT2 Receptor Agonists
Vasopressins
Virulence Factors, Bordetella
Serotonin 5-HT1 Receptor Agonists
Dogs
Histamine Agonists
Ciliary Body
Adenylate Cyclase
Adenylate Cyclase Toxin
Locus Coeruleus
Phenoxybenzamine
Lipolysis
Analgesics, Non-Narcotic
Adrenergic alpha-1 Receptor Antagonists
Bucladesine
Triamcinolone
Acetylcholine
Bronchodilator Agents
Naloxone
Signal Transduction
RNA, Messenger
Myocardium
GTP-Binding Proteins
Mitochondrial Proteins
Rabbits
Vasoconstriction
Serotonin
Stimulation, Chemical
Ion Channels
Hemodynamics
Glucagon
Cannabinoid Receptor Agonists
Enzyme Inhibitors
Protein Kinase C
Receptors, Opioid, mu
Sheep
Vasoactive Intestinal Peptide
Sympathetic Nervous System
Administration, Inhalation
Insulin
Pulmonary Edema
Receptors, Opioid, kappa
Liver
Administration, Topical
Pulmonary Alveoli
Analysis of Variance
Spinal Cord
Radioligand Assay
Enzyme Activation
Nitric Oxide
Reflex
Adipose Tissue
Cyclic AMP-Dependent Protein Kinases
Receptors, Opioid, delta
Body Temperature Regulation
Serotonin 5-HT4 Receptor Agonists
Ligands
Muscle Contraction
Asthma
Membrane Potentials
Theophylline
Amiloride
Carrier Proteins
Receptors, Dopamine D2
Mesenteric Arteries
Phosphorylation
Cell Membrane
Double-Blind Method
Enkephalin, Ala(2)-MePhe(4)-Gly(5)-
Glucose
Halothane
Body Weight
Adenosine
Mice, Knockout
Pain
Gene Expression Regulation
Receptors, Opioid
Serotonin Antagonists
Glucocorticoids
Calcimycin
Calcium Channel Agonists
Adipocytes
Molecular Sequence Data
Brain
2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine
Phenethylamines
CHO Cells
Binding, Competitive
Cannabinoids
Receptors, Purinergic P1
Cyclic GMP
Cricetinae
Biological Transport
Characterization of alpha1-adrenoceptor subtypes mediating vasoconstriction in human umbilical vein. (1/329)
1. The present study attempted to characterize pharmacologically the subtypes of alpha-adrenoceptors mediating contractions in human umbilical vein (HUV). 2. HUV rings were mounted in isolated organ baths and cumulative concentration-response curves were constructed for the alpha-adrenoceptor agonists phenylephrine and adrenaline. Adrenaline was more potent than phenylephrine (pD2=7.29 and 6.04 respectively). 3. Isoproterenol exhibited no agonism on KCl pre-contracted HUV rings. Propranolol (1 microM) and rauwolscine (0.1 microM) did not affect the concentration-response curves to adrenaline. These results demonstrate the lack of involvement of functional beta-or alpha2-adrenoceptors in adrenaline-induced vasoconstriction. 4. The non subtype selective alpha1-adrenoceptor antagonist prazosin was evaluated on phenylephrine and adrenaline concentration-response curves. The effects of the competitive alpha1A and alpha1D-adrenoceptor antagonists, 5-methyl urapidil and BMY 7378 and the irreversible alpha1B selective compound chloroethylclonidine (CEC) were also evaluated on adrenaline concentration-response curves. 5. The potencies of prazosin against responses mediated by adrenaline (pA2= 10.87) and phenylephrine (pA2= 10.70) indicate the involvement of prazosin-sensitive functional alpha1-adrenoceptor subtype in vasoconstriction of the HUV. 6. The potencies of 5-methyl urapidil (pA2 = 6.70) and BMY 7378 (pA2= 7.34) were not consistent with the activation of an alpha1A- or alpha1D-adrenoceptor population. 7. Exposure to a relatively low CEC concentration (3 microM) abolished the maximum response to adrenaline suggesting that this response was mediated by an alpha1B-adrenoceptor subtype. 8. We conclude that HUV express a prazosin-sensitive functional alpha1-adrenoceptor resembling the alpha1B-subtype according with the low pA2 values for both 5-methyl urapidil and BMY 7378 and the high sensitivity to CEC. (+info)Sympathovagal balance: how should we measure it? (2/329)
There are complex interactions between the sympathetic and parasympathetic nervous system inputs to the sinus node. The concept of "sympathovagal balance" reflects the autonomic state resulting from the sympathetic and parasympathetic influences. Despite widespread usage of a variety of heart rate (HR) variability parameters as indexes of sympathovagal balance, no index has been validated as a measure of sympathovagal balance. This study evaluated the utility of HR, HR variability, and a new parameter termed the vagal-sympathetic effect (VSE) as indexes of sympathovagal balance. The ideal parameter had to satisfy the following criteria: 1) the index should vary similarly among subjects in response to different autonomic conditions; 2) the variability in the index among subjects exposed to the same autonomic conditions should be small; and 3) the response of the index to various autonomic conditions should reflect the underlying changes in physiological state and have a meaningful interpretation. Volunteers [8 men, 6 women; mean age 28.5 +/- 4.8 (SD) yr] were evaluated for the effects of sympathetic and parasympathetic stimulation and blockade on HR and HR variability. VSE was defined as the ratio of the R-R interval to the intrinsic R-R interval. VSE and R-R interval consistently changed in the expected directions with parasympathetic and sympathetic stimulation and blockade. A general linearized model was used to evaluate the response of each parameter. VSE and R-R interval had r2 values of 0.847 and 0.852, respectively. Natural logarithm of the low-frequency power had an r2 value of 0.781 with lower r2 values for all the other HR variability parameters. The coefficient of variation was also lowest for each condition tested for the VSE and the R-R interval. VSE and R-R interval best satisfy the criteria for the ideal index of sympathovagal balance. Because it is impractical under most conditions to measure the VSE as the index of sympathovagal balance, the most suitable index is the R-R interval. (+info)"Uncaging" using optical fibers to deliver UV light directly to the sample. (3/329)
Photolysis or "uncaging" of caged compounds represents a significant tool in cell biology and chemistry. It provides a means for quantitative control of compound delivery with temporal and spatial resolution while observing their consequences for cellular signaling. We discuss the use of ultraviolet-transmitting optical fibers to directly deliver UV energy to the sample, combined with a nitrogen pulsed laser as a source of UV light. In this approach the size of the photolysis area is regulated by the exit aperture of the fiber tip which is controlled by pulling the optical fibers to desirable diameters. A diode (red) laser that is also coupled to the optical fiber aids the location of UV energy delivery through the fiber. We used this method to quantitatively uncage norepinephrine and calcium. The major advantage of this photolysis approach is its independence of microscope objectives and traditional optical pathways. Because the optical pathway of the microscope needs no modification to accommodate this photolysis system, integration with other experimental methods, such as electrochemistry, electrophysiology, confocal microscopy, and wide-field epifluorescence microscopy, is relatively simple. (+info)Contributions of adenosine receptor activation to the ocular actions of epinephrine. (4/329)
PURPOSE: Epinephrine is an effective drug for glaucoma treatment. However, the mechanisms responsible for the ocular hypotensive action of this compound are not completely understood. Adenosine is an autacoid released by all cells. This study evaluated the role of adenosine receptor activation in epinephrine-induced changes in ocular function. METHODS: Rabbits were pretreated topically with the moderately selective adenosine A1 antagonist 8-(p-sulfophenyl)theophylline (8-SPT) or the adenosine A2 antagonist 3,7-dimethyl-l-propargylxanthine (DMPX). Epinephrine (500 microg) was then administered, and intraocular pressures (IOPs), pupil diameters (PDs), or total outflow facility was evaluated. In a separate group of animals, epinephrine or vehicle was administered, and aqueous humor samples obtained to evaluate changes in aqueous humor purine levels by means of high-performance liquid chromatography. RESULTS: In control animals, epinephrine produced a biphasic change in IOP: an initial rise in IOP of approximately 1 mm Hg from 1/2 to 1 hour followed by significant reduction in IOP of 8 to 9 mm Hg from 3 to 5 hours postadministration. These animals also exhibited a significant increase in PD of 2 to 3 mm from 1/2 to 2 hours postadministration. Pretreatment with 8-SPT (1000 microg) enhanced the initial rise in IOP, while significantly inhibiting the ocular hypotensive response. Pretreatment with 8-SPT also significantly enhanced the epinephrine-induced increase in PD. Inhibition of the epinephrine-induced reduction in IOP by 8-SPT was dose-related with an IC50 of 446 microg. Administration of 8-SPT alone did not significantly alter IOP or PD. The A2 antagonist DMPX did not alter the epinephrine-induced change in IOP or PD. In rabbits pretreated with 8-SPT, the epinephrine-induced increase in outflow facility was significantly reduced by 60% when compared with those in rabbits treated with epinephrine alone. In vehicle-treated rabbits, aqueous humor adenosine and inosine levels were 2.7 +/- 0.38 and 29 +/- 4.2 ng/100 microl, respectively. Three hours after epinephrine administration, adenosine and inosine levels had significantly increased to 11 +/- 1.6 and 66 +/- 4.4 ng/100 microl, respectively. CONCLUSIONS: These results support the idea that in rabbits epinephrine administration stimulates adenosine release in the anterior segment. This rise in endogenous levels of adenosine then leads to the activation of ocular adenosine receptors and is in part responsible for the ocular hypotensive action of epinephrine. (+info)Activation of a thioesterase specific for very-long-chain fatty acids by adrenergic agonists in perfused hearts. (5/329)
We have recently described an acyl-CoA thioesterase specific for very-long-chain fatty acids, named ARTISt, that regulates steroidogenesis through the release of arachidonic acid in adrenal zona fasciculata cells. In this paper we demonstrate the presence of the protein as a 43 kDa band and its mRNA in cardiac tissue. The activity of the protein was measured using an heterologous cell-free assay in which it is recombined with adrenal microsomes and mitochondria to activate mitochondrial steroidogenesis. Isoproterenol and phenylephrine activate the enzyme in a dose-dependent manner (10(-10)-10(-6) M). Both propranolol (10(-5) M) and prazosin (10(-5) M) block the action of isoproterenol and phenylephrine respectively. Antipeptide antibodies against the serine lipase motif of the protein and the Cys residue present in the catalytic domain also block the activity of the protein. Taken together, our results confirm the presence of ARTISt in heart and provide evidence for a catecholamine-activated regulatory pathway of the enzyme in that tissue. (+info)Influence of G protein type on agonist efficacy. (6/329)
An agonist at a specific G protein-coupled receptor may exhibit a range of efficacies for any given response in a cell-specific manner. We report that the relationship between different states of agonism is regulated by the type of G protein expressed in the cell. In NIH-3T3 alpha(2)-adrenergic receptor (AR) transfectants, the alpha(2)-AR agonists clonidine, oxymetazoline, UK-14304, and epinephrine increased [(35)S]guanosine-5'-O-(3-thio)triphosphate binding in a dose-dependent manner from a basal value of 101.2 +/- 6. 5 fmol/mg to a maximal response (100 microM) of 196.6 +/- 9.8, 182.3 +/- 2, 328.1 +/- 11.2, and 340.6 +/- 3 fmol/mg, respectively. Thus, clonidine and oxymetazoline behaved as partial agonists. Receptor-mediated activation of G proteins in membrane preparations was blocked by cell pretreatment with pertussis toxin, indicating receptor coupling to the subgroup of pertussis toxin-sensitive G protein (Gialpha2,3) expressed in NIH-3T3 cells. Ectopic expression of Goalpha1 but not Gialpha1 increased the relative efficacy of clonidine and oxymetazoline such that the two ligands now behaved as close to full agonists in this assay system. The relationship between full and partial agonists in the different genetic backgrounds was not altered by progressive reduction in the amount of G protein available for coupling to receptor. The increased efficacy observed for clonidine in the Goalpha1 transfectants was not due to changes in the relative affinities or amounts of high-affinity, Gpp(NH)p-sensitive binding of agonist. These data suggest that there is little difference in the ability of clonidine to interact with or stabilize alpha(2)-AR-Gialpha2/Gialpha3 versus alpha(2)-AR-Goalpha1 complexes, but that the subsequent step of signal transfer from receptor to G protein is more readily achieved for the clonidine/alpha(2)-AR/Goalpha1 complex. Such observations have important implications for receptor theory and drug development. (+info)Differential effects of epinephrine and norepinephrine on cAMP response and g(i3)alpha protein expression in cultured sympathetic neurons. (7/329)
The effect of 24-h pretreatment with epinephrine (EPI) or norepinephrine (NE) on alpha(2)- and beta-adrenoceptor agonist-induced, cAMP responses and G(i3)alpha-protein expression was studied in primary cultures of rat superior cervical ganglionic (SCG) neurons. SCG neurons, 10 to 12 days in culture, accumulated cAMP when stimulated with the beta-adrenoceptor agonist isoproterenol and the preferential beta(2)-adrenoceptor antagonist ICI 118,551 blocked this response. Similarly, the preferential alpha(2)-adrenoceptor agonist UK14,304 inhibited forskolin-stimulated cAMP accumulation, implying that cultured SCG neurons possess functional alpha(2)- and beta(2)-adrenoceptors. A 24-h treatment of SCG neurons with EPI or NE induced desensitization of the cAMP response to the beta-adrenoceptor agonist isoproterenol. Simultaneously, EPI treatment increased the maximal inhibitory cAMP response to the alpha(2)-adrenoceptor agonist UK14,304 and NE was without effect. Immunoblotting analyses of G(i3)alpha subunits revealed that 24-h EPI but not NE treatment induces a 3- to 4-fold increase in the expression of G(i3)alpha subunits. Furthermore, EPI-induced up-regulation of alpha-subunit expression can be blocked by the preferential beta(2)-adrenoceptor antagonist ICI 118,551 but not by the preferential beta(1)-adrenoceptor antagonist CGP 20712A. Our results suggest that changes in alpha(2)-adrenoceptor responsiveness induced by EPI may involve activation of beta(2)-adrenoceptors that influence the expression of inhibitory G proteins. Thus, primary cultures of sympathetic neurons by possessing functional alpha(2)- and beta-adrenoceptors may be a suitable model system to study the signaling mechanisms of "cross talk" between these adrenoceptor subtypes, which are known to play a central role in cardiovascular function. (+info)Mental well-being in alcohol withdrawal: relationship to alpha2-adrenoceptor function. (8/329)
The possible relationship between postsynaptic alpha2-adrenoceptor function, as assessed by the growth hormone (GH) response to clonidine (CLON) and aspects of mental well-being by self-report of mood using the Swedish Mood Adjective Check List, was investigated in alcohol-dependent patients in the early withdrawal period. Patients had blunted GH responses to CLON and worse mental well-being than control subjects immediately after the end of alcohol intake. No relation was found between mental well-being and postsynaptic alpha2-adrenoceptor function. After 1 week, the GH responses to CLON remained blunted, whereas the state of mental well-being had improved to levels similar to those of control subjects. The results further support a downregulated alpha2-adrenoceptor function during 1 week of alcohol withdrawal. Furthermore, even if subsensitive postsynaptic alpha2-adrenoceptor function was not generally related to state of mood, patients with the lowest postsynaptic alpha2-adrenoceptor function reported the highest levels in the dimensions pleasantness/unpleasantness and activation/deactivation when sober. (+info)Symptoms of pulmonary edema may include:
* Shortness of breath (dyspnea)
* Coughing up frothy sputum
* Chest pain or tightness
* Fatigue
* Confusion or disorientation
Pulmonary edema can be diagnosed through physical examination, chest x-rays, electrocardiogram (ECG), and blood tests. Treatment options include oxygen therapy, diuretics, and medications to manage underlying conditions such as heart failure or sepsis. In severe cases, hospitalization may be necessary to provide mechanical ventilation.
Prevention measures for pulmonary edema include managing underlying medical conditions, avoiding exposure to pollutants and allergens, and seeking prompt medical attention if symptoms persist or worsen over time.
In summary, pulmonary edema is a serious condition that can impair lung function and lead to shortness of breath, chest pain, and other respiratory symptoms. Prompt diagnosis and treatment are essential to prevent complications and improve outcomes for patients with this condition.
Asthma can cause recurring episodes of wheezing, coughing, chest tightness, and shortness of breath. These symptoms occur when the muscles surrounding the airways contract, causing the airways to narrow and swell. This can be triggered by exposure to environmental allergens or irritants such as pollen, dust mites, pet dander, or respiratory infections.
There is no cure for asthma, but it can be managed with medication and lifestyle changes. Treatment typically includes inhaled corticosteroids to reduce inflammation, bronchodilators to open up the airways, and rescue medications to relieve symptoms during an asthma attack.
Asthma is a common condition that affects people of all ages, but it is most commonly diagnosed in children. According to the American Lung Association, more than 25 million Americans have asthma, and it is the third leading cause of hospitalization for children under the age of 18.
While there is no cure for asthma, early diagnosis and proper treatment can help manage symptoms and improve quality of life for those affected by the condition.
Body weight is an important health indicator, as it can affect an individual's risk for certain medical conditions, such as obesity, diabetes, and cardiovascular disease. Maintaining a healthy body weight is essential for overall health and well-being, and there are many ways to do so, including a balanced diet, regular exercise, and other lifestyle changes.
There are several ways to measure body weight, including:
1. Scale: This is the most common method of measuring body weight, and it involves standing on a scale that displays the individual's weight in kg or lb.
2. Body fat calipers: These are used to measure body fat percentage by pinching the skin at specific points on the body.
3. Skinfold measurements: This method involves measuring the thickness of the skin folds at specific points on the body to estimate body fat percentage.
4. Bioelectrical impedance analysis (BIA): This is a non-invasive method that uses electrical impulses to measure body fat percentage.
5. Dual-energy X-ray absorptiometry (DXA): This is a more accurate method of measuring body composition, including bone density and body fat percentage.
It's important to note that body weight can fluctuate throughout the day due to factors such as water retention, so it's best to measure body weight at the same time each day for the most accurate results. Additionally, it's important to use a reliable scale or measuring tool to ensure accurate measurements.
There are several different types of pain, including:
1. Acute pain: This type of pain is sudden and severe, and it usually lasts for a short period of time. It can be caused by injuries, surgery, or other forms of tissue damage.
2. Chronic pain: This type of pain persists over a long period of time, often lasting more than 3 months. It can be caused by conditions such as arthritis, fibromyalgia, or nerve damage.
3. Neuropathic pain: This type of pain results from damage to the nervous system, and it can be characterized by burning, shooting, or stabbing sensations.
4. Visceral pain: This type of pain originates in the internal organs, and it can be difficult to localize.
5. Psychogenic pain: This type of pain is caused by psychological factors such as stress, anxiety, or depression.
The medical field uses a range of methods to assess and manage pain, including:
1. Pain rating scales: These are numerical scales that patients use to rate the intensity of their pain.
2. Pain diaries: These are records that patients keep to track their pain over time.
3. Clinical interviews: Healthcare providers use these to gather information about the patient's pain experience and other relevant symptoms.
4. Physical examination: This can help healthcare providers identify any underlying causes of pain, such as injuries or inflammation.
5. Imaging studies: These can be used to visualize the body and identify any structural abnormalities that may be contributing to the patient's pain.
6. Medications: There are a wide range of medications available to treat pain, including analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), and muscle relaxants.
7. Alternative therapies: These can include acupuncture, massage, and physical therapy.
8. Interventional procedures: These are minimally invasive procedures that can be used to treat pain, such as nerve blocks and spinal cord stimulation.
It is important for healthcare providers to approach pain management with a multi-modal approach, using a combination of these methods to address the physical, emotional, and social aspects of pain. By doing so, they can help improve the patient's quality of life and reduce their suffering.
There are several different types of obesity, including:
1. Central obesity: This type of obesity is characterized by excess fat around the waistline, which can increase the risk of health problems such as type 2 diabetes and cardiovascular disease.
2. Peripheral obesity: This type of obesity is characterized by excess fat in the hips, thighs, and arms.
3. Visceral obesity: This type of obesity is characterized by excess fat around the internal organs in the abdominal cavity.
4. Mixed obesity: This type of obesity is characterized by both central and peripheral obesity.
Obesity can be caused by a variety of factors, including genetics, lack of physical activity, poor diet, sleep deprivation, and certain medications. Treatment for obesity typically involves a combination of lifestyle changes, such as increased physical activity and a healthy diet, and in some cases, medication or surgery may be necessary to achieve weight loss.
Preventing obesity is important for overall health and well-being, and can be achieved through a variety of strategies, including:
1. Eating a healthy, balanced diet that is low in added sugars, saturated fats, and refined carbohydrates.
2. Engaging in regular physical activity, such as walking, jogging, or swimming.
3. Getting enough sleep each night.
4. Managing stress levels through relaxation techniques, such as meditation or deep breathing.
5. Avoiding excessive alcohol consumption and quitting smoking.
6. Monitoring weight and body mass index (BMI) on a regular basis to identify any changes or potential health risks.
7. Seeking professional help from a healthcare provider or registered dietitian for personalized guidance on weight management and healthy lifestyle choices.
1) They share similarities with humans: Many animal species share similar biological and physiological characteristics with humans, making them useful for studying human diseases. For example, mice and rats are often used to study diseases such as diabetes, heart disease, and cancer because they have similar metabolic and cardiovascular systems to humans.
2) They can be genetically manipulated: Animal disease models can be genetically engineered to develop specific diseases or to model human genetic disorders. This allows researchers to study the progression of the disease and test potential treatments in a controlled environment.
3) They can be used to test drugs and therapies: Before new drugs or therapies are tested in humans, they are often first tested in animal models of disease. This allows researchers to assess the safety and efficacy of the treatment before moving on to human clinical trials.
4) They can provide insights into disease mechanisms: Studying disease models in animals can provide valuable insights into the underlying mechanisms of a particular disease. This information can then be used to develop new treatments or improve existing ones.
5) Reduces the need for human testing: Using animal disease models reduces the need for human testing, which can be time-consuming, expensive, and ethically challenging. However, it is important to note that animal models are not perfect substitutes for human subjects, and results obtained from animal studies may not always translate to humans.
6) They can be used to study infectious diseases: Animal disease models can be used to study infectious diseases such as HIV, TB, and malaria. These models allow researchers to understand how the disease is transmitted, how it progresses, and how it responds to treatment.
7) They can be used to study complex diseases: Animal disease models can be used to study complex diseases such as cancer, diabetes, and heart disease. These models allow researchers to understand the underlying mechanisms of the disease and test potential treatments.
8) They are cost-effective: Animal disease models are often less expensive than human clinical trials, making them a cost-effective way to conduct research.
9) They can be used to study drug delivery: Animal disease models can be used to study drug delivery and pharmacokinetics, which is important for developing new drugs and drug delivery systems.
10) They can be used to study aging: Animal disease models can be used to study the aging process and age-related diseases such as Alzheimer's and Parkinson's. This allows researchers to understand how aging contributes to disease and develop potential treatments.
Adrenergic agonist
Alpha-adrenergic agonist
Beta2-adrenergic agonist
Beta3-adrenergic agonist
Beta1-adrenergic agonist
Beta-adrenergic agonist
Use of beta-adrenergic agonists in livestock
Rhinitis medicamentosa
Appetite stimulant
Benzodiazepine
Mydriasis
Discovery and development of beta2 agonists
Concentrated animal feeding operation
Opioid use disorder
Brimonidine
Tretoquinol
Zinterol
Gabriella Campadelli-Fiume
Tocolytic
Phenylpropanolamine
Opioid withdrawal
Triethyloxonium tetrafluoroborate
Emma Parmee
Chronic obstructive pulmonary disease
Xylazine
Lofexidine
Mivazerol
Talipexole
Alifedrine
Cimaterol
List of investigational anxiolytics
Gastrin
Sigma-1 receptor
Sympathoadrenal system
Metabotropic glutamate receptor
Arrestin
Bronchoconstriction
TEAD3
Isoetarine
Bitolterol
Moxonidine
Cannabigerol
Index of biochemistry articles
Glaucoma
Hydroxyzine
Carmoterol
Halostachine
Intermittent claudication
3,4-Methylenedioxyamphetamine
ACTH receptor
Raymond C. Stevens
Phenethylamine
ICI-118,551
Fenoldopam
Yohimbine
Overflow incontinence
Atypical antipsychotic
Rotigotine
Bronchiolitis
Corynanthine
DailyMed - Search Results for Adrenergic Agonists
DailyMed - Search Results for Adrenergic Agonists
Pediatric Third-Degree Acquired Atrioventricular Block Medication: Beta1/Beta2 Adrenergic Agonists
Beta-2 Adrenergic Agonists - PubMed
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DailyMed - Search Results for beta2-Adrenergic Agonist
Alpha₂-adrenergic agonists for the management of opioid withdrawal - PubMed
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Agonist and antagonist binding to alpha 2-adrenergic receptors in purified membranes from human platelets. Implications of...
Adrenergic Agonists & Antagonists | Morgan & Mikhail's Clinical Anesthesiology, 6e | AccessMedicine | McGraw Hill Medical
Subjects: Adrenergic alpha-Agonists -- administration & dosage - Digital Collections - National Library of Medicine Search...
DailyMed - Search Results for Adrenergic Agonists
Regulation of protein kinase B and glycogen synthase kinase-3 by insulin and beta-adrenergic agonists in rat epididymal fat...
Classification of drugs -adrenergic-agonists
ß2-adrenergic receptor agonist counteracts skeletal muscle atrophy and oxidative stress in uremic mice. | Sci Rep;11(1): 9130,...
Repurposing beta-3 adrenergic receptor agonists for Alzheimer's disease: beneficial effects in a mouse model
Beta-3 Adrenergic Agonist Archives - menMD
Postoperative pain-from mechanisms to treatment : PAIN Reports
MEDLINE Data Changes 2011: Revised Entry Combinations Table. NLM Technical Bulletin. 2010 Nov-Dec
What are the main side effects of adrenergic agonists? - Steadyprintshop.com
Salbutamol Free Base
-
Adrenergic beta-Agonists, Tocolytic Agents, Bronchodilator Agents, ATC:R03AC
Symptoms & Causes of Urinary Retention - NIDDK
Welfare traits of Bos indicus cattle castrated immunologically and fed beta-adrenergic agonists
online solution: Discuss the Salmeterol beta 2 adrenergic agonists in detail? - Gee writers
Ephedrine Hcl 30mg pills,An alpha- and beta-adrenergic agonist
Guarana: MedlinePlus Supplements
Efficacy and tolerability of budesonide/formoterol added to tiotropium in patients with chronic obstructive pulmonary disease
Receptor agonist6
- ß2-adrenergic receptor agonist counteracts skeletal muscle atrophy and oxidative stress in uremic mice. (bvsalud.org)
- Albuterol, a moderately selective beta(2)-receptor agonist similar in structure to terbutaline, is widely used as a bronchodilator to manage asthma and other chronic obstructive airway diseases. (pharmacycode.com)
- Activation of Human Brown Adipose Tissue by a β3-Adrenergic Receptor Agonist. (nih.gov)
- Stimulation of 3T3-L1 adipocytes with insulin or the beta(3)-adrenergic receptor agonist CL316243 (termed CL) indicated that insulin preferentially phosphorylated/activated PDE3B associated with internal membranes (endoplasmic reticulum/Golgi), whereas CL preferentially phosphorylated/activated PDE3B associated with caveolae. (lu.se)
- Regulation of mitochondrial dynamics and energetics in the diabetic renal proximal tubule by the β2-adrenergic receptor agonist formoterol. (nih.gov)
- We previously demonstrated that the β2-adrenergic receptor agonist formoterol induced mitochondrial biogenesis and promoted recovery from acute kidney injury. (nih.gov)
Receptors8
- Direct agonists directly interact with the adrenergic receptors, whereas indirect agonists typically stimulate the release of endogenous catecholamines. (nih.gov)
- Agonist and antagonist binding to alpha 2-adrenergic receptors in purified membranes from human platelets. (aspetjournals.org)
- Adrenergic agonists and antagonists produce their clinical effects by interacting with the adrenergic receptors (ie, adrenoceptors). (mhmedical.com)
- Direct-acting sympathomimetic drugs act directly on 1 or more of the adrenergic receptors. (mhmedical.com)
- However, certain non-catecholamines with both direct and indirect effects on adrenergic receptors show significant β 2 activity and are used clinically for these effects. (mhmedical.com)
- Brown fat cells have β3-adrenergic receptors on their surface. (nih.gov)
- Several other tissues also have β3-adrenergic receptors, including white fat and the bladder. (nih.gov)
- Dr. Aaron Cypess-now at NIH's National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK), while working at the Joslin Diabetes Center in Boston-and colleagues examined whether this drug might activate β3-adrenergic receptors on brown fat cells to increase metabolism in humans. (nih.gov)
Epinephrine3
- The beta-2 adrenergic agonists are a large group of drugs that mimic the actions of naturally occurring catecholamines such as norepinephrine, epinephrine and dopamine. (nih.gov)
- The term adrenergic originally referred to the effects of epinephrine ( adren aline), although norepinephrine (noradrenaline) is the primary neurotransmitter responsible for most of the adrenergic activity of the sympathetic nervous system. (mhmedical.com)
- Although minor compared to those of epinephrine, beta agonists usually have mild to moderate adverse effects, which include anxiety, hypertension, increased heart rate, and insomnia. (steadyprintshop.com)
Formoterol1
- To assess the efficacy and tolerability of budesonide/formoterol added to tiotropium in patients eligible for inhaled corticosteroid/long-acting beta(2)-agonist combination therapy. (nih.gov)
Albuterol1
- Albuterol is an adrenergic agonist that increases the plasma insulin concentration, which may, in turn, help shift K + into the intracellular space. (medscape.com)
Anticholinergics1
- The preferred bronchodilator has changed from methylxanthines, and anticholinergics methylxanthines to beta -adrenergic agonists. (cdc.gov)
Salmeterol1
- online solution: Discuss the Salmeterol beta 2 adrenergic agonists in detail? (geewriters.com)
Norepinephrine1
- An alpha- and beta-adrenergic agonist that may also enhance release of norepinephrine. (ariflam.com)
Insulin1
- The complexes present in insulin-stimulated cells contained tyrosine-phosphorylated IRS-1 (insulin receptor substrate 1) and its downstream signalling proteins, whereas CL-activated complexes contained beta(3)-adrenergic receptor, PKA-RII [PKA (cAMP-dependent protein kinase)-regulatory subunit] and HSL. (lu.se)
Clonidine1
- Randomised controlled trials comparing alpha2-adrenergic agonists (clonidine, lofexidine, guanfacine, tizanidine) with reducing doses of methadone, symptomatic medications or placebo, or comparing different alpha2-adrenergic agonists to modify the signs and symptoms of withdrawal in participants who were opioid dependent. (nih.gov)
Brown Adipos2
- Brown adipose tissue (BAT) is the main thermogenic driver in mammals and its stimulation, through β3 adrenergic receptor (β3AR) agonists or cold acclimation, counteracts metabolic deficits in rodents and humans. (nih.gov)
- Brown adipose tissue, or brown fat, produces β3-adrenergic receptor at levels higher than nearly every other organ in the body. (nih.gov)
Medication1
- The liver injury typically arises within a few days of starting high dose intravenous beta adrenergic agonists, is usually asymptomatic, not associated with jaundice, and rapidly reversed once the medication is stopped. (nih.gov)
Indirect1
- Adrenergic agonists can be categorized as direct or indirect. (mhmedical.com)
Asthma3
- The beta-2 adrenergic agonists are used largely as bronchodilators in the management of asthma, both in control of acute symptomatic attacks as well as chronic, long term prevention and management. (nih.gov)
- The use of beta adrenergic agonists in asthma has not been associated with elevations in serum aminotransferase or alkaline phosphatase levels or in causing clinically apparent liver disease. (nih.gov)
- Inhaled beta(2)-adrenoceptor agonists (beta(2)-agonists) are the most commonly used asthma medications in many Western countries. (steadyprintshop.com)
Beta10
- The beta-2 adrenergic agonists act mainly on the smooth muscle of the vasculature, bronchial tree, intestines and uterus. (nih.gov)
- When given in large doses or after intentional overdose, beta adrenergic agonists can cause liver injury. (nih.gov)
- Which of the following is the most common side effect of beta 2 agonist? (steadyprintshop.com)
- 7] The most common side effects of beta-2 agonists involve the cardiac, metabolic, or musculoskeletal system. (steadyprintshop.com)
- Which condition is an adverse effect of a beta adrenergic agonist? (steadyprintshop.com)
- Which of the following is a side effect of beta-adrenergic blockers? (steadyprintshop.com)
- Which of the following is an adverse effect of beta 2 agonist Hypo? (steadyprintshop.com)
- Among these additives, beta-adrenergic agonists (β-AAs), such as zilpaterol hydrochloride (ZH) and ractopamine hydrochloride (RH), which are synthetic and nonhormonal compounds with a powerful anabolic effect on skeletal muscle, have been used to improve animal performance and lean meat production [ 1 - 3 ]. (animbiosci.org)
- Evidence for involvement of an adrenal catecholamine in the beta-adrenergic inhibition of oxytocin release in lactating rats. (nih.gov)
- Use of any known adrenergic agonists, CYP3A or CYP2D6 substrates, cardiac beta-blockers, calcium channel blockers, systemic corticosteroids, monoamine oxidase (Nirengi et al. (nih.gov)
Agents1
- Adrenergic agonist agents cause vasoconstriction and bronchodilation and reduce vascular permeability. (medscape.com)
Selective2
- It has become less extensively used with the advent of more selective agonists. (ariflam.com)
- A short-acting β 1 -selective adrenergic blocking agent (β-blocker). (drugs.com)
Doses1
- To assess the effectiveness of interventions involving the use of alpha2-adrenergic agonists compared with placebo, reducing doses of methadone, symptomatic medications, or an alpha2-adrenergic agonist regimen different to the experimental intervention, for the management of the acute phase of opioid withdrawal. (nih.gov)
Effects4
- It has alpha-agonist effects that include increased peripheral vascular resistance and reduced vascular permeability. (medscape.com)
- What are the main side effects of adrenergic agonists? (steadyprintshop.com)
- Classification of adrenergic receptor agonists (sympathomimetic amines) and drugs that produce sympathomimetic-like effects. (mhmedical.com)
- Effects of the β-adrenergic agonist metaproterenol were studied daily gain, carcass composition and feed consumption of Varamini female lambs were studied. (ac.ir)
Stimulation2
- Since metabolic disorders and AD share strong pathogenic links, we hypothesized that BAT stimulation through a β3AR agonist could exert benefits in AD as well. (nih.gov)
- SAN automaticity was also responsive to β-adrenergic and cholinergic pharmacological stimulation, showing a consequent shift in the localization of the origin of pacemaker activity. (nature.com)
Metabolic1
- As β3AR agonists are being clinically developed for metabolic disorders, repurposing them in AD could be a valuable therapeutic strategy. (nih.gov)
Peripheral1
- Here, we show that β3AR agonist administration decreased body weight and improved peripheral glucose metabolism and BAT thermogenesis in both non-transgenic and 3xTg-AD mice. (nih.gov)
Treatment2
- Next, the effect of the ß2- adrenergic receptor (ß2-AR) agonist, clenbuterol , was evaluated as a potential treatment for uremic sarcopenia . (bvsalud.org)
- One-month treatment with a β3AR agonist increased recognition index by 19% in 16-month-old 3xTg-AD mice compared to pre-treatment (14-month-old). (nih.gov)
Increase1
- Although the ß2-AR agonist can increase the muscular mass with ROS reduction, development of therapeutic interventions for restoring skeletal muscle function is still awaited. (bvsalud.org)
Previously1
- We previously identified spinophilin as a regulator of α 2 adrenergic receptor (α 2 AR) trafficking and signaling in vitro and in vivo (Science 304:1940-1944, 2004). (elsevierpure.com)