Drugs that act on adrenergic receptors or affect the life cycle of adrenergic transmitters. Included here are adrenergic agonists and antagonists and agents that affect the synthesis, storage, uptake, metabolism, or release of adrenergic transmitters.
Drugs that mimic the effects of stimulating postganglionic adrenergic sympathetic nerves. Included here are drugs that directly stimulate adrenergic receptors and drugs that act indirectly by provoking the release of adrenergic transmitters.
Drugs that bind to and activate adrenergic receptors.
The active sympathomimetic hormone from the ADRENAL MEDULLA. It stimulates both the alpha- and beta- adrenergic systems, causes systemic VASOCONSTRICTION and gastrointestinal relaxation, stimulates the HEART, and dilates BRONCHI and cerebral vessels. It is used in ASTHMA and CARDIAC FAILURE and to delay absorption of local ANESTHETICS.
A nonselective alpha-adrenergic antagonist. It is used in the treatment of hypertension and hypertensive emergencies, pheochromocytoma, vasospasm of RAYNAUD DISEASE and frostbite, clonidine withdrawal syndrome, impotence, and peripheral vascular disease.
Isopropyl analog of EPINEPHRINE; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant.
A widely used non-cardioselective beta-adrenergic antagonist. Propranolol has been used for MYOCARDIAL INFARCTION; ARRHYTHMIA; ANGINA PECTORIS; HYPERTENSION; HYPERTHYROIDISM; MIGRAINE; PHEOCHROMOCYTOMA; and ANXIETY but adverse effects instigate replacement by newer drugs.
Cell-surface proteins that bind epinephrine and/or norepinephrine with high affinity and trigger intracellular changes. The two major classes of adrenergic receptors, alpha and beta, were originally discriminated based on their cellular actions but now are distinguished by their relative affinity for characteristic synthetic ligands. Adrenergic receptors may also be classified according to the subtypes of G-proteins with which they bind; this scheme does not respect the alpha-beta distinction.
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.
A selective adrenergic alpha-1 antagonist used in the treatment of HEART FAILURE; HYPERTENSION; PHEOCHROMOCYTOMA; RAYNAUD DISEASE; PROSTATIC HYPERTROPHY; and URINARY RETENTION.
Drugs that selectively bind to and activate alpha adrenergic receptors.
An alpha-1 adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent.
Drugs that bind to but do not activate alpha-adrenergic receptors thereby blocking the actions of endogenous or exogenous adrenergic agonists. Adrenergic alpha-antagonists are used in the treatment of hypertension, vasospasm, peripheral vascular disease, shock, and pheochromocytoma.
Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.
One of two major pharmacologically defined classes of adrenergic receptors. The beta adrenergic receptors play an important role in regulating CARDIAC MUSCLE contraction, SMOOTH MUSCLE relaxation, and GLYCOGENOLYSIS.
Drugs used to cause constriction of the blood vessels.
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.
The escape of diagnostic or therapeutic material from the vessel into which it is introduced into the surrounding tissue or body cavity.
Abnormally low BLOOD PRESSURE that can result in inadequate blood flow to the brain and other vital organs. Common symptom is DIZZINESS but greater negative impacts on the body occur when there is prolonged depravation of oxygen and nutrients.
Sepsis associated with HYPOTENSION or hypoperfusion despite adequate fluid resuscitation. Perfusion abnormalities may include, but are not limited to LACTIC ACIDOSIS; OLIGURIA; or acute alteration in mental status.
An adrenergic beta-2 agonist used to control PREMATURE LABOR.
Antidiuretic hormones released by the NEUROHYPOPHYSIS of all vertebrates (structure varies with species) to regulate water balance and OSMOLARITY. In general, vasopressin is a nonapeptide consisting of a six-amino-acid ring with a cysteine 1 to cysteine 6 disulfide bridge or an octapeptide containing a CYSTINE. All mammals have arginine vasopressin except the pig with a lysine at position 8. Vasopressin, a vasoconstrictor, acts on the KIDNEY COLLECTING DUCTS to increase water reabsorption, increase blood volume and blood pressure.

Neuroregulation by vasoactive intestinal peptide (VIP) of mucus secretion in ferret trachea: activation of BK(Ca) channels and inhibition of neurotransmitter release. (1/296)

1. The aims of this study were to determine: (1) whether vasoactive intestinal peptide (VIP) regulates cholinergic and 'sensory-efferent' (tachykininergic) 35SO4 labelled mucus output in ferret trachea in vitro, using a VIP antibody, (2) the class of potassium (K+) channel involved in VIP-regulation of cholinergic neural secretion using glibenclamide (an ATP-sensitive K+ (K(ATP)) channel inhibitor), iberiotoxin (a large conductance calcium activated K+ (BK(ca)) channel blocker), and apamin (a small conductance K(ca) (SK(ca)) channel blocker), and (3) the effect of VIP on cholinergic neurotransmission using [3H]-choline overflow as a marker for acetylcholine (ACh) release. 2. Exogenous VIP (1 and 10 microM) alone increased 35SO4 output by up to 53% above baseline, but suppressed (by up to 80% at 1 microM) cholinergic and tachykininergic neural secretion without altering secretion induced by ACh or substance P (1 microM each). Endogenous VIP accounted for the minor increase in non-adrenergic, non-cholinergic (NANC), non-tachykininergic neural secretion, which was compatible with the secretory response of exogenous VIP. 3. Iberiotoxin (3 microM), but not apamin (1 microM) or glibenclamide (0.1 microM), reversed the inhibition by VIP (10 nM) of cholinergic neural secretion. 4. Both endogenous VIP (by use of the VIP antibody; 1:500 dilution) and exogenous VIP (0.1 microM), the latter by 34%, inhibited ACh release from cholinergic nerve terminals and this suppression was completely reversed by iberiotoxin (0.1 microM). 5. We conclude that, in ferret trachea in vitro, endogenous VIP has dual activity whereby its small direct stimulatory action on mucus secretion is secondary to its marked regulation of cholinergic and tachykininergic neurogenic mucus secretion. Regulation is via inhibition of neurotransmitter release, consequent upon opening of BK(Ca) channels. In the context of neurogenic mucus secretion, we propose that VIP joins NO as a neurotransmitter of i-NANC nerves in ferret trachea.  (+info)

alpha-adrenergic stimulation mediates glucose uptake through phosphatidylinositol 3-kinase in rat heart. (2/296)

We examined whether insulin and catecholamines share common pathways for their stimulating effects on glucose uptake. We perfused isolated working rat hearts with Krebs-Henseleit buffer containing [2-3H]glucose (5 mmol/L, 0.05 microCi/mL) and sodium oleate (0.4 mmol/L). In the absence or presence of the phosphatidylinositol 3-kinase (PI3-K) inhibitor wortmannin (3 micromol/L), we added insulin (1 mU/mL), epinephrine (1 micromol/L), phenylephrine (100 micromol/L) plus propranolol (10 micromol/L, selective alpha-adrenergic stimulation), or isoproterenol (1 micromol/L) plus phentolamine (10 micromol/L, selective beta-adrenergic stimulation) to the perfusate. Cardiac power was found to be stable in all groups (between 8.07+/-0.68 and 10.7+/-0. 88 mW) and increased (25% to 47%) with addition of epinephrine, but not with selective alpha- and beta-adrenergic stimulation. Insulin and epinephrine, as well as selective alpha- and beta-receptor stimulation, increased glucose uptake (the following values are in micromol/[min. g dry weight]: basal, 1.19+/-0.13; insulin, 3.89+/-0.36; epinephrine, 3.46+/-0.27; alpha-stimulation, 4.08+/-0.40; and beta-stimulation, 3.72+/-0.34). Wortmannin completely inhibited insulin-stimulated and selective alpha-stimulated glucose uptake, but it did not affect the epinephrine-stimulated or selective beta-stimulated glucose uptake. Sequential addition of insulin and epinephrine or insulin and alpha-selective stimulation showed additive effects on glucose uptake in both cases. Wortmannin further blocked the effects of insulin on glycogen synthesis. We conclude that alpha-adrenergic stimulation mediates glucose uptake in rat heart through a PI3-K-dependent pathway. However, the additive effects of alpha-adrenergic stimulation and insulin suggest 2 different isoforms of PI3-K, compartmentation of PI3-K, potentiation, or inhibition by wortmannin of another intermediate of the alpha-adrenergic signaling cascade. The stimulating effects of both the alpha- and the beta-adrenergic pathways on glucose uptake are independent of changes in cardiac performance.  (+info)

S-16924, a novel, potential antipsychotic with marked serotonin1A agonist properties. IV. A drug discrimination comparison with clozapine. (3/296)

The novel benzodioxopyrrolidine (S-16924) displays a clozapine-like profile of interaction with multiple monoaminergic receptors, in addition to potent agonist activity at serotonin (5-HT)1A receptors. S-16924 (2.5 mg/kg i.p.) and clozapine (5.0 mg/kg i.p.) generated robust discriminative stimuli (DS) and displayed full mutual generalization. The D4 antagonists L-745,870 and S-18126, the D1/D5 antagonist SCH-39166, and the D3 antagonist S-14297 showed at most partial generalization to S-16924 and clozapine. The D2/D3 antagonist raclopride fully generalized to S-16924, but only partially generalized to clozapine. The 5-HT2A antagonist MDL-100, 907 fully generalized to S-16924 and two further 5-HT2A antagonists, fananserin and SR-46349, showed partial generalization. However, MDL-100,907, fananserin, and SR-46349 showed less pronounced generalization to clozapine. Similarly, the 5-HT2C antagonists SB-200,646 and SB-206,553 more markedly generalized to S-16924 than to clozapine. The 5-HT1A receptor agonist (+/-)-8-dihydroxy-2-(di-n-propylamino) tetralin generalized fully to S-16924 but not to clozapine. Full generalization was obtained to both S-16924 and clozapine for the clozapine congeners, olanzapine and quetiapine. In distinction, the benzisoxazole, risperidone, and the phenylindole, sertindole, weakly generalized to S-16924 and clozapine. However, the benzisoxazole ziprasidone, which possesses 5-HT1A agonist properties, generalized fully to S-16924 but not to clozapine. Finally, the muscarinic antagonist scopolamine generalized fully to clozapine and partially to S-16924. In conclusion, S-16924 and clozapine display both communalities and differences in their "compound" DS; this likely reflects their respective complex patterns of interaction with multiple monoaminergic receptors. Although no specific receptor was identified as underlying the clozapine DS, 5-HT1A agonist as well as D2 and 5-HT2A/2C antagonist properties contribute to the S-16924 DS.  (+info)

beta2-adrenergic cAMP signaling is uncoupled from phosphorylation of cytoplasmic proteins in canine heart. (4/296)

BACKGROUND: Recent studies of beta-adrenergic receptor (beta-AR) subtype signaling in in vitro preparations have raised doubts as to whether the cAMP/protein kinase A (PKA) signaling is activated in the same manner in response to beta2-AR versus beta1-AR stimulation. METHODS AND RESULTS: The present study compared, in the intact dog, the magnitude and characteristics of chronotropic, inotropic, and lusitropic effects of cAMP accumulation, PKA activation, and PKA-dependent phosphorylation of key effector proteins in response to beta-AR subtype stimulation. In addition, many of these parameters and L-type Ca2+ current (ICa) were also measured in single canine ventricular myocytes. The results indicate that although the cAMP/PKA-dependent phosphorylation cascade activated by beta1-AR stimulation could explain the resultant modulation of cardiac function, substantial beta2-AR-mediated chronotropic, inotropic, and lusitropic responses occurred in the absence of PKA activation and phosphorylation of nonsarcolemmal proteins, including phospholamban, troponin I, C protein, and glycogen phosphorylase kinase. However, in single canine myocytes, we found that beta2-AR-stimulated increases in both ICa and contraction were abolished by PKA inhibition. Thus, the beta2-AR-directed cAMP/PKA signaling modulates sarcolemmal L-type Ca2+ channels but does not regulate PKA-dependent phosphorylation of cytoplasmic proteins. CONCLUSIONS: These results indicate that the dissociation of beta2-AR signaling from cAMP regulatory systems is only apparent and that beta2-AR-stimulated cAMP/PKA signaling is uncoupled from phosphorylation of nonsarcolemmal regulatory proteins involved in excitation-contraction coupling.  (+info)

Neurometabolic effects of psilocybin, 3,4-methylenedioxyethylamphetamine (MDE) and d-methamphetamine in healthy volunteers. A double-blind, placebo-controlled PET study with [18F]FDG. (5/296)

The neurometabolic effects of the hallucinogen psilocybin (PSI; 0.2 mg/kg), the entactogen 3,4-methylenedioxyethylamphetamine (MDE; 2 mg/kg) and the stimulant d-methamphetamine (METH; 0.2-0.4 mg/kg) and the drugs' interactions with a prefrontal activation task were investigated in a double-blind, placebo-controlled human [F-18]fluorodeoxyglucoseFDG-positron emission tomographicPET study (each group: n = 8). Subjects underwent two scans (control: word repetition; activation word association) within 2-4 weeks. Psilocybin increased rMRGlu in distinct right hemispheric frontotemporal cortical regions, particularly in the anterior cingulate and decreased rMRGlu in the thalamus. Both MDE and METH induced cortical hypometabolism and cerebellar hypermetabolism. In the MDE group, cortical hypometabolism was more pronounced in frontal regions, with the exception of the right anterior cingulate, which tended to be hyperactive. Cognitive activation-related increases in left frontocortical regions were attenuated under all three psychoactive substances, but less so under MDE. Taking into account performance data and subjective reports on task difficulty, these effects may result from different mechanisms across the three groups. Our PSI data are in line with studies on acute schizophrenic patients suggesting frontal overactivity at rest, but diminished capacity to activate prefrontal regions upon cognitive demand. The MDE data support the hypothesis that entactogens constitute a distinct psychoactive substance class, which takes an intermediate position between stimulants and hallucinogens.  (+info)

Glucose uptake during centrally induced stress is insulin independent and enhanced by adrenergic blockade. (6/296)

Glucose utilization increases markedly in the normal dog during stress induced by the intracerebroventricular (ICV) injection of carbachol. To determine the extent to which insulin, glucagon, and selective (alpha/beta)-adrenergic activation mediate the increment in glucose metabolic clearance rate (MCR) and glucose production (R(a)), we used five groups of normal mongrel dogs: 1) pancreatic clamp (PC; n = 7) with peripheral somatostatin (0.8 microg x kg(-1) x min(-1)) and intraportal replacement of insulin (1,482 +/- 84 pmol x kg(-1) x min(-1)) and glucagon (0.65 ng x kg(-1) x min(-1)) infusions; 2) PC plus combined alpha (phentolamine)- and beta (propranolol)-blockade (7 and 5 microg x kg(-1) x min(-1), respectively; alpha+beta; n = 5); 3) PC plus alpha-blockade (alpha; n = 6); 4) PC plus beta-blockade (beta; n = 5); and 5) a carbachol control group without PC (Con; n = 10). During ICV carbachol stress (0-120 min), catecholamines, ACTH, and cortisol increased in all groups. Baseline insulin and glucagon levels were maintained in all groups except Con, where glucagon rose 33%, and alpha, where insulin increased slightly but significantly. Stress increased (P < 0.05) plasma glucose in Con, PC, and alpha but decreased it in beta and alpha+beta. The MCR increment was greater (P < 0.05) in beta and alpha+beta than in Con, PC, and alpha. R(a) increased (P < 0.05) in all groups but was attenuated in alpha+beta. Stress-induced lipolysis was abolished in beta (P < 0.05). The marked rise in lactate in Con, PC, and alpha was abolished in alpha+beta and beta. We conclude that the stress-induced increase in MCR is largely independent of changes in insulin, markedly augmented by beta-blockade, and related, at least in part, to inhibition of lipolysis and glycogenolysis, and that R(a) is augmented by glucagon and alpha- and beta-catecholamine effects.  (+info)

beta-adrenergic agonists stimulate Na+-K+-Cl- cotransport by inducing intracellular Ca2+ liberation in crypt cells. (7/296)

Epinephrine and beta-adrenergic agonists (beta1 and beta2 for isoproterenol, beta1 for dobutamine, beta2 for salbutamol) stimulated K+ (or 86Rb) influx mediated by the Na+-K+-2Cl- cotransporter and the Na+-K+ pump in isolated colonic crypt cells. Preincubation with bumetanide abolished the epinephrine effect on the Na+-K+ pump, suggesting that the primary effect is on the cotransporter. Maximal effect was obtained with 1 microM epinephrine with an EC50 of 91.6 +/- 9.98 nM. Epinephrine-induced K+ transport was blocked by propranolol with an IC50 of 134 +/- 28.2 nM. alpha-Adrenergic drugs did not modify K+ transport mechanisms. Neither Ba2+ nor tetraethylammonium nor DIDS modified the adrenergic enhancement on the cotransporter. In addition, epinephrine did not affect K+ efflux. Dibutyryl cAMP did not alter K+ transport. Reduction of extracellular Ca2+ to 30 nM did not influence the response to epinephrine. However, 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid-AM abolished epinephrine-induced K+ transport. Ionomycin increased Na+-K+-2Cl- cotransport activity. Moreover, epinephrine increased intracellular Ca2+ concentration in a process inhibited by propranolol. In conclusion, epinephrine stimulated the Na+-K+-2Cl- cotransporter in a process mediated by beta1- and beta2-receptors and modulated by intracellular Ca2+ liberation.  (+info)

Sympathetic inhibition, leptin, and uncoupling protein subtype expression in normal fasting rats. (8/296)

To further investigate neural effects on leptin and uncoupling proteins (UCPs), we studied in vivo perturbations intended to block adrenergic input to peripheral tissues. We examined plasma leptin, leptin mRNA, and adipose and muscle UCP subtype mRNA in rats treated with alpha-methyl-p-tyrosine methyl ester (AMPT-ME), which inhibits catecholamine synthesis and 6-hydroxydopamine (6HDA), which is toxic to catecholinergic nerve terminals but, unlike AMPT-ME, does not enter the central nervous system. Intraperitoneal AMPT-ME, 250 mg/kg, was administered at 1800 and 0700 the following day, and rats were killed at 1200-1400. All rats were fasted with free access to water during this time. Intraperitoneal AMPT-ME increased plasma leptin by 15-fold, increased interscapular brown adipose tissue (IBAT) and epididymal fat leptin mRNA by 2- to 2.5-fold, and also increased plasma insulin and glucose concentrations. Intraperitoneal AMPT-ME decreased IBAT UCP-3 mRNA to 40% of control, while it increased epididymal adipose UCP-3 mRNA approximately twofold. Intravenous AMPT-ME, 250 mg/kg, administered to conscious rats for 5 h decreased lumbar sympathetic nerve activity, increased plasma leptin (5.89 +/- 1.43 compared with 2.75 +/- 0.31 ng/ml in vehicle-treated rats, n = 7, P < 0.05), and decreased cardiac rate with no sustained change in blood pressure. Intraperitoneal 6HDA, 100 mg/kg, as a single dose at 1800, increased plasma leptin approximately twofold after 18-20 h, increased IBAT (but not epididymal fat) leptin mRNA by two- to threefold, and decreased IBAT UCP-3 mRNA to 30-40% of control. Neither AMPT-ME nor 6HDA significantly altered mRNA encoding gastrocnemius muscle UCP-3, IBAT UCP-1, or IBAT and epididymal UCP-2. In summary, AMPT-ME and 6HDA increased plasma leptin and upregulated leptin mRNA expression. AMPT-ME also resulted in complex tissue and subtype-specific modulation of adipose UCP mRNA. These data are consistent with interaction between leptin and sympathetic nerve activity (SNA) in regulation of fat cell energy utilization. However, the in vivo modulation of leptin and UCPs appears complex and, beyond a causal effect of SNA per se, may depend on concurrent changes in plasma insulin, glucose, and circulatory hemodynamics.  (+info)

Adrenergic agents are a class of drugs that bind to and activate adrenergic receptors, which are cell surface receptors found in the nervous system and other tissues. These receptors are activated by neurotransmitters such as norepinephrine and epinephrine (also known as adrenaline), which are released by the sympathetic nervous system in response to stress or excitement.

Adrenergic agents can be classified based on their mechanism of action and the specific receptors they bind to. There are two main types of adrenergic receptors: alpha and beta receptors, each with several subtypes. Some adrenergic agents bind to both alpha and beta receptors, while others are selective for one or the other.

Adrenergic agents have a wide range of therapeutic uses, including the treatment of asthma, cardiovascular diseases, glaucoma, and neurological disorders. They can also be used as diagnostic tools to test the function of the sympathetic nervous system. Some examples of adrenergic agents include:

* Alpha-agonists: These drugs bind to alpha receptors and cause vasoconstriction (narrowing of blood vessels), which can be useful in the treatment of hypotension (low blood pressure) or nasal congestion. Examples include phenylephrine and oxymetazoline.
* Alpha-antagonists: These drugs block the action of alpha receptors, leading to vasodilation (widening of blood vessels) and a decrease in blood pressure. Examples include prazosin and doxazosin.
* Beta-agonists: These drugs bind to beta receptors and cause bronchodilation (opening of the airways), increased heart rate, and increased force of heart contractions. They are used in the treatment of asthma, chronic obstructive pulmonary disease (COPD), and other respiratory disorders. Examples include albuterol and salmeterol.
* Beta-antagonists: These drugs block the action of beta receptors, leading to a decrease in heart rate, blood pressure, and bronchodilation. They are used in the treatment of hypertension, angina (chest pain), and heart failure. Examples include metoprolol and atenolol.
* Nonselective alpha- and beta-antagonists: These drugs block both alpha and beta receptors and are used in the treatment of hypertension, angina, and heart failure. Examples include labetalol and carvedilol.

Sympathomimetic drugs are substances that mimic or stimulate the actions of the sympathetic nervous system. The sympathetic nervous system is one of the two divisions of the autonomic nervous system, which regulates various automatic physiological functions in the body. The sympathetic nervous system's primary function is to prepare the body for the "fight-or-flight" response, which includes increasing heart rate, blood pressure, respiratory rate, and metabolism while decreasing digestive activity.

Sympathomimetic drugs can exert their effects through various mechanisms, including directly stimulating adrenergic receptors (alpha and beta receptors) or indirectly causing the release of norepinephrine and epinephrine from nerve endings. These drugs are used in various clinical settings to treat conditions such as asthma, nasal congestion, low blood pressure, and attention deficit hyperactivity disorder (ADHD). Examples of sympathomimetic drugs include epinephrine, norepinephrine, dopamine, dobutamine, albuterol, pseudoephedrine, and methylphenidate.

It is important to note that sympathomimetic drugs can also have adverse effects, particularly when used in high doses or in individuals with certain medical conditions. These adverse effects may include anxiety, tremors, palpitations, hypertension, arrhythmias, and seizures. Therefore, these medications should be used under the close supervision of a healthcare provider.

Adrenergic agonists are medications or substances that bind to and activate adrenergic receptors, which are a type of receptor in the body that respond to neurotransmitters such as norepinephrine and epinephrine (also known as adrenaline).

There are two main types of adrenergic receptors: alpha and beta receptors. Alpha-adrenergic agonists activate alpha receptors, while beta-adrenergic agonists activate beta receptors. These medications can have a variety of effects on the body, depending on which type of receptor they act on.

Alpha-adrenergic agonists are often used to treat conditions such as nasal congestion, glaucoma, and low blood pressure. Examples include phenylephrine, oxymetazoline, and clonidine.

Beta-adrenergic agonists are commonly used to treat respiratory conditions such as asthma and COPD (chronic obstructive pulmonary disease). They work by relaxing the smooth muscle in the airways, which makes it easier to breathe. Examples include albuterol, salmeterol, and formoterol.

It's important to note that adrenergic agonists can have both desired and undesired effects on the body. They should be used under the guidance of a healthcare professional, who can monitor their effectiveness and potential side effects.

Epinephrine, also known as adrenaline, is a hormone and a neurotransmitter that is produced in the body. It is released by the adrenal glands in response to stress or excitement, and it prepares the body for the "fight or flight" response. Epinephrine works by binding to specific receptors in the body, which causes a variety of physiological effects, including increased heart rate and blood pressure, improved muscle strength and alertness, and narrowing of the blood vessels in the skin and intestines. It is also used as a medication to treat various medical conditions, such as anaphylaxis (a severe allergic reaction), cardiac arrest, and low blood pressure.

Phentolamine is a non-selective alpha-blocker drug, which means it blocks both alpha-1 and alpha-2 receptors. It works by relaxing the muscle around blood vessels, which increases blood flow and lowers blood pressure. Phentolamine is used medically for various purposes, including the treatment of high blood pressure, the diagnosis and treatment of pheochromocytoma (a tumor that releases hormones causing high blood pressure), and as an antidote to prevent severe hypertension caused by certain medications or substances. It may also be used in diagnostic tests to determine if a patient's blood pressure is reactive to drugs, and it can be used during some surgical procedures to help lower the risk of hypertensive crises.

Phentolamine is available in two forms: an injectable solution and oral tablets. The injectable form is typically administered by healthcare professionals in a clinical setting, while the oral tablets are less commonly used due to their short duration of action and potential for causing severe drops in blood pressure. As with any medication, phentolamine should be taken under the supervision of a healthcare provider, and patients should follow their doctor's instructions carefully to minimize the risk of side effects and ensure the drug's effectiveness.

Isoproterenol is a medication that belongs to a class of drugs called beta-adrenergic agonists. Medically, it is defined as a synthetic catecholamine with both alpha and beta adrenergic receptor stimulating properties. It is primarily used as a bronchodilator to treat conditions such as asthma and chronic obstructive pulmonary disease (COPD) by relaxing the smooth muscles in the airways, thereby improving breathing.

Isoproterenol can also be used in the treatment of bradycardia (abnormally slow heart rate), cardiac arrest, and heart blocks by increasing the heart rate and contractility. However, due to its non-selective beta-agonist activity, it may cause various side effects such as tremors, palpitations, and increased blood pressure. Its use is now limited due to the availability of more selective and safer medications.

Propranolol is a medication that belongs to a class of drugs called beta blockers. Medically, it is defined as a non-selective beta blocker, which means it blocks the effects of both epinephrine (adrenaline) and norepinephrine (noradrenaline) on the heart and other organs. These effects include reducing heart rate, contractility, and conduction velocity, leading to decreased oxygen demand by the myocardium. Propranolol is used in the management of various conditions such as hypertension, angina pectoris, arrhythmias, essential tremor, anxiety disorders, and infants with congenital heart defects. It may also be used to prevent migraines and reduce the risk of future heart attacks. As with any medication, it should be taken under the supervision of a healthcare provider due to potential side effects and contraindications.

Adrenergic receptors are a type of G protein-coupled receptor that bind and respond to catecholamines, which include the neurotransmitters norepinephrine (noradrenaline) and epinephrine (adrenaline). These receptors play a crucial role in the body's "fight or flight" response and are involved in regulating various physiological functions such as heart rate, blood pressure, respiration, and metabolism.

There are nine different subtypes of adrenergic receptors, which are classified into two main groups based on their pharmacological properties: alpha (α) and beta (β) receptors. Alpha receptors are further divided into two subgroups, α1 and α2, while beta receptors are divided into three subgroups, β1, β2, and β3. Each subtype has a unique distribution in the body and mediates distinct physiological responses.

Activation of adrenergic receptors occurs when catecholamines bind to their specific binding sites on the receptor protein. This binding triggers a cascade of intracellular signaling events that ultimately lead to changes in cell function. Different subtypes of adrenergic receptors activate different G proteins and downstream signaling pathways, resulting in diverse physiological responses.

In summary, adrenergic receptors are a class of G protein-coupled receptors that bind catecholamines and mediate various physiological functions. Understanding the function and regulation of these receptors is essential for developing therapeutic strategies to treat a range of medical conditions, including hypertension, heart failure, asthma, and anxiety disorders.

Adrenergic receptors are a type of G protein-coupled receptor that bind and respond to catecholamines, such as epinephrine (adrenaline) and norepinephrine (noradrenaline). Alpha adrenergic receptors (α-ARs) are a subtype of adrenergic receptors that are classified into two main categories: α1-ARs and α2-ARs.

The activation of α1-ARs leads to the activation of phospholipase C, which results in an increase in intracellular calcium levels and the activation of various signaling pathways that mediate diverse physiological responses such as vasoconstriction, smooth muscle contraction, and cell proliferation.

On the other hand, α2-ARs are primarily located on presynaptic nerve terminals where they function to inhibit the release of neurotransmitters, including norepinephrine. The activation of α2-ARs also leads to the inhibition of adenylyl cyclase and a decrease in intracellular cAMP levels, which can mediate various physiological responses such as sedation, analgesia, and hypotension.

Overall, α-ARs play important roles in regulating various physiological functions, including cardiovascular function, mood, and cognition, and are also involved in the pathophysiology of several diseases, such as hypertension, heart failure, and neurodegenerative disorders.

**Prazosin** is an antihypertensive drug, which belongs to the class of medications called alpha-blockers. It works by relaxing the muscles in the blood vessels, which helps to lower blood pressure and improve blood flow. Prazosin is primarily used to treat high blood pressure (hypertension), but it may also be used for the management of symptoms related to enlarged prostate (benign prostatic hyperplasia).

In a medical definition context:

Prazosin: A selective α1-adrenergic receptor antagonist, used in the treatment of hypertension and benign prostatic hyperplasia. It acts by blocking the action of norepinephrine on the smooth muscle of blood vessels, resulting in vasodilation and decreased peripheral vascular resistance. This leads to a reduction in blood pressure and an improvement in urinary symptoms associated with an enlarged prostate.

Adrenergic alpha-agonists are a type of medication that binds to and activates adrenergic alpha receptors, which are found in the nervous system and other tissues throughout the body. These receptors are activated naturally by chemicals called catecholamines, such as norepinephrine and epinephrine (also known as adrenaline), that are released in response to stress or excitement.

When adrenergic alpha-agonists bind to these receptors, they mimic the effects of catecholamines and cause various physiological responses, such as vasoconstriction (constriction of blood vessels), increased heart rate and force of heart contractions, and relaxation of smooth muscle in the airways.

Adrenergic alpha-agonists are used to treat a variety of medical conditions, including hypertension (high blood pressure), glaucoma, nasal congestion, and attention deficit hyperactivity disorder (ADHD). Examples of adrenergic alpha-agonists include phenylephrine, clonidine, and guanfacine.

It's important to note that adrenergic alpha-agonists can have both beneficial and harmful effects, depending on the specific medication, dosage, and individual patient factors. Therefore, they should only be used under the guidance of a healthcare professional.

Phenylephrine is a medication that belongs to the class of drugs known as sympathomimetic amines. It primarily acts as an alpha-1 adrenergic receptor agonist, which means it stimulates these receptors, leading to vasoconstriction (constriction of blood vessels). This effect can be useful in various medical situations, such as:

1. Nasal decongestion: When applied topically in the nose, phenylephrine causes constriction of the blood vessels in the nasal passages, which helps to relieve congestion and swelling. It is often found in over-the-counter (OTC) cold and allergy products.
2. Ocular circulation: In ophthalmology, phenylephrine is used to dilate the pupils before eye examinations. The increased pressure from vasoconstriction helps to open up the pupil, allowing for a better view of the internal structures of the eye.
3. Hypotension management: In some cases, phenylephrine may be given intravenously to treat low blood pressure (hypotension) during medical procedures like spinal anesthesia or septic shock. The vasoconstriction helps to increase blood pressure and improve perfusion of vital organs.

It is essential to use phenylephrine as directed, as improper usage can lead to adverse effects such as increased heart rate, hypertension, arrhythmias, and rebound congestion (when used as a nasal decongestant). Always consult with a healthcare professional for appropriate guidance on using this medication.

Adrenergic alpha-antagonists, also known as alpha-blockers, are a class of medications that block the effects of adrenaline and noradrenaline at alpha-adrenergic receptors. These receptors are found in various tissues throughout the body, including the smooth muscle of blood vessels, the heart, the genitourinary system, and the eyes.

When alpha-blockers bind to these receptors, they prevent the activation of the sympathetic nervous system, which is responsible for the "fight or flight" response. This results in a relaxation of the smooth muscle, leading to vasodilation (widening of blood vessels), decreased blood pressure, and increased blood flow.

Alpha-blockers are used to treat various medical conditions, such as hypertension (high blood pressure), benign prostatic hyperplasia (enlarged prostate), pheochromocytoma (a rare tumor of the adrenal gland), and certain types of glaucoma.

Examples of alpha-blockers include doxazosin, prazosin, terazosin, and tamsulosin. Side effects of alpha-blockers may include dizziness, lightheadedness, headache, weakness, and orthostatic hypotension (a sudden drop in blood pressure upon standing).

Norepinephrine, also known as noradrenaline, is a neurotransmitter and a hormone that is primarily produced in the adrenal glands and is released into the bloodstream in response to stress or physical activity. It plays a crucial role in the "fight-or-flight" response by preparing the body for action through increasing heart rate, blood pressure, respiratory rate, and glucose availability.

As a neurotransmitter, norepinephrine is involved in regulating various functions of the nervous system, including attention, perception, motivation, and arousal. It also plays a role in modulating pain perception and responding to stressful or emotional situations.

In medical settings, norepinephrine is used as a vasopressor medication to treat hypotension (low blood pressure) that can occur during septic shock, anesthesia, or other critical illnesses. It works by constricting blood vessels and increasing heart rate, which helps to improve blood pressure and perfusion of vital organs.

Adrenergic receptors are a type of G protein-coupled receptor that binds and responds to catecholamines, such as epinephrine (adrenaline) and norepinephrine (noradrenaline). Beta adrenergic receptors (β-adrenergic receptors) are a subtype of adrenergic receptors that include three distinct subclasses: β1, β2, and β3. These receptors are widely distributed throughout the body and play important roles in various physiological functions, including cardiovascular regulation, bronchodilation, lipolysis, and glucose metabolism.

β1-adrenergic receptors are primarily located in the heart and regulate cardiac contractility, chronotropy (heart rate), and relaxation. β2-adrenergic receptors are found in various tissues, including the lungs, vascular smooth muscle, liver, and skeletal muscle. They mediate bronchodilation, vasodilation, glycogenolysis, and lipolysis. β3-adrenergic receptors are mainly expressed in adipose tissue, where they stimulate lipolysis and thermogenesis.

Agonists of β-adrenergic receptors include catecholamines like epinephrine and norepinephrine, as well as synthetic drugs such as dobutamine (a β1-selective agonist) and albuterol (a non-selective β2-agonist). Antagonists of β-adrenergic receptors are commonly used in the treatment of various conditions, including hypertension, angina pectoris, heart failure, and asthma. Examples of β-blockers include metoprolol (a β1-selective antagonist) and carvedilol (a non-selective β-blocker with additional α1-adrenergic receptor blocking activity).

Vasoconstrictor agents are substances that cause the narrowing of blood vessels by constricting the smooth muscle in their walls. This leads to an increase in blood pressure and a decrease in blood flow. They work by activating the sympathetic nervous system, which triggers the release of neurotransmitters such as norepinephrine and epinephrine that bind to alpha-adrenergic receptors on the smooth muscle cells of the blood vessel walls, causing them to contract.

Vasoconstrictor agents are used medically for a variety of purposes, including:

* Treating hypotension (low blood pressure)
* Controlling bleeding during surgery or childbirth
* Relieving symptoms of nasal congestion in conditions such as the common cold or allergies

Examples of vasoconstrictor agents include phenylephrine, oxymetazoline, and epinephrine. It's important to note that prolonged use or excessive doses of vasoconstrictor agents can lead to rebound congestion and other adverse effects, so they should be used with caution and under the guidance of a healthcare professional.

Ephedrine is a medication that stimulates the nervous system and is used to treat low blood pressure, asthma, and nasal congestion. It works by narrowing the blood vessels and increasing heart rate, which can help to increase blood pressure and open up the airways in the lungs. Ephedrine may also be used as a bronchodilator to treat COPD (chronic obstructive pulmonary disease).

Ephedrine is available in various forms, including tablets, capsules, and solutions for injection. It is important to follow the instructions of a healthcare provider when taking ephedrine, as it can have side effects such as rapid heart rate, anxiety, headache, and dizziness. Ephedrine should not be used by people with certain medical conditions, such as heart disease, high blood pressure, or narrow-angle glaucoma, and it should not be taken during pregnancy or breastfeeding without consulting a healthcare provider.

In addition to its medical uses, ephedrine has been used as a performance-enhancing drug and is banned by many sports organizations. It can also be found in some over-the-counter cold and allergy medications, although these products are required to carry warnings about the potential for misuse and addiction.

Extravasation of diagnostic and therapeutic materials refers to the unintended leakage or escape of these substances from the intended vasculature into the surrounding tissues. This can occur during the administration of various medical treatments, such as chemotherapy, contrast agents for imaging studies, or other injectable medications.

The extravasation can result in a range of complications, depending on the type and volume of the material that has leaked, as well as the location and sensitivity of the surrounding tissues. Possible consequences include local tissue damage, inflammation, pain, and potential long-term effects such as fibrosis or necrosis.

Prompt recognition and management of extravasation are essential to minimize these complications. Treatment may involve local cooling or heating, the use of hyaluronidase or other agents to facilitate dispersion of the extravasated material, or surgical intervention in severe cases.

Hypotension is a medical term that refers to abnormally low blood pressure, usually defined as a systolic blood pressure less than 90 millimeters of mercury (mm Hg) or a diastolic blood pressure less than 60 mm Hg. Blood pressure is the force exerted by the blood against the walls of the blood vessels as the heart pumps blood.

Hypotension can cause symptoms such as dizziness, lightheadedness, weakness, and fainting, especially when standing up suddenly. In severe cases, hypotension can lead to shock, which is a life-threatening condition characterized by multiple organ failure due to inadequate blood flow.

Hypotension can be caused by various factors, including certain medications, medical conditions such as heart disease, endocrine disorders, and dehydration. It is important to seek medical attention if you experience symptoms of hypotension, as it can indicate an underlying health issue that requires treatment.

Septic shock is a serious condition that occurs as a complication of an infection that has spread throughout the body. It's characterized by a severe drop in blood pressure and abnormalities in cellular metabolism, which can lead to organ failure and death if not promptly treated.

In septic shock, the immune system overreacts to an infection, releasing an overwhelming amount of inflammatory chemicals into the bloodstream. This leads to widespread inflammation, blood vessel dilation, and leaky blood vessels, which can cause fluid to leak out of the blood vessels and into surrounding tissues. As a result, the heart may not be able to pump enough blood to vital organs, leading to organ failure.

Septic shock is often caused by bacterial infections, but it can also be caused by fungal or viral infections. It's most commonly seen in people with weakened immune systems, such as those who have recently undergone surgery, have chronic medical conditions, or are taking medications that suppress the immune system.

Prompt diagnosis and treatment of septic shock is critical to prevent long-term complications and improve outcomes. Treatment typically involves aggressive antibiotic therapy, intravenous fluids, vasopressors to maintain blood pressure, and supportive care in an intensive care unit (ICU).

Ritodrine is a medication that was previously used to prevent or delay premature labor in women at high risk. It is a beta-2 adrenergic agonist, which works by relaxing uterine muscles and slowing down contractions. However, its use in clinical practice has been largely discontinued due to the availability of more effective and safer alternatives for tocolysis (the suppression of premature labor). It's important to note that Ritodrine is not currently a commonly used medication in obstetrics.

Vasopressin, also known as antidiuretic hormone (ADH), is a hormone that helps regulate water balance in the body. It is produced by the hypothalamus and stored in the posterior pituitary gland. When the body is dehydrated or experiencing low blood pressure, vasopressin is released into the bloodstream, where it causes the kidneys to decrease the amount of urine they produce and helps to constrict blood vessels, thereby increasing blood pressure. This helps to maintain adequate fluid volume in the body and ensure that vital organs receive an adequate supply of oxygen-rich blood. In addition to its role in water balance and blood pressure regulation, vasopressin also plays a role in social behaviors such as pair bonding and trust.

Adrenergic blocking agents treat certain diseases through blocking the adrenergic receptor, preventing it from being activated ... Adrenergic blocking agents are a class of drugs that exhibit its pharmacological action through inhibiting the action of the ... The following examples are the common adrenergic blocking agents used clinically. Phenoxybenzamine Phentolamine Prazosin ... selective alpha blockers are caused by the autonomic response to the systemic changes induced by the adrenergic blocking agents ...
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... a beta-adrenergic agent. Chemistry, pharmacokinetics, pharmacodynamics, adverse effects and clinical efficacy in asthma". ...
... s are a class of sympathomimetic agents that selectively stimulates alpha adrenergic receptors. The ... Alpha blocker Adrenergic agonist Beta-adrenergic agonist Declerck I, Himpens B, Droogmans G, Casteels R (September 1990). "The ... Media related to Alpha-adrenergic agonists at Wikimedia Commons Adrenergic+alpha-Agonists at the U.S. National Library of ... Cirazoline is an α1 adrenergic agonist and an α2 adrenergic antagonist". Journal of Pharmacology and Experimental Therapeutics ...
Clark BK (May 1992). "Beta-adrenergic blocking agents: their current status". AACN Clinical Issues in Critical Care Nursing. 3 ... The selective agents (atenolol, metoprolol) are preferred to the non-selective agents (propranolol). There are several ( ... These agents should be avoided whenever possible as there is upwards of seven times more beta-adrenoceptor antagonism than ... Adrenergic (Epinephrine and metanephrine) More likely to indicate an adrenal tumor[non-primary source needed] When plasma ...
Gross ME (2001). "Tranquilizers, α2-adrenergic agonists, and related agents". In Adams RH (ed.). Veterinary Pharmacology and ... A reversal agent for benzodiazepines exists, flumazenil (Anexate). Its use as an antidote is not routinely recommended because ... Although they are second-line agents, benzodiazepines can be used for a limited time to relieve severe anxiety and agitation. ... Kintz P (2007). "Bioanalytical procedures for detection of chemical agents in hair in the case of drug-facilitated crimes". ...
... is an antihypertensive agent. It is used in the form of its sulfate. Guanadrel is a postganglionic adrenergic ... Adrenergic release inhibitors, Antihypertensive agents, Guanidines, Ketals, Spiro compounds). ... blocking agent. Uptake of guanadrel and storage in sympathetic neurons occurs via the norepinephrine pump; guanadrel slowly ...
It acts as a blocking agent for adrenergic neurons. When radiolabeled, it can be used in nuclear medicinal diagnostic and ... It localizes to adrenergic tissue and thus can be used to identify the location of tumors such as pheochromocytomas and ... MIBG is absorbed by and accumulated in granules of adrenal medullary chromaffin cells, as well as in pre-synaptic adrenergic ... It also accumulates in norepinephrine transporters in adrenergic nerves in the heart, lungs, adrenal medulla, salivary glands, ...
Direct intraspinal injection of the catecholamines epinephrine and norepinephrine, and the α-adrenergic agents dexmedetomidine ... "Spinal administration of adrenergic agents produces analgesia in amphibians". European Journal of Pharmacology. 316 (2): 205- ... The relative analgesic potency of 11 opioid agents (μ-opioid receptor agonists - fentanyl, levorphanol, methadone, morphine, ... relative analgesic potency of μ-opioids in amphibians was correlated with the relative analgesic potency of these same agents ...
... clenbuterol and other β2 adrenergic agents remain banned not as a beta-agonist, but rather an anabolic agent. These effects are ... Other adrenergic receptors Alpha-1 adrenergic receptor Alpha-2 adrenergic receptor Beta-1 adrenergic receptor Beta-3 adrenergic ... The beta-2 adrenergic receptor (β2 adrenoreceptor), also known as ADRB2, is a cell membrane-spanning beta-adrenergic receptor ... "Insulin stimulates sequestration of beta-adrenergic receptors and enhanced association of beta-adrenergic receptors with Grb2 ...
Kjaergaard N, Kjaergaard B, Lauritsen JG (June 1988). "Prazosin, an adrenergic blocking agent inadequate as male contraceptive ... Phenoxybenzamine forms a permanent covalent bond with adrenergic receptors. Based on known information about the structures of ... Alkylating agents, Alpha-1 blockers, Alpha-2 blockers, IARC Group 2B carcinogens, Irreversible antagonists, Organochlorides, ... "Phenoxybenzamine binding reveals the helical orientation of the third transmembrane domain of adrenergic receptors". The ...
A Beta-Adrenergic Blocking Agent for the Treatment of Glaucoma". Archives of Ophthalmology. 95 (4): 601-4. doi:10.1001/archopht ... Yale researcher Marvin Sears, observed that timolol, a beta-adrenergic agent, had an intraocular pressure lowering effect in ... This agent was subsequently used to effectively treat Herpes Simplex keratitis, the primary cause of corneal blindness in the ... IDU was proven effective and resulted in the discovery of the first antiviral agent used in humans to treat an active viral ...
"Beta-adrenergic-blocking agents in bronchospastic diseases: a therapeutic dilemma". Pharmacotherapy. 19 (8): 974-978. doi: ... It works by blocking β1-adrenergic receptors in the heart and dilating blood vessels. Nebivolol was patented in 1983 and came ... February 2016). "β3 Adrenergic Stimulation Restores Nitric Oxide/Redox Balance and Enhances Endothelial Function in ... Bakris G (May 2009). "An in-depth analysis of vasodilation in the management of hypertension: focus on adrenergic blockade". ...
Kjaergaard N, Kjaergaard B, Lauritsen JG (June 1988). "Prazosin, an adrenergic blocking agent inadequate as male contraceptive ... February 2021). "Triptonide is a reversible non-hormonal male contraceptive agent in mice and non-human primates". Nature ...
"Effect of antidepressant agents on β-adrenergic receptor and neurotransmitter regulatory systems". Pharmacology Biochemistry ... Tetrabenazine, a similar agent to reserpine, which also depletes catecholamine stores, and to a lesser degree 5-HT, was shown ... This was accounted for on the basis of the energizing effect that these agents have. Moreover, NRIs have the additional adverse ... Moreover, both antidepressant agents were demonstrated to prevent reserpine-induced sedation. Likewise, administration of DOPA ...
Falkay G, Kovács L (1986). "Affinity of tocolytic agents on human placental and myometrial beta-adrenergic receptors". Journal ... Giorgino FL, Egan CG (2010). "Use of isoxsuprine hydrochloride as a tocolytic agent in the treatment of preterm labour: a ... Beta-adrenergic agonists, Equine medications, NMDA receptor antagonists, Phenol ethers, Phenols, Phenylethanolamines, ...
"Effect of antidepressant agents on beta-adrenergic receptor and neurotransmitter regulatory systems". Pharmacology, ... as potential central nervous system agents. 2. Compounds containing a heteroatom attached to nitrogen". Journal of Medicinal ...
"Cardiovascular adverse drug reaction associated with combined beta-adrenergic and calcium entry-blocking agents". Journal of ... Peroutka SJ (November 1983). "The pharmacology of calcium channel antagonists: a novel class of anti-migraine agents?". ...
It stimulates β adrenergic receptors. Abou-Mohamed G, Nagarajan R, Ibrahim TM, Caldwell RW (March 1996). "Characterization of ... the adrenergic activity of arbutamine, a novel agent for pharmacological stress testing". Cardiovascular Drugs and Therapy. 10 ... Beta-adrenergic agonists, Catecholamines, Cardiac stimulants, Phenylethanolamines, All stub articles, Cardiovascular system ...
"Effect of Adrenergic Blocking Agents on the Calcium Pump of the Fragmented Cardiac Sarcoplasmic Reticulum". Nature. 220 (5162 ...
These agents also commonly have action at α-adrenergic receptors and/or 5-HT receptors. This lack of receptor selectivity is ... Agents where the main therapeutic effect is mediated by negative modulation of histamine receptors are termed antihistamines; ... They can be classified on the basis of chemical structure, and agents within these groups have similar properties. Two aromatic ... Patient response and occurrence of adverse drug reactions vary greatly between classes and between agents within classes. The ...
An adrenergic agent is a drug, or other substance, which has effects similar to, or the same as, epinephrine (adrenaline). Thus ... the adrenergic receptors). Directly acting adrenergic agonists act on adrenergic receptors. All adrenergic receptors are G- ... Ephedrine Pseudoephedrine Adrenergic receptor Alpha adrenergic agonist List of adrenergic drugs Siegel, George J; et al. (2006 ... An adrenergic agonist is a drug that stimulates a response from the adrenergic receptors. The five main categories of ...
... can also be a side effect of alpha-1 blockers (alpha1 adrenergic blocking agents). Alpha1 blockers ...
Sympatholytic agents, such as the alpha-adrenergic blocker prazosin, may provide temporary relief to secondary Raynaud's ...
Chocolate, Coffee, Tea Caffeine, cocaine, beta-adrenergic agonists Encainide, Lorcainide Antiarrhythmic agent Electrophysiology ... A Pro-arrhythmic agent is a chemical, drug, or food that promotes cardiac arrhythmias. Omega 3 fatty acids. ...
"Shock and Hypotension in the Newborn Medication: Alpha/Beta Adrenergic Agonists, Vasodilators, Inotropic agents, Volume ... Inotropic agents, Motivation, Neurotransmitters, Norepinephrine-dopamine releasing agents, TAAR1 agonists, Biology of attention ... Similar dopamine antagonist drugs are also some of the most effective anti-nausea agents. Restless legs syndrome and attention ... Some of the most effective therapeutic agents for ADHD are psychostimulants such as methylphenidate (Ritalin, Concerta) and ...
Other stimulators include the powerful vasoconstriction-inducing agents, angiotensin II, endothelins, and alpha adrenergic ... Many agents stimulate cells and tissues to produce 20-HETE in vitro and in vivo. Androgens are particularly potent stimulators ... There are a variety of pharmacological agents which inhibit the synthesis of 20-HETE including various fatty acid analogs that ... This platelet hyper-responsiveness to epinephrine, particularly if also exhibited to other platelet-aggregating agents, could ...
Rapid response to the alpha-1 adrenergic agent phenylephrine in the perioperative period is impacted by genomics and ancestry. ...
Several agents, including alpha adrenergic blockers (such as tamsulosin) and calcium channel blockers (such as nifedipine), may ... intravenous agents or even instillation of certain irrigating agents directly onto the stone can be performed, using antegrade ... Uroliths present in the kidneys, ureters, or bladder may be better defined by the use of this contrast agent. Stones can also ... Normal urine contains chelating agents, such as citrate, that inhibit the nucleation, growth, and aggregation of calcium- ...
Adrenergic blocking agents treat certain diseases through blocking the adrenergic receptor, preventing it from being activated ... Adrenergic blocking agents are a class of drugs that exhibit its pharmacological action through inhibiting the action of the ... The following examples are the common adrenergic blocking agents used clinically. Phenoxybenzamine Phentolamine Prazosin ... selective alpha blockers are caused by the autonomic response to the systemic changes induced by the adrenergic blocking agents ...
Definition: Drugs that act on adrenergic receptors or affect the life cycle of adrenergic transmitters. [d] [e] ... Retrieved from "https://citizendium.org/wiki/index.php?title=Talk:Adrenergic_agent&oldid=692745" ...
Beta-Adrenergic Blocking Agents. Class Summary. Beta blockers inhibit chronotropic, inotropic, and vasodilatory responses to ... Alpha-Adrenergic Agonists. Class Summary. The centrally acting alpha2 -adrenergic agonists clonidine and guanfacine have been ... They are antidepressant agents that are chemically unrelated to tricyclic, tetracyclic, or other available antidepressants. ... SSRIs are first-line agents for managing anxiety, depression, avoidance behavior, and intrusive recollections. ...
Short Acting Adrenergic Bronchodilator Agents essay example for your inspiration. ✔️ 2451 words. ✍ Read and download unique ... Home / Health Care / Asthma / Short Acting Adrenergic Bronchodilator Agents. Short Acting Adrenergic Bronchodilator Agents. ... Short Acting Adrenergic Bronchodilator Agents. These medications are also known as short-acting beta-agonists (SABAs). SABAs ... The short acting adrenergic bronchodilator agents are available in four forms namely pills, injectable, inhaler, and liquids ( ...
Interactions between Alpha-Adrenergic Agents, Prostaglandin E1, Nicotinic Acid, and Adenosine in Regulation of Lipolysis in ... The antilipolytic activity of the alpha-adrenergic agent clonidine was studied using fat cells from the epididymal fat bodies ... Interactions between Alpha-Adrenergic Agents, Prostaglandin E1, Nicotinic Acid, and Adenosine in Regulation of Lipolysis in ... Interactions between Alpha-Adrenergic Agents, Prostaglandin E1, Nicotinic Acid, and Adenosine in Regulation of Lipolysis in ...
Adrenergic agonists. Class Summary. Adrenergic agents can produce constriction of skeletal and vascular muscle. ... Anticholinergic agents. Class Summary. The goal in using anticholinergic agents is to enhance sinoatrial (SA) activity and to ... Atropine is a parasympatholytic agent used to eliminate vagal influence on the SA and AV nodes. This agent is not effective for ... This agent increases water resorption at the distal renal tubular epithelium (ADH effect) and promotes smooth muscle ...
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... is a combination of a corticosteroid and a beta2-adrenergic bronchodilator used to treat asthma or chronic obstructive ... Beta-Adrenergic Receptor Blocking Agents. Beta-blockers not only block the pulmonary effect of beta-agonists, such as ... However, under certain circumstances, there may be no acceptable alternatives to the use of beta-adrenergic blocking agents for ... Use of long acting agents like salmeterol, an active ingredient in Advair, may increase the risk of asthma-related death. ...
Prazosin is an alpha-adrenergic blocking agent used to treat hypertension and benign prostatic hyperplasia. Accordingly, ... Prazosin is a selective inhibitor of the alpha1 subtype of alpha adrenergic receptors. In the human prostate, Prazosin ...
Explore the 1 paper that mention a possible interaction between Glucose and Beta Adrenergic Agent. ... Beta adrenergic activity contributes to the maintenance of elevated circulating levels of glucose , free fatty acids and total ... effects of cyclooxygenase inhibitors and of alpha and beta adrenergic blockade. ...
Metaraminol acts on both α1-adrenergic receptors but appears to have no effect on β-adrenergic receptors. It acts by increasing ...
Alpha-2 Adrenergic Agonists. Class Summary. Agents in this class may decrease vasomotor tone and heart rate by stimulating ... Clonidine is a central alpha-adrenergic agonist that is commonly used as an antihypertensive agent. It stimulates alpha2- ... Propranolol is a nonselective beta-adrenergic receptor blocking agent. It has been found to relieve exaggerated startle ... Prazosin is an alpha-1 adrenergic blocker that is indicated for hypertension. Studies indicate that a nighttime dose of ...
neurotransmitter agent. 16726. adrenergic agent. 9181. adrenergic uptake inhibitor. 4808. (R,R)-tramadol +. 36. ... ARI; NERI; NRI; adrenergic reuptake inhibitor; adrenergic reuptake inhibitors; adrenergic uptake inhibitors; norepinephrine ... Adrenergic uptake inhibitors are drugs that block the transport of adrenergic transmitters into axon terminals or into storage ... antidepressants and amphetamines are among the therapeutically important drugs that may act via inhibition of adrenergic ...
Preparations: Pressor Infusions - Beta adrenergic agents (primarily) *Precautions. *Inotropic and chronotropic agents with risk ... Preparations: Pressor Infusions - Alpha adrenergic agents (primarily) * Preparations: Pressor Infusions - Beta adrenergic ... Preparations: Pressor Infusions - Alpha adrenergic agents (primarily) * Preparations: Pressor Infusions - Beta adrenergic ... Preparations: Pressor Infusions - Alpha adrenergic agents (primarily) * Norepinephrine *Indications. *Preferred first-line ...
In addition, beta-adrenergic agents have been reported to produce electrocardiogram (ECG) changes, such as flattening of the T ... Beta-adrenergic agents. Caution is advised in the co-administration of COMBIVENT Inhalation Aerosol and other sympathomimetic ... Beta-receptor blocking agents and albuterol inhibit the effect of each other. Beta-receptor blocking agents should be used with ... Beta-adrenergic agents may also produce significant hypokalemia in some patients (possibly through intracellular shunting) ...
By Erica Hoe,2019-05-06T11:31:28-04:00May 6th, 2019,Comments Off on In which patient should β-adrenergic blocking agents be ... In which patient should β-adrenergic blocking agents be considered as part of the ED treatment?. ...
β-Adrenergic blocking agents. Possible additive effects on heart rate; may increase risk of severe bradycardia and heart block ... If resting heart rate ,50 bpm, may initiate siponimod in patients receiving stable dosages of a β-adrenergic blocking agent ... May initiate β-adrenergic blocking agents in patients receiving stable dosages of siponimod ... Initiation of siponimod in individuals receiving a β-Adrenergic blocking agent (propranolol) resulted in additive negative ...
E-Pilo-2 is a brand name medication included in a group of medications called Adrenergic and dopaminergic agents. For more ...
Alpha-Adrenergic Agents Antihypertensive effect of alpha-adrenergic blockers such as guanethidine, betanidine, reserpine, alpha ... A variety of adverse reactions not listed above have been reported with other beta-adrenergic blocking agents and should be ... Beta- adrenergic blockers may also potentiate the postural hypotensive effect of the first dose of prazosin, probably by ... Metoprolol tartrate is a selective beta 1-adrenoreceptor blocking agent, available as 25 mg, 37.5 mg, 50 mg, 75 mg and 100 mg ...
Beta-adrenergic blocking agents (See INDICATIONS AND USAGE and WARNINGS). Experience in over 1400 patients in a non-comparative ... and about half had concomitant treatment with beta-adrenergic blocking agents. The most common adverse events were: Incidence ... Nifedipine is an antianginal drug belonging to a class of pharmacological agents, the calcium channel blockers. Nifedipine is 3 ... Controlled studies in small numbers of patients suggest concomitant use of nifedipine and betablocking agents may be beneficial ...
Adrenergic Agent; Antihypertensive Agent; Metabolite; Adrenergic beta-Antagonist; Synthetic Compound; Adrenergic beta-1 ... Adrenergic Receptors Tocris Bioscience 387. Atenolol is a selective ?1 receptor antagonist.; Target: Adrenergic Receptor; ... Cardioselective beta-adrenergic blocker. Antihypertensive, antianginal and antiarrhythmic. S-enantiomer also available. Tocris ... Cardioselective beta-adrenergic blocker. Antihypertensive, antianginal, antiarrhythmic. S-enantiomer (Cat. No. 0393) also ...
Drugs of the Autonomic Nervous System: Adrenergic Agents. Pharmacotherapy for Hypertension Treatment. ...
Alpha- and beta-adrenergic agonist agents (eg, epinephrine). * First-generation antihistamines (eg, diphenhydramine, ... Physically induced angioedema is caused by physical agents, such as cold, heat pressure, vibration, and ultraviolet radiation. ... Agents for treatment or prophylaxis: C1 INH concentrates, ecallantide, lanadelumab, and icatibant. ... 13] Affected patients describe subjective pruritus, sometimes associated with hypersensitivity to an offending agent (eg, a ...
Beta-adrenergic blocking agents: Severe hypertension and reflex bradycardia may occur with non-selective beta-blocking drugs ... Alpha-adrenergic blocking agents: Alpha-blockers such as phentolamine antagonise the vasoconstriction and hypertension effects ... Antihypertensive agents: Adrenaline specifically reverses the antihypertensive effects of adrenergic neurone blockers such as ... Antidepressant agents: Tricyclic antidepressants such as imipramine, inhibit reuptake of directly acting sympathomimetic agents ...
alpha-adrenergic agonist An agent that selectively binds to and activates alpha. -adrenergic receptors. ... alpha-adrenergic agonist An agent that selectively binds to and activates alpha. -adrenergic receptors. ... sympathomimetic agent A drug that mimics the effects of stimulating postganglionic adrenergic sympathetic nerves. Included in ... sympathomimetic agent A drug that mimics the effects of stimulating postganglionic adrenergic sympathetic nerves. Included in ...
Metoprolol (metroprolol) is a beta-adrenergic blocking agent ("beta blocker"). Beta-blockers affect the heart and circulation ( ...
Pharmacologically induced mydriasis produced by adrenergic agonists or parasympatholytic agents. Approved by the FDA. ...
Beta-adrenergic blocking agents. Indications and usages, anatomical therapeutic chemical and diseases classification codes:. ...
BETA-ADRENERGIC BLOCKING AGENT. 711,168. 7.35%. $6,860,753. 2.06%. 142,017. HMG-COA REDUCTASE INHIBITORS. 699,898. 7.23%. $ ...
  • The centrally acting alpha 2 -adrenergic agonists clonidine and guanfacine have been used to treat children with attention deficit hyperactivity disorder (ADHD). (medscape.com)
  • adrenergic agonists (LABA), such as salmeterol, one of the active ingredients in AirDuo RespiClick, increase the risk of asthma-related death. (tevapharm.com)
  • Epinephrine oral inhalation is in a class of medications called alpha- and beta-adrenergic agonists (sympathomimetic agents). (medlineplus.gov)
  • thus α2-adrenergic agonists are contraindicated in children younger than 2 years. (aao.org)
  • Aim 2: Determine how agents that augment PKA, especially therapeutic beta-adrenergic agonists, dampen dust extract-induced PKC isoform activation and attenuate lung inflammation in vitro and in vivo. (cdc.gov)
  • These chemicals will act on adrenergic receptors, with subtypes Alpha-1, Alpha-2, Beta-1, Beta-2, Beta-3, which ultimately allow the body to trigger a "fight-or-flight" response to handle external stress. (wikipedia.org)
  • The common adverse effects of alpha blockers are due to the blockade of alpha-1 adrenergic receptors in tissue that requires high level of alpha adrenergic sympathetic input such as arterial resistance, vascular capacitance and the outflow tract of the urinary bladder. (wikipedia.org)
  • Drugs that act on adrenergic receptors or affect the life cycle of adrenergic transmitters. (citizendium.org)
  • Metaproterenol acts like any other beta adrenergic agonist through beta-2 adrenergic receptors which are predominant in bronchial smooth muscles. (essaywriter.org)
  • In the smooth muscle, it causes relaxation by acting on intracellular adenyl cyclase beta-2 adrenergic receptors that cause increases in cyclic AMP through the conversation of ATP ("Metaproterenol: Indications, Side Effects, Warnings - Drugs.com", 2017). (essaywriter.org)
  • This agent increases water resorption at the distal renal tubular epithelium (ADH effect) and promotes smooth muscle contraction throughout the vascular bed via stimulation of V1 receptors (vasopressor effect). (medscape.com)
  • Accordingly, Prazosin is a selective inhibitor of the alpha1 subtype of alpha adrenergic receptors. (pharmacycode.com)
  • Metaraminol acts on both α1-adrenergic receptors but appears to have no effect on β-adrenergic receptors. (pharmacycode.com)
  • Included in this class are drugs that directly stimulate adrenergic receptors and drugs that act indirectly by provoking the release of adrenergic transmitters. (ebi.ac.uk)
  • An agent that selectively binds to and activates alpha -adrenergic receptors. (ebi.ac.uk)
  • It is a partial agonist at beta adrenergic receptors and acts as a coronary vasodilator and cardiotonic agent. (bvsalud.org)
  • In particular, the drug belongs to beta-adrenergic agonist class which is a group of medications which work the same way and treats the similar medical problem. (essaywriter.org)
  • Teva Pharmaceutical Industries Ltd., (NYSE and TASE:TEVA) today announced the simultaneous launch of AirDuo ™ RespiClick ® (fluticasone propionate and salmeterol) inhalation powder and its authorized generic for the treatment of asthma in patients aged 12 years and older who are uncontrolled on an inhaled corticosteroid (ICS) or whose disease severity clearly warrants the use of an ICS/long-acting beta 2 -adrenergic agonist (LABA) combination. (tevapharm.com)
  • The α2-adrenergic agonist apraclonidine is better tolerated systemically in children, but the risk of follicular conjunctivitis increases with long-term use. (aao.org)
  • Adrenergic blocking agents are a class of drugs that exhibit its pharmacological action through inhibiting the action of the sympathetic nervous system in the body. (wikipedia.org)
  • Adrenergic blocking agents treat certain diseases through blocking the adrenergic receptor, preventing it from being activated by noradrenaline and epinephrine. (wikipedia.org)
  • The adverse effects of non-selective alpha blockers are caused by the autonomic response to the systemic changes induced by the adrenergic blocking agents. (wikipedia.org)
  • In which patient should β-adrenergic blocking agents be considered as part of the ED treatment? (emergencymedicinecases.com)
  • The mechanism of the antihypertensive effects of beta-blocking agents has not been fully elucidated. (nih.gov)
  • Among the adrenergic blocking agents rauwolscine and yohimbine afforded protection, while dihydergotamine was ineffective. (erowid.org)
  • The paper is geared at the compressive analysis of three short acting adrenergic bronchodilator agents namely Metaproterenol, Albuterol, and Levalbuterol. (essaywriter.org)
  • Advair Diskus and Advair HFA (fluticasone propionate and salmeterol oral inhaler) is a combination of a corticosteroid and a beta2-adrenergic bronchodilator used to treat asthma or chronic obstructive pulmonary disease ( COPD ) associated with chronic bronchitis . (medicinenet.com)
  • Combivent (ipratropium bromide and albuterol sulfate ) is an inhaler that is a combination of an anticholinergic bronchodilator and a selective beta2-adrenergic bronchodilator used to treat and prevent symptoms ( wheezing and shortness of breath) caused by ongoing lung disease ( chronic obstructive pulmonary disease - COPD which includes bronchitis and emphysema ). (rxlist.com)
  • Albuterol sulfate, chemically known as (1,3-benzenedimethanol, α'-[[(1,1dimethylethyl) amino] methyl]-4-hydroxy, sulfate (2:1)(salt), (±)- is a relatively selective beta 2 -adrenergic bronchodilator. (rxlist.com)
  • Topical β-adrenergic antagonists, or β-blocker agents, must be used with caution in children. (aao.org)
  • Adrenergic uptake inhibitors are drugs that block the transport of adrenergic transmitters into axon terminals or into storage vesicles within terminals. (mcw.edu)
  • Propranolol is a nonselective beta-adrenergic receptor blocking agent. (medscape.com)
  • They can be used to treat signs and symptoms of benign prostatic hyperplasia, hypertension (but not as first line agent), pheochromocytoma, extravasation management and reversal of local anesthesia. (wikipedia.org)
  • Prazosin is an alpha-adrenergic blocking agent used to treat hypertension and benign prostatic hyperplasia. (pharmacycode.com)
  • The goal in using anticholinergic agents is to enhance sinoatrial (SA) activity and to improve conduction through the SA or atrioventricular (AV) node by reducing vagal tone via muscarinic receptor blockade. (medscape.com)
  • Plasma prostaglandin levels and circulating fuel levels in rats with diabetic ketoacidosis: effects of cyclooxygenase inhibitors and of alpha and beta adrenergic blockade. (supp.ai)
  • Metoprolol is a beta 1 -selective (cardioselective) adrenergic receptor blocker. (nih.gov)
  • A drug that mimics the effects of stimulating postganglionic adrenergic sympathetic nerves. (ebi.ac.uk)
  • Its role is to blocks the effects of adrenergic drugs, such as adrenaline or epinephrine, on nerves of the sympathetic nervous system. (umc-cares.org)
  • Atropine is a parasympatholytic agent used to eliminate vagal influence on the SA and AV nodes. (medscape.com)
  • Beta blockers inhibit chronotropic, inotropic, and vasodilatory responses to beta-adrenergic stimulation. (medscape.com)
  • The Metaproterenol should not be used with other beta adrenergic aerosol bronchodilators as it can result in additive effects. (essaywriter.org)
  • Metoprolol tartrate is a selective beta 1 -adrenoreceptor blocking agent, available as 25 mg, 37.5 mg, 50 mg, 75 mg and 100 mg tablets for oral administration. (nih.gov)
  • Tenormin is a beta-adrenergic blocking agent. (umc-cares.org)
  • The tachycardic effects of beta-adrenergic agents may be enhanced by Buscopan. (janusinfo.se)
  • Elevation of intraocular pressure may be produced by the administration of anticholinergic agents such as Buscopan in patients with undiagnosed and therefore untreated narrow angle glaucoma. (janusinfo.se)
  • This activity describes the indications, actions, adverse effects, and contraindications of sildenafil as an agent in the clinical setting. (nih.gov)
  • The antilipolytic activity of the alpha -adrenergic agent clonidine was studied using fat cells from the epididymal fat bodies of golden hamsters. (aspetjournals.org)
  • From these data we conclude that the sensitivity of fat cells to the antilipolytic effects of clonidine, prostaglandin E 1 , and nicotinic acid is strongly influenced by the presence of adenosine produced by the incubated cells and that optimal antilipolytic activity of these agents is seen only in the absence of adenosine. (aspetjournals.org)
  • They are antidepressant agents that are chemically unrelated to tricyclic, tetracyclic, or other available antidepressants. (medscape.com)
  • The tricyclic antidepressants and amphetamines are among the therapeutically important drugs that may act via inhibition of adrenergic transport. (mcw.edu)
  • E-Pilo-2 is a brand name medication included in a group of medications called Adrenergic and dopaminergic agents . (rxwiki.com)
  • The systemic absorption of these agents is considerable-even with topical application-and can cause bronchospasm, bradycardia, and hypotension in susceptible children. (aao.org)
  • Cardiovascular Drugs / Antilipemic Agents / HMG-CoA Reductase Inhibitors (i.e. (tevausa.com)
  • Topical β-blockers, topical carbonic anhydrase inhibitors (CAIs), and prostaglandin analogues are reasonable first-line agents in children. (aao.org)
  • Adrenergic agents can produce constriction of skeletal and vascular muscle. (medscape.com)
  • class 1C antiarrhythmic drugs (flecainide, propafenone) and class 1A agents (procainamide, disopyramide). (nih.gov)
  • The rats implanted with DB in MAR had prolonged diestrus, and their uteri showed decidual reaction, indicating that an α-adrenergic mechanism is involved in the release of PTF from the median eminence. (karger.com)
  • Nifedipine is an antianginal drug belonging to a class of pharmacological agents, the calcium channel blockers. (nih.gov)
  • Various pharmacological agents were tested for their ability to block reserpine-induced (0.5 mg/kg) emesis in pigeons. (erowid.org)
  • however, some authorities question its clinical effectiveness in humans This agent is used to increase coronary and cerebral blood flow during cardiopulmonary resuscitation (CPR) and may enhance automaticity during asystole. (medscape.com)
  • however, this agent has not been demonstrated to influence the final clinical outcome. (medscape.com)
  • This agent is not effective for infranodal third-degree heart block, PEA, and asystole. (medscape.com)