A specific category of drugs that prevent sleepiness by specifically targeting sleep-mechanisms in the brain. They are used to treat DISORDERS OF EXCESSIVE SOMNOLENCE such as NARCOLEPSY. Note that this drug category does not include broadly-acting central nervous system stimulants such as AMPHETAMINES.
A subclass of alpha-adrenergic receptors found on both presynaptic and postsynaptic membranes where they signal through Gi-Go G-PROTEINS. While postsynaptic alpha-2 receptors play a traditional role in mediating the effects of ADRENERGIC AGONISTS, the subset of alpha-2 receptors found on presynaptic membranes signal the feedback inhibition of NEUROTRANSMITTER release.
Drugs that are used to treat RHEUMATOID ARTHRITIS.
A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated.
Cell surface receptors that bind TUMOR NECROSIS FACTORS and trigger changes which influence the behavior of cells.
Serum glycoprotein produced by activated MACROPHAGES and other mammalian MONONUCLEAR LEUKOCYTES. It has necrotizing activity against tumor cell lines and increases ability to reject tumor transplants. Also known as TNF-alpha, it is only 30% homologous to TNF-beta (LYMPHOTOXIN), but they share TNF RECEPTORS.
Antibodies produced by a single clone of cells.
The major immunoglobulin isotype class in normal human serum. There are several isotype subclasses of IgG, for example, IgG1, IgG2A, and IgG2B.
Plasma glycoprotein member of the serpin superfamily which inhibits TRYPSIN; NEUTROPHIL ELASTASE; and other PROTEOLYTIC ENZYMES.
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.
Chemical substances which inhibit the function of the endocrine glands, the biosynthesis of their secreted hormones, or the action of hormones upon their specific sites.
Drugs that bind to but do not activate DOPAMINE RECEPTORS, thereby blocking the actions of dopamine or exogenous agonists. Many drugs used in the treatment of psychotic disorders (ANTIPSYCHOTIC AGENTS) are dopamine antagonists, although their therapeutic effects may be due to long-term adjustments of the brain rather than to the acute effects of blocking dopamine receptors. Dopamine antagonists have been used for several other clinical purposes including as ANTIEMETICS, in the treatment of Tourette syndrome, and for hiccup. Dopamine receptor blockade is associated with NEUROLEPTIC MALIGNANT SYNDROME.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Drugs that bind to but do not activate excitatory amino acid receptors, thereby blocking the actions of agonists.
Compounds that inhibit or block the activity of NEUROKININ-1 RECEPTORS.
Agents inhibiting the effect of narcotics on the central nervous system.
Drugs that bind to and block the activation of ADRENERGIC ALPHA-1 RECEPTORS.
Drugs that selectively bind to but do not activate histamine H2 receptors, thereby blocking the actions of histamine. Their clinically most important action is the inhibition of acid secretion in the treatment of gastrointestinal ulcers. Smooth muscle may also be affected. Some drugs in this class have strong effects in the central nervous system, but these actions are not well understood.
A ligand that binds to but fails to activate the INTERLEUKIN 1 RECEPTOR. It plays an inhibitory role in the regulation of INFLAMMATION and FEVER. Several isoforms of the protein exist due to multiple ALTERNATIVE SPLICING of its mRNA.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
Hypoxia-inducible factor 1, alpha subunit is a basic helix-loop-helix transcription factor that is regulated by OXYGEN availability and is targeted for degradation by VHL TUMOR SUPPRESSOR PROTEIN.
Drugs that bind to nicotinic cholinergic receptors (RECEPTORS, NICOTINIC) and block the actions of acetylcholine or cholinergic agonists. Nicotinic antagonists block synaptic transmission at autonomic ganglia, the skeletal neuromuscular junction, and at central nervous system nicotinic synapses.
Drugs that bind to but do not activate MUSCARINIC RECEPTORS, thereby blocking the actions of endogenous ACETYLCHOLINE or exogenous agonists. Muscarinic antagonists have widespread effects including actions on the iris and ciliary muscle of the eye, the heart and blood vessels, secretions of the respiratory tract, GI system, and salivary glands, GI motility, urinary bladder tone, and the central nervous system.
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.
Drugs that bind to but do not activate GABA RECEPTORS, thereby blocking the actions of endogenous GAMMA-AMINOBUTYRIC ACID and GABA RECEPTOR AGONISTS.
A member of the NICOTINIC ACETYLCHOLINE RECEPTOR subfamily of the LIGAND-GATED ION CHANNEL family. It consists entirely of pentameric a7 subunits expressed in the CNS, autonomic nervous system, vascular system, lymphocytes and spleen.
Drugs that selectively bind to but do not activate histamine H1 receptors, thereby blocking the actions of endogenous histamine. Included here are the classical antihistaminics that antagonize or prevent the action of histamine mainly in immediate hypersensitivity. They act in the bronchi, capillaries, and some other smooth muscles, and are used to prevent or allay motion sickness, seasonal rhinitis, and allergic dermatitis and to induce somnolence. The effects of blocking central nervous system H1 receptors are not as well understood.
Compounds that bind to and block the stimulation of PURINERGIC P1 RECEPTORS.
A family of hexahydropyridines.
A subclass of alpha-adrenergic receptors that mediate contraction of SMOOTH MUSCLE in a variety of tissues such as ARTERIOLES; VEINS; and the UTERUS. They are usually found on postsynaptic membranes and signal through GQ-G11 G-PROTEINS.
Drugs that bind to and block the activation of ADRENERGIC ALPHA-2 RECEPTORS.

alpha1-adrenergic receptor subtypes in human peripheral blood lymphocytes. (1/2042)

We investigated the expression of alpha1-adrenergic receptor subtypes in intact human peripheral blood lymphocytes using reverse transcription-polymerase chain reaction (RT-PCR) and radioligand binding assay techniques combined with antibodies against the three subtypes of alpha1-adrenergic receptors (alpha1A, alpha1B, and alpha1D). RT-PCR amplified in peripheral blood lymphocytes a 348-bp alpha1A-adrenergic receptor fragment, a 689-bp alpha1B-adrenergic receptor fragment, and a 540-bp alpha1D-adrenergic receptor fragment. Radioligand binding assay with [3H]prazosin as radioligand revealed a high-affinity binding with a dissociation constant value of 0. 65+/-0.05 nmol/L and a maximum density of binding sites of 175. 3+/-20.5 fmol/10(6) cells. The pharmacological profile of [3H]prazosin binding to human peripheral blood lymphocytes was consistent with the labeling of alpha1-adrenergic receptors. Antibodies against alpha1A-, alpha1B-, and alpha1D-receptor subtypes decreased [3H]prazosin binding to a different extent. This indicates that human peripheral blood lymphocytes express the three alpha1-adrenergic receptor subtypes. Of the three different alpha1-adrenergic receptor subtypes, the alpha1B is the most represented and the alpha1D, the least. Future studies should clarify the functional relevance of alpha1-adrenergic receptors expressed by peripheral blood lymphocytes. The identification of these sites may represent a step for evaluating whether they represent a marker of alpha1-adrenergic receptors in cardiovascular disorders or for assessing responses to drug treatment on these receptors.  (+info)

Modulation of basal intracellular calcium by inverse agonists and phorbol myristate acetate in rat-1 fibroblasts stably expressing alpha1d-adrenoceptors. (2/2042)

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

Transcriptional regulation of alpha1-adrenoceptor gene in the rat liver during different phases of sepsis. (3/2042)

Changes in alpha1-adrenoceptor (alpha1AR) gene expression in the rat liver during different phases of sepsis were studied. Sepsis was induced by cecal ligation and puncture (CLP). Septic rats exhibit two metabolically distinct phases: an initial hyperglycemic phase (9 h after CLP, early sepsis) followed by a hypoglycemic phase (18 h after CLP; late sepsis). The [3H]prazosin binding studies show that the density of alpha1AR was increased by 30% during the early phase while it was decreased by 24% during the late phase of sepsis. Western blot analyses reveal that alpha1AR protein level was elevated by 48% during early sepsis but was decreased by 55% during late sepsis. Northern blot analyses depict that the steady-state level of alpha1bAR mRNA was enhanced by 21% during the early phase but was declined by 29% during the late phase of sepsis. Nuclear run-off assays show that the transcription rate of alpha1bAR gene transcript was increased by 76% during early sepsis while it was decreased by 29% during late sepsis. The actinomycin D pulse-chase studies indicate that the half-life of alpha1bAR mRNA remained unaffected during the early and the late phases of sepsis. These findings demonstrate that during the early phase of sepsis, the increase in the rate of transcription of alpha1bAR gene paralleled with the elevations in the alpha1bAR mRNA abundance and alpha1AR protein level, while during the late phase of sepsis, the decrease in the rate of transcription of alpha1bAR gene coincided with the declines in the alpha1bAR mRNA abundance and the alpha1AR protein level in the rat liver. These observations indicate that the altered expression of alpha1AR genes in the rat liver during the progression of sepsis was regulated transcriptionally.  (+info)

Facilitation and depression of ATP and noradrenaline release from sympathetic nerves of rat tail artery. (4/2042)

1. Excitatory junction currents (EJCs) were used to measure ATP release; noradrenaline (NA) oxidation currents and fractional overflow of labelled NA, [3H]NA, were used to monitor the release of endogenous and exogenous NA, respectively, from post-ganglionic sympathetic nerves of rat tail artery. 2. During nerve stimulation with 100 pulses at 5-20 Hz the EJCs initially grew in size (maximally by 23 %, at 2-10 Hz), and then depressed, maximally by 68 % at 20 Hz. 3. The peak amplitude of NA oxidation currents in response to nerve stimulation with 100 pulses at 2-20 Hz grew in size with frequency, while the area was independent of frequency and roughly constant. 4. The size of the NA oxidation currents evoked by nerve stimulation with 4-100 pulses at 20 Hz grew linearly with train length between pulses 4-16. Between pulses 20-100 there was a train length-dependent depression of the signal. 5. Fractional overflow of [3H]NA in response to nerve stimulation with 5-100 pulses at 20 Hz behaved similarly to the EJCs. It initially grew roughly linearly between pulses 5-25, and then showed a dramatic depression similar to that of the EJCs. 6. The alpha2-adrenoceptor antagonists rauwolscine and yohimbine increased the overflow of [3H]NA and the amplitude of NA oxidation currents, but not that of the EJCs. 7. It is concluded that during high-frequency stimulation (i) the release of ATP and NA is first briefly facilitated then markedly depressed, (ii) facilitation and depression of the two transmitters are similar in magnitude and time course, and (iii) alpha2-adrenoceptor antagonists differentially modify EJCs and the NA signals. The results obtained in the absence of drugs are compatible with the hypothesis that ATP and NA are released in parallel, while the effects of alpha2-adrenoceptor antagonists seem to suggest dissociated release.  (+info)

Homologous regulation of the alpha2C-adrenoceptor subtype in human hepatocarcinoma, HepG2. (5/2042)

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

Effects of heptanol on the neurogenic and myogenic contractions of the guinea-pig vas deferens. (6/2042)

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

Nitric oxide mediates sympathetic vasoconstriction at supraspinal, spinal, and synaptic levels. (7/2042)

The purposes of this study were to investigate the level of the sympathetic nervous system in which nitric oxide (NO) mediates regional sympathetic vasoconstriction and to determine whether neural mechanisms are involved in vasoconstriction after NO inhibition. Ganglionic blockade (hexamethonium), alpha1-receptor blockade (prazosin), and spinal section at T1 were used to study sympathetic involvement. NO was blocked with Nomega-nitro-L-arginine methyl ester (L-NAME). Regional blood flow in the mesenteric and renal arteries and terminal aorta was monitored by electromagnetic flowmetry in conscious rats. L-NAME (3-5 mg/kg iv) increased arterial pressure and peripheral resistance. Ganglionic blockade (25 mg/kg iv) significantly reduced the increase in resistance in the mesentery and kidney in intact and spinal-sectioned rats. Ganglionic blockade significantly decreased hindquarter resistance in intact rats but not in spinal-sectioned rats. Prazosin (200 micrograms/kg iv) significantly reduced the increased hindquarter resistance. We concluded that NO suppresses sympathetic vasoconstriction in the mesentery and kidney at the spinal level, whereas hindquarter tone is mediated at supraspinal and synaptic levels.  (+info)

Facilitatory beta2-adrenoceptors on cholinergic and adrenergic nerve endings of the guinea pig trachea. (8/2042)

Using electrical field stimulation of epithelium-denuded intact guinea pig tracheal tube preparations, we studied the presence and role of prejunctional beta2-adrenoceptors by measuring evoked endogenous acetylcholine (ACh) and norepinephrine (NE) release directly. Analysis of ACh and NE was through two HPLC systems with electrochemical detection. Electrical field stimulation (150 mA, 0.8 ms, 16 Hz, 5 min, biphasic pulses) released 29.1 +/- 2.5 pmol ACh/g tissue and 70.2 +/- 6.2 pmol NE/g tissue. Preincubation for 15 min with the selective beta2-adrenoceptor agonist fenoterol (1 microM) increased both ACh and NE overflow to 178 +/- 28 (P < 0.01) and 165 +/- 12% (P < 0.01), respectively, of control values, increases that were abolished completely by the selective beta2-adrenoceptor antagonist ICI-118551 (1 microM). Further experiments with increasing fenoterol concentrations (0.1-100 microM) and different preincubation periods (1, 5, and 15 min) showed a strong and concentration-dependent facilitation of NE release, with maximum response levels decreasing (from nearly 5-fold to only 2.5-fold of control value) with increasing agonist contact time. In contrast, sensitivity of facilitatory beta2-adrenoceptors on cholinergic nerves to fenoterol gradually increased when the incubation period was prolonged; in addition, a bell-shaped concentration-response relationship was found at 15 min of preincubation. Fenoterol concentration-response relationships (15-min agonist preincubation) in the presence of atropine and yohimbine (1 microM each) were similar in the case of NE release, but in the case of ACh release, the bell shape was lost. The results indicate a differential capacity and response time profile of facilitatory prejunctional beta2-adrenoceptors on adrenergic and cholinergic nerve terminals in the guinea pig trachea and suggest that the receptors on adrenergic nerves are more susceptible to desensitization.  (+info)

Wakefulness-promoting agents are a class of medications that are used to promote and maintain alertness and wakefulness. They work by stimulating the brain's arousal centers, increasing the release of neurotransmitters such as dopamine, norepinephrine, and histamine, which help to counteract the effects of sleep-promoting substances in the brain.

Wakefulness-promoting agents are typically used to treat excessive daytime sleepiness associated with conditions such as narcolepsy, obstructive sleep apnea, shift work sleep disorder, and other disorders that cause disrupted sleep patterns. Some examples of wakefulness-promoting agents include modafinil, armodafinil, pitolisant, and solriamfetol.

It is important to note that while these medications can help to promote alertness and reduce excessive daytime sleepiness, they are not a substitute for getting adequate amounts of quality sleep. It is also important to use them under the guidance of a healthcare provider, as they may have potential side effects and interactions with other medications.

Alpha-2 adrenergic receptors are a type of G protein-coupled receptor that binds catecholamines, such as norepinephrine and epinephrine. These receptors are widely distributed in the central and peripheral nervous system, as well as in various organs and tissues throughout the body.

Activation of alpha-2 adrenergic receptors leads to a variety of physiological responses, including inhibition of neurotransmitter release, vasoconstriction, and reduced heart rate. These receptors play important roles in regulating blood pressure, pain perception, and various cognitive and emotional processes.

There are several subtypes of alpha-2 adrenergic receptors, including alpha-2A, alpha-2B, and alpha-2C, which may have distinct physiological functions and be targeted by different drugs. For example, certain medications used to treat hypertension or opioid withdrawal target alpha-2 adrenergic receptors to produce their therapeutic effects.

Antirheumatic agents are a class of drugs used to treat rheumatoid arthritis, other inflammatory types of arthritis, and related conditions. These medications work by reducing inflammation in the body, relieving symptoms such as pain, swelling, and stiffness in the joints. They can also help slow down or prevent joint damage and disability caused by the disease.

There are several types of antirheumatic agents, including:

1. Nonsteroidal anti-inflammatory drugs (NSAIDs): These medications, such as ibuprofen and naproxen, reduce inflammation and relieve pain. They are often used to treat mild to moderate symptoms of arthritis.
2. Corticosteroids: These powerful anti-inflammatory drugs, such as prednisone and cortisone, can quickly reduce inflammation and suppress the immune system. They are usually used for short-term relief of severe symptoms or in combination with other antirheumatic agents.
3. Disease-modifying antirheumatic drugs (DMARDs): These medications, such as methotrexate and hydroxychloroquine, work by slowing down the progression of rheumatoid arthritis and preventing joint damage. They can take several weeks or months to become fully effective.
4. Biologic response modifiers (biologics): These are a newer class of DMARDs that target specific molecules involved in the immune response. They include drugs such as adalimumab, etanercept, and infliximab. Biologics are usually used in combination with other antirheumatic agents for patients who have not responded to traditional DMARD therapy.
5. Janus kinase (JAK) inhibitors: These medications, such as tofacitinib and baricitinib, work by blocking the action of enzymes called JAKs that are involved in the immune response. They are used to treat moderate to severe rheumatoid arthritis and can be used in combination with other antirheumatic agents.

It is important to note that antirheumatic agents can have significant side effects and should only be prescribed by a healthcare provider who is experienced in the management of rheumatoid arthritis. Regular monitoring and follow-up are essential to ensure safe and effective treatment.

Rheumatoid arthritis (RA) is a systemic autoimmune disease that primarily affects the joints. It is characterized by persistent inflammation, synovial hyperplasia, and subsequent damage to the articular cartilage and bone. The immune system mistakenly attacks the body's own tissues, specifically targeting the synovial membrane lining the joint capsule. This results in swelling, pain, warmth, and stiffness in affected joints, often most severely in the hands and feet.

RA can also have extra-articular manifestations, affecting other organs such as the lungs, heart, skin, eyes, and blood vessels. The exact cause of RA remains unknown, but it is believed to involve a complex interplay between genetic susceptibility and environmental triggers. Early diagnosis and treatment are crucial in managing rheumatoid arthritis to prevent joint damage, disability, and systemic complications.

Tumor Necrosis Factor (TNF) Receptors are cell surface receptors that bind to tumor necrosis factor cytokines. They play crucial roles in the regulation of a variety of immune cell functions, including inflammation, immunity, and cell survival or death (apoptosis).

There are two major types of TNF receptors: TNFR1 (also known as p55 or CD120a) and TNFR2 (also known as p75 or CD120b). TNFR1 is widely expressed in most tissues, while TNFR2 has a more restricted expression pattern and is mainly found on immune cells.

TNF receptors have an intracellular domain called the death domain, which can trigger signaling pathways leading to apoptosis when activated by TNF ligands. However, they can also activate other signaling pathways that promote cell survival, differentiation, and inflammation. Dysregulation of TNF receptor signaling has been implicated in various diseases, including cancer, autoimmune disorders, and neurodegenerative conditions.

Tumor Necrosis Factor-alpha (TNF-α) is a cytokine, a type of small signaling protein involved in immune response and inflammation. It is primarily produced by activated macrophages, although other cell types such as T-cells, natural killer cells, and mast cells can also produce it.

TNF-α plays a crucial role in the body's defense against infection and tissue injury by mediating inflammatory responses, activating immune cells, and inducing apoptosis (programmed cell death) in certain types of cells. It does this by binding to its receptors, TNFR1 and TNFR2, which are found on the surface of many cell types.

In addition to its role in the immune response, TNF-α has been implicated in the pathogenesis of several diseases, including autoimmune disorders such as rheumatoid arthritis, inflammatory bowel disease, and psoriasis, as well as cancer, where it can promote tumor growth and metastasis.

Therapeutic agents that target TNF-α, such as infliximab, adalimumab, and etanercept, have been developed to treat these conditions. However, these drugs can also increase the risk of infections and other side effects, so their use must be carefully monitored.

Monoclonal antibodies are a type of antibody that are identical because they are produced by a single clone of cells. They are laboratory-produced molecules that act like human antibodies in the immune system. They can be designed to attach to specific proteins found on the surface of cancer cells, making them useful for targeting and treating cancer. Monoclonal antibodies can also be used as a therapy for other diseases, such as autoimmune disorders and inflammatory conditions.

Monoclonal antibodies are produced by fusing a single type of immune cell, called a B cell, with a tumor cell to create a hybrid cell, or hybridoma. This hybrid cell is then able to replicate indefinitely, producing a large number of identical copies of the original antibody. These antibodies can be further modified and engineered to enhance their ability to bind to specific targets, increase their stability, and improve their effectiveness as therapeutic agents.

Monoclonal antibodies have several mechanisms of action in cancer therapy. They can directly kill cancer cells by binding to them and triggering an immune response. They can also block the signals that promote cancer growth and survival. Additionally, monoclonal antibodies can be used to deliver drugs or radiation directly to cancer cells, increasing the effectiveness of these treatments while minimizing their side effects on healthy tissues.

Monoclonal antibodies have become an important tool in modern medicine, with several approved for use in cancer therapy and other diseases. They are continuing to be studied and developed as a promising approach to treating a wide range of medical conditions.

Immunoglobulin G (IgG) is a type of antibody, which is a protective protein produced by the immune system in response to foreign substances like bacteria or viruses. IgG is the most abundant type of antibody in human blood, making up about 75-80% of all antibodies. It is found in all body fluids and plays a crucial role in fighting infections caused by bacteria, viruses, and toxins.

IgG has several important functions:

1. Neutralization: IgG can bind to the surface of bacteria or viruses, preventing them from attaching to and infecting human cells.
2. Opsonization: IgG coats the surface of pathogens, making them more recognizable and easier for immune cells like neutrophils and macrophages to phagocytose (engulf and destroy) them.
3. Complement activation: IgG can activate the complement system, a group of proteins that work together to help eliminate pathogens from the body. Activation of the complement system leads to the formation of the membrane attack complex, which creates holes in the cell membranes of bacteria, leading to their lysis (destruction).
4. Antibody-dependent cellular cytotoxicity (ADCC): IgG can bind to immune cells like natural killer (NK) cells and trigger them to release substances that cause target cells (such as virus-infected or cancerous cells) to undergo apoptosis (programmed cell death).
5. Immune complex formation: IgG can form immune complexes with antigens, which can then be removed from the body through various mechanisms, such as phagocytosis by immune cells or excretion in urine.

IgG is a critical component of adaptive immunity and provides long-lasting protection against reinfection with many pathogens. It has four subclasses (IgG1, IgG2, IgG3, and IgG4) that differ in their structure, function, and distribution in the body.

Alpha 1-antitrypsin (AAT, or α1-antiproteinase, A1AP) is a protein that is primarily produced by the liver and released into the bloodstream. It belongs to a group of proteins called serine protease inhibitors, which help regulate inflammation and protect tissues from damage caused by enzymes involved in the immune response.

Alpha 1-antitrypsin is particularly important for protecting the lungs from damage caused by neutrophil elastase, an enzyme released by white blood cells called neutrophils during inflammation. In the lungs, AAT binds to and inhibits neutrophil elastase, preventing it from degrading the extracellular matrix and damaging lung tissue.

Deficiency in alpha 1-antitrypsin can lead to chronic obstructive pulmonary disease (COPD) and liver disease. The most common cause of AAT deficiency is a genetic mutation that results in abnormal folding and accumulation of the protein within liver cells, leading to reduced levels of functional AAT in the bloodstream. This condition is called alpha 1-antitrypsin deficiency (AATD) and can be inherited in an autosomal codominant manner. Individuals with severe AATD may require augmentation therapy with intravenous infusions of purified human AAT to help prevent lung damage.

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.

Hormone antagonists are substances or drugs that block the action of hormones by binding to their receptors without activating them, thereby preventing the hormones from exerting their effects. They can be classified into two types: receptor antagonists and enzyme inhibitors. Receptor antagonists bind directly to hormone receptors and prevent the hormone from binding, while enzyme inhibitors block the production or breakdown of hormones by inhibiting specific enzymes involved in their metabolism. Hormone antagonists are used in the treatment of various medical conditions, such as cancer, hormonal disorders, and cardiovascular diseases.

Dopamine antagonists are a class of drugs that block the action of dopamine, a neurotransmitter in the brain associated with various functions including movement, motivation, and emotion. These drugs work by binding to dopamine receptors and preventing dopamine from attaching to them, which can help to reduce the symptoms of certain medical conditions such as schizophrenia, bipolar disorder, and gastroesophageal reflux disease (GERD).

There are several types of dopamine antagonists, including:

1. Typical antipsychotics: These drugs are primarily used to treat psychosis, including schizophrenia and delusional disorders. Examples include haloperidol, chlorpromazine, and fluphenazine.
2. Atypical antipsychotics: These drugs are also used to treat psychosis but have fewer side effects than typical antipsychotics. They may also be used to treat bipolar disorder and depression. Examples include risperidone, olanzapine, and quetiapine.
3. Antiemetics: These drugs are used to treat nausea and vomiting. Examples include metoclopramide and prochlorperazine.
4. Dopamine agonists: While not technically dopamine antagonists, these drugs work by stimulating dopamine receptors and can be used to treat conditions such as Parkinson's disease. However, they can also have the opposite effect and block dopamine receptors in high doses, making them functionally similar to dopamine antagonists.

Common side effects of dopamine antagonists include sedation, weight gain, and movement disorders such as tardive dyskinesia. It's important to use these drugs under the close supervision of a healthcare provider to monitor for side effects and adjust the dosage as needed.

A dose-response relationship in the context of drugs refers to the changes in the effects or symptoms that occur as the dose of a drug is increased or decreased. Generally, as the dose of a drug is increased, the severity or intensity of its effects also increases. Conversely, as the dose is decreased, the effects of the drug become less severe or may disappear altogether.

The dose-response relationship is an important concept in pharmacology and toxicology because it helps to establish the safe and effective dosage range for a drug. By understanding how changes in the dose of a drug affect its therapeutic and adverse effects, healthcare providers can optimize treatment plans for their patients while minimizing the risk of harm.

The dose-response relationship is typically depicted as a curve that shows the relationship between the dose of a drug and its effect. The shape of the curve may vary depending on the drug and the specific effect being measured. Some drugs may have a steep dose-response curve, meaning that small changes in the dose can result in large differences in the effect. Other drugs may have a more gradual dose-response curve, where larger changes in the dose are needed to produce significant effects.

In addition to helping establish safe and effective dosages, the dose-response relationship is also used to evaluate the potential therapeutic benefits and risks of new drugs during clinical trials. By systematically testing different doses of a drug in controlled studies, researchers can identify the optimal dosage range for the drug and assess its safety and efficacy.

Excitatory amino acid antagonists are a class of drugs that block the action of excitatory neurotransmitters, particularly glutamate and aspartate, in the brain. These drugs work by binding to and blocking the receptors for these neurotransmitters, thereby reducing their ability to stimulate neurons and produce an excitatory response.

Excitatory amino acid antagonists have been studied for their potential therapeutic benefits in a variety of neurological conditions, including stroke, epilepsy, traumatic brain injury, and neurodegenerative disorders such as Alzheimer's disease and Parkinson's disease. However, their use is limited by the fact that blocking excitatory neurotransmission can also have negative effects on cognitive function and memory.

There are several types of excitatory amino acid receptors, including N-methyl-D-aspartate (NMDA), alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), and kainite receptors. Different excitatory amino acid antagonists may target one or more of these receptor subtypes, depending on their specific mechanism of action.

Examples of excitatory amino acid antagonists include ketamine, memantine, and dextromethorphan. These drugs have been used in clinical practice for various indications, such as anesthesia, sedation, and treatment of neurological disorders. However, their use must be carefully monitored due to potential side effects and risks associated with blocking excitatory neurotransmission.

Neurokinin-1 (NK-1) receptor antagonists are a class of drugs that block the action of substance P, a neuropeptide involved in pain transmission and inflammation. These drugs work by binding to NK-1 receptors found on nerve cells, preventing substance P from activating them and transmitting pain signals. NK-1 receptor antagonists have been studied for their potential use in treating various conditions associated with pain and inflammation, such as migraine headaches, depression, and irritable bowel syndrome. Some examples of NK-1 receptor antagonists include aprepitant, fosaprepitant, and rolapitant.

Narcotic antagonists are a class of medications that block the effects of opioids, a type of narcotic pain reliever, by binding to opioid receptors in the brain and blocking the activation of these receptors by opioids. This results in the prevention or reversal of opioid-induced effects such as respiratory depression, sedation, and euphoria. Narcotic antagonists are used for a variety of medical purposes, including the treatment of opioid overdose, the management of opioid dependence, and the prevention of opioid-induced side effects in certain clinical situations. Examples of narcotic antagonists include naloxone, naltrexone, and methylnaltrexone.

Adrenergic alpha-1 receptor antagonists, also known as alpha-blockers, are a class of medications that block the effects of the neurotransmitter norepinephrine at alpha-1 receptors. These receptors are found in various tissues throughout the body, including the smooth muscle of blood vessels, the bladder, and the eye.

When norepinephrine binds to alpha-1 receptors, it causes smooth muscle to contract, leading to vasoconstriction (constriction of blood vessels), increased blood pressure, and other effects. By blocking these receptors, alpha-blockers can cause relaxation of smooth muscle, leading to vasodilation (expansion of blood vessels), decreased blood pressure, and other effects.

Alpha-blockers are used in the treatment of various medical conditions, including hypertension (high blood pressure), benign prostatic hyperplasia (enlarged prostate), and pheochromocytoma (a rare tumor of the adrenal gland). Examples of alpha-blockers include doxazosin, prazosin, and terazosin.

It's important to note that while alpha-blockers can be effective in treating certain medical conditions, they can also have side effects, such as dizziness, lightheadedness, and orthostatic hypotension (a sudden drop in blood pressure when standing up). As with any medication, it's important to use alpha-blockers under the guidance of a healthcare provider.

Histamine H2 antagonists, also known as H2 blockers, are a class of medications that work by blocking the action of histamine on the H2 receptors in the stomach. Histamine is a chemical that is released by the body during an allergic reaction and can also be released by certain cells in the stomach in response to food or other stimuli. When histamine binds to the H2 receptors in the stomach, it triggers the release of acid. By blocking the action of histamine on these receptors, H2 antagonists reduce the amount of acid produced by the stomach, which can help to relieve symptoms such as heartburn, indigestion, and stomach ulcers. Examples of H2 antagonists include ranitidine (Zantac), famotidine (Pepcid), and cimetidine (Tagamet).

Interleukin-1 Receptor Antagonist Protein (IL-1Ra) is a naturally occurring protein that acts as a competitive inhibitor of the interleukin-1 (IL-1) receptor. IL-1 is a pro-inflammatory cytokine involved in various physiological processes, including the immune response and inflammation. The binding of IL-1 to its receptor triggers a signaling cascade that leads to the activation of inflammatory genes and cellular responses.

IL-1Ra shares structural similarities with IL-1 but does not initiate the downstream signaling pathway. Instead, it binds to the same receptor site as IL-1, preventing IL-1 from interacting with its receptor and thus inhibiting the inflammatory response.

Increased levels of IL-1Ra have been found in various inflammatory conditions, such as rheumatoid arthritis, inflammatory bowel disease, and sepsis, where it acts to counterbalance the pro-inflammatory effects of IL-1. Recombinant IL-1Ra (Anakinra) is used clinically as a therapeutic agent for the treatment of rheumatoid arthritis and other inflammatory diseases.

Sprague-Dawley rats are a strain of albino laboratory rats that are widely used in scientific research. They were first developed by researchers H.H. Sprague and R.C. Dawley in the early 20th century, and have since become one of the most commonly used rat strains in biomedical research due to their relatively large size, ease of handling, and consistent genetic background.

Sprague-Dawley rats are outbred, which means that they are genetically diverse and do not suffer from the same limitations as inbred strains, which can have reduced fertility and increased susceptibility to certain diseases. They are also characterized by their docile nature and low levels of aggression, making them easier to handle and study than some other rat strains.

These rats are used in a wide variety of research areas, including toxicology, pharmacology, nutrition, cancer, and behavioral studies. Because they are genetically diverse, Sprague-Dawley rats can be used to model a range of human diseases and conditions, making them an important tool in the development of new drugs and therapies.

Hypoxia-Inducible Factor 1 (HIF-1) is a transcription factor that plays a crucial role in the body's response to low oxygen levels, also known as hypoxia. HIF-1 is a heterodimeric protein composed of two subunits: an alpha subunit (HIF-1α) and a beta subunit (HIF-1β).

The alpha subunit, HIF-1α, is the regulatory subunit that is subject to oxygen-dependent degradation. Under normal oxygen conditions (normoxia), HIF-1α is constantly produced in the cell but is rapidly degraded by proteasomes due to hydroxylation of specific proline residues by prolyl hydroxylase domain-containing proteins (PHDs). This hydroxylation reaction requires oxygen as a substrate, and under hypoxic conditions, the activity of PHDs is inhibited, leading to the stabilization and accumulation of HIF-1α.

Once stabilized, HIF-1α translocates to the nucleus, where it heterodimerizes with HIF-1β and binds to hypoxia-responsive elements (HREs) in the promoter regions of target genes. This binding results in the activation of gene transcription programs that promote cellular adaptation to low oxygen levels. These adaptive responses include increased erythropoiesis, angiogenesis, glucose metabolism, and pH regulation, among others.

Therefore, HIF-1α is a critical regulator of the body's response to hypoxia, and its dysregulation has been implicated in various pathological conditions, including cancer, cardiovascular disease, and neurodegenerative disorders.

Nicotinic antagonists are a class of drugs that block the action of nicotine at nicotinic acetylcholine receptors (nAChRs). These receptors are found in the nervous system and are activated by the neurotransmitter acetylcholine, as well as by nicotine. When nicotine binds to these receptors, it can cause the release of various neurotransmitters, including dopamine, which can lead to rewarding effects and addiction.

Nicotinic antagonists work by binding to nAChRs and preventing nicotine from activating them. This can help to reduce the rewarding effects of nicotine and may be useful in treating nicotine addiction. Examples of nicotinic antagonists include mecamylamine, varenicline, and cytisine.

It's important to note that while nicotinic antagonists can help with nicotine addiction, they can also have side effects, such as nausea, vomiting, and abnormal dreams. Additionally, some people may experience more serious side effects, such as seizures or cardiovascular problems, so it's important to use these medications under the close supervision of a healthcare provider.

Muscarinic antagonists, also known as muscarinic receptor antagonists or parasympatholytics, are a class of drugs that block the action of acetylcholine at muscarinic receptors. Acetylcholine is a neurotransmitter that plays an important role in the parasympathetic nervous system, which helps to regulate various bodily functions such as heart rate, digestion, and respiration.

Muscarinic antagonists work by binding to muscarinic receptors, which are found in various organs throughout the body, including the eyes, lungs, heart, and gastrointestinal tract. By blocking the action of acetylcholine at these receptors, muscarinic antagonists can produce a range of effects depending on the specific receptor subtype that is affected.

For example, muscarinic antagonists may be used to treat conditions such as chronic obstructive pulmonary disease (COPD) and asthma by relaxing the smooth muscle in the airways and reducing bronchoconstriction. They may also be used to treat conditions such as urinary incontinence or overactive bladder by reducing bladder contractions.

Some common muscarinic antagonists include atropine, scopolamine, ipratropium, and tiotropium. It's important to note that these drugs can have significant side effects, including dry mouth, blurred vision, constipation, and confusion, especially when used in high doses or for prolonged periods of time.

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).

GABA (gamma-aminobutyric acid) antagonists are substances that block the action of GABA, which is the primary inhibitory neurotransmitter in the central nervous system. GABA plays a crucial role in regulating neuronal excitability and reducing the transmission of nerve impulses.

GABA antagonists work by binding to the GABA receptors without activating them, thereby preventing the normal function of GABA and increasing neuronal activity. These agents can cause excitation of the nervous system, leading to various effects depending on the specific type of GABA receptor they target.

GABA antagonists are used in medical treatments for certain conditions, such as sleep disorders, depression, and cognitive enhancement. However, they can also have adverse effects, including anxiety, agitation, seizures, and even neurotoxicity at high doses. Examples of GABA antagonists include picrotoxin, bicuculline, and flumazenil.

The alpha7 nicotinic acetylcholine receptor (α7nAChR) is a type of cholinergic receptor found in the nervous system that is activated by the neurotransmitter acetylcholine. It is a ligand-gated ion channel that is widely distributed throughout the central and peripheral nervous systems, including in the hippocampus, cortex, thalamus, and autonomic ganglia.

The α7nAChR is composed of five subunits arranged around a central pore, and it has a high permeability to calcium ions (Ca2+). When acetylcholine binds to the receptor, it triggers a conformational change that opens the ion channel, allowing Ca2+ to flow into the cell. This influx of Ca2+ can activate various intracellular signaling pathways and have excitatory or inhibitory effects on neuronal activity, depending on the location and function of the receptor.

The α7nAChR has been implicated in a variety of physiological processes, including learning and memory, attention, sensory perception, and motor control. It has also been studied as a potential therapeutic target for various neurological and psychiatric disorders, such as Alzheimer's disease, schizophrenia, and pain.

Histamine H1 antagonists, also known as H1 blockers or antihistamines, are a class of medications that work by blocking the action of histamine at the H1 receptor. Histamine is a chemical mediator released by mast cells and basophils in response to an allergic reaction or injury. It causes various symptoms such as itching, sneezing, runny nose, and wheal and flare reactions (hives).

H1 antagonists prevent the binding of histamine to its receptor, thereby alleviating these symptoms. They are commonly used to treat allergic conditions such as hay fever, hives, and eczema, as well as motion sickness and insomnia. Examples of H1 antagonists include diphenhydramine (Benadryl), loratadine (Claritin), cetirizine (Zyrtec), and doxylamine (Unisom).

Purinergic P1 receptor antagonists are a class of pharmaceutical drugs that block the activity of purinergic P1 receptors, which are a type of G-protein coupled receptor found in many tissues throughout the body. These receptors are activated by extracellular nucleotides such as adenosine and ATP, and play important roles in regulating a variety of physiological processes, including cardiovascular function, neurotransmission, and immune response.

Purinergic P1 receptor antagonists work by binding to these receptors and preventing them from being activated by nucleotides. This can have various therapeutic effects, depending on the specific receptor subtype that is targeted. For example, A1 receptor antagonists have been shown to improve cardiac function in heart failure, while A2A receptor antagonists have potential as anti-inflammatory and neuroprotective agents.

However, it's important to note that the use of purinergic P1 receptor antagonists is still an area of active research, and more studies are needed to fully understand their mechanisms of action and therapeutic potential.

Piperidines are not a medical term per se, but they are a class of organic compounds that have important applications in the pharmaceutical industry. Medically relevant piperidines include various drugs such as some antihistamines, antidepressants, and muscle relaxants.

A piperidine is a heterocyclic amine with a six-membered ring containing five carbon atoms and one nitrogen atom. The structure can be described as a cyclic secondary amine. Piperidines are found in some natural alkaloids, such as those derived from the pepper plant (Piper nigrum), which gives piperidines their name.

In a medical context, it is more common to encounter specific drugs that belong to the class of piperidines rather than the term itself.

Alpha-1 adrenergic receptors (also known as α1-adrenoreceptors) are a type of G protein-coupled receptor that binds catecholamines, such as norepinephrine and epinephrine. These receptors are primarily found in the smooth muscle of various organs, including the vasculature, heart, liver, kidneys, gastrointestinal tract, and genitourinary system.

When an alpha-1 adrenergic receptor is activated by a catecholamine, it triggers a signaling cascade that leads to the activation of phospholipase C, which in turn activates protein kinase C and increases intracellular calcium levels. This ultimately results in smooth muscle contraction, increased heart rate and force of contraction, and vasoconstriction.

Alpha-1 adrenergic receptors are also found in the central nervous system, where they play a role in regulating wakefulness, attention, and anxiety. There are three subtypes of alpha-1 adrenergic receptors (α1A, α1B, and α1D), each with distinct physiological roles and pharmacological properties.

In summary, alpha-1 adrenergic receptors are a type of G protein-coupled receptor that binds catecholamines and mediates various physiological responses, including smooth muscle contraction, increased heart rate and force of contraction, vasoconstriction, and regulation of wakefulness and anxiety.

Adrenergic alpha-2 receptor antagonists are a class of medications that block the action of norepinephrine, a neurotransmitter and hormone, at adrenergic alpha-2 receptors. These receptors are found in the central and peripheral nervous system and play a role in regulating various physiological functions such as blood pressure, heart rate, and insulin secretion.

By blocking the action of norepinephrine at these receptors, adrenergic alpha-2 receptor antagonists can increase sympathetic nervous system activity, leading to vasodilation, increased heart rate, and increased insulin secretion. These effects make them useful in the treatment of conditions such as hypotension (low blood pressure), opioid-induced sedation and respiratory depression, and diagnostic procedures that require vasodilation.

Examples of adrenergic alpha-2 receptor antagonists include yohimbine, idazoxan, and atipamezole. It's important to note that these medications can have significant side effects, including hypertension, tachycardia, and agitation, and should be used under the close supervision of a healthcare provider.

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... a novel alpha-adrenergic antagonist". Biopharmaceutics & Drug Disposition. 10 (6): 581-9. doi:10.1002/bdd.2510100607. PMID ... Metazosin is an antihypertensive α1-adrenergic receptor antagonist. Trcka, V; König, J; Mácová, S; Smíd, M; Helfert, I; ... Alpha-1 blockers, All stub articles, Antihypertensive agent stubs). ...
Earl CQ, Prozialeck WC, Weiss B.: Interaction of alpha adrenergic antagonists with calmodulin. Life Sci. 1984 Jul 30;35(5):525- ... alpha adrenergic antagonists [23]and phenothiazineantipsychotic drugs were potent inhibitors of calmodulin activated enzymes [ ... in that older animals evidence a decrease in beta-adrenergic receptors and a reduced response to adrenergic stimuli [34,35,36 ... Greenberg, L.H. and Weiss, B.: Beta adrenergic receptors in aged rat brain: reduced number and capacity of pineal gland to ...
Systemic Alpha-1 adrenergic receptor antagonists have been implicated in Intraoperative Floppy Iris Syndrome (IFIS). Bunazosin ... Bunazosin (INN) is an α1-adrenergic receptor antagonist. Bunazosin was initially developed to treat benign prostatic ... Alpha blockers, Carboxamides, Catechol ethers, Diazepanes, Quinazolines, All stub articles, Antihypertensive agent stubs). ...
Conversely, coadministration of NMDA-antagonists with alpha-2 adrenergic antagonists, like yohimbine, could theoretically ... Drugs that work to suppress NAT include anticholinergics, benzodiazepines, barbiturates and Alpha-adrenergic agonists, such as ... NMDA receptor antagonists include physician-prescribed drugs for therapeutic treatment of human diseases such as memantine for ... Auer RN (1996). "Effect of age and sex on N-methyl-D-aspartate antagonist-induced neuronal necrosis in rats". Stroke. 27 (4): ...
... a specific antagonist radioligand for brain alpha 2-adrenergic receptors". European Journal of Pharmacology. 76 (4): 461-4. doi ... Alpha-2 blockers, 5-HT1A agonists, 5-HT2A antagonists, 5-HT2B antagonists, Methyl esters, Heterocyclic compounds with 5 rings) ... Rauwolscine acts predominantly as a α2-adrenergic receptor antagonist. It has also been shown to function as a 5-HT1A receptor ... Wainscott DB, Sasso DA, Kursar JD, Baez M, Lucaites VL, Nelson DL (January 1998). "[3H]Rauwolscine: an antagonist radioligand ...
... s (also called alpha-adrenergic blocking agents or alpha-1 antagonists) constitute a variety of drugs that block ... a variety of drugs have been developed from non-selective alpha-1 antagonists to selective alpha-1 antagonists and alpha-1 ... Wikimedia Commons has media related to Alpha-1 blockers. DrugDigest - Alpha blockers RxList.com - Tamsulosin alpha-Adrenergic+ ... Prazosin has been established as an effective and safe centrally active alpha-1 adrenergic receptor antagonist. It can be used ...
4. Synthesis and pharmacological activity of chiral 2-alkylaminomethylbenzodioxans, competitive .alpha.-adrenergic antagonists ... Formerly investigated by Fourneau as an α-adrenergic-blocking agent, they demonstrated that it also antagonized histamine- ... Alpha blockers, Antihistamines, Benzodioxans, French inventions, 1-Piperidinyl compounds). ...
... an alpha-1 adrenergic antagonist, has been used in veterans with PTSD to reduce nightmares. Studies show variability in the ... adrenergic inhibitors, antipsychotics, and even anticonvulsants), benzodiazepines should be considered relatively ...
Adrenergic competitive antagonists are shorter lasting than the other two types of antagonists. While the antagonists for alpha ... There are few non-cardiovascular uses for adrenergic antagonists. Alpha-adrenergic antagonists are also used for treatment of ... The α-adrenergic antagonists have different effects from the β-adrenergic antagonists. Adrenergic ligands are endogenous ... While only a few α-adrenergic antagonists are competitive, all β-adrenergic antagonists are competitive antagonists. ...
Yang G, Wei Q, Li H, Yang Y, Zhang S, Dong Q (2006). "The effect of alpha-adrenergic antagonists in chronic prostatitis/chronic ...
"The effect of alpha 1-acid glycoprotein on the pharmacological activity of alpha 1-adrenergic antagonists in rabbit aortic ... Tiodazosin is an α1-adrenergic receptor antagonist. Terazosin Chiang, J; Hermodsson, G; Oie, S (1991). " ... Alpha-1 blockers, Quinazolines, Oxadiazoles, Thioethers, All stub articles, Pharmacology stubs). ...
An alpha-adrenergic antagonist with equal affinity for α1 and α2 receptors, monotherapy with phentolamine has been ... Phentolamine is an alpha blocker that relaxes blood vessel muscles, allowing more blood to flow to the penis. While the active ...
"Effect of methoxy substitution on the adrenergic activity of three structurally related alpha 2-adrenoreceptor antagonists". ... It acts as an α2-adrenergic receptor antagonist similarly to other imidazoles like idazoxan. It was never marketed. ... Fenmetozole (DH-524) is a drug which was patented as an antidepressant, but was later studied as an antagonist of the effects ...
... relationships between alpha-adrenergic activity and binding affinity of alpha-adrenoceptor agonists and antagonists". Journal ... Alpha-1 adrenergic receptor agonists, Alpha-2 adrenergic receptor agonists, Antihypertensive agents, Chloroarenes, Imidazolines ... It is a centrally-acting α2 adrenergic receptor agonist (IC50 = 9.1 nM). It also acts as an α1-adrenergic receptor agonist to a ... Roden DM, Nadeau JH, Primm RK (June 1988). "Electrophysiologic and hemodynamic effects of chronic oral therapy with the alpha 2 ...
They are primarily postsynaptic adrenergic receptor antagonists (alpha and beta adrenergic receptor antagonists, or "blockers ... ICI-118,551 Highly selective β2-adrenergic receptor antagonist - No known clinical applications, but used in experiments due to ... α1 antagonist) Doxazosin (alpha blocker) Beta blockers Non-selective agents Alprenolol Bucindolol Carteolol Carvedilol (has ... preventing postsynaptic adrenergic receptor activation and downstream signaling. Another way to inhibit adrenergic receptor ...
... related to ketanserin such as ritanserin are more selective 5-HT2A receptor antagonists with low affinity for alpha-adrenergic ... Another antagonist is cyproheptadine. Pizotifen is a non-selective antagonist. LY-367,265 - dual 5-HT2A antagonist / SSRI with ... Trazodone is a potent 5-HT2A antagonist, as well as an antagonist on other serotonin receptors. Brexpiprazole an atypical ... However, there is at least one antagonist at this site which has been shown to up-regulate 5-HT2A receptors. Additionally, a ...
... is an α1-adrenergic receptor antagonist. Alpha blocker Tham TC, Guy S, Shanks RG, Harron DW (April 1992). "Dose-dependent alpha ... Alpha-1 blockers, Quinolines, Norsalsolinol ethers, All stub articles, Antihypertensive agent stubs, Genito-urinary system drug ... 1-adrenoceptor antagonist activity of the anti-arrhythmic drug, abanoquil (UK-52,046), without reduction in blood pressure in ...
... beta-adrenergic antagonists, alpha-adrenergic agonists, and carbonic anhydrase inhibitors etc. The UGH Syndrome was originally ...
... alpha-adrenergic agonist, alpha 1 antagonists). Urinary symptoms may include frequency, urgency, incontinence or recurrent ... Alpha blockers can also reduce outlet resistance and allow complete emptying if there is adequate bladder muscle function. ...
... needle ablation of the prostate as an alternative to transurethral resection of the prostate when alpha-adrenergic antagonist ...
Antagonists L-765,314 Risperidone Brexpiprazole Alpha-1B adrenergic receptor has been shown to interact with AP2M1. A role in ... 1994). "Cloning, expression and characterization of human alpha adrenergic receptors alpha 1a, alpha 1b and alpha 1c". Biochem ... The alpha-1B adrenergic receptor (α1B-adrenoreceptor), also known as ADRA1B, is an alpha-1 adrenergic receptor, and also ... There are 3 alpha-1 adrenergic receptor subtypes: alpha-1A, -1B and -1D, all of which signal through the Gq/11 family of G- ...
5-HT1A antagonists, Alpha-2 adrenergic receptor agonists, Phytocannabinoids, CB1 receptor antagonists, Resorcinols, Terpeno- ... It appears to be unique among cannabinoid compounds by also having high affinity and activity at alpha-2 adrenergic receptors ... the activity of cannabigerol at alpha-2 adrenergic receptors in vitro raises concerns about its safety for human consumption, ... plant cannabinoid cannabigerol is a highly potent alpha2-adrenoceptor agonist and moderately potent 5HT1A receptor antagonist ...
... relationships between alpha-adrenergic activity and binding affinity of alpha-adrenoceptor agonists and antagonists". Journal ... Adrenergic receptor Graham RM, Perez DM, Hwa J, Piascik MT (May 1996). "alpha 1-adrenergic receptor subtypes. Molecular ... "Renal alpha-1 and alpha-2 adrenergic receptors: biochemical and pharmacological correlations". The Journal of Pharmacology and ... alpha-1 (α1) adrenergic receptors are G protein-coupled receptors (GPCRs) associated with the Gq heterotrimeric G protein. α1- ...
... is a drug used in benign prostatic hypertrophy which acts as a selective α1-adrenergic receptor antagonist or alpha-1 blocker. ... Alpha-1 blockers, Antihypertensive agents, Calcium channel blockers, N-(2-methoxyphenyl)piperazines, Naphthol ethers, ...
... a cholinergic and alpha-1 adrenergic antagonist, to achieve a shorter recovery time. Treatment with a combination of different ... Competitive antagonists of AChE can be used for pre-treatment. They can reduce mortality, which is caused by exposure to AzM. ... These two treatments are also used together, some patients are namely treated with atropine (a competitive antagonist of AChE) ...
"Alpha 1 Adrenergic Receptor Antagonists", LiverTox: Clinical and Research Information on Drug-Induced Liver Injury, Bethesda ( ... Adrenergic neurone blockers, commonly known as adrenergic antagonists, are a group of drugs that inhibit the sympathetic ... When non-selective alpha blockers are used, norepinephrine cannot bind to alpha 1 or alpha 2 receptors. As a result, activation ... Alpha 2 blockers Alpha 2 blockers inhibit the activation of adenylyl cyclase via Gi protein by antagonising alpha 2 receptors, ...
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There are no studies to date confirming if aripiprazole function as an agonist or antagonist at alpha-adrenergic receptors such ... 5-HT2A antagonists, 5-HT2B antagonists, 5-HT2C agonists, 5-HT7 antagonists, Alpha-1 blockers, Alpha-2 blockers, Atypical ... but the orthostatic hypotension observed with aripiprazole may be explained by its antagonist activity at adrenergic α1A ... D3 antagonists, D3 receptor agonists, Ethers, H1 receptor antagonists, Mood stabilizers, Otsuka Pharmaceutical, Serotonin- ...
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Alpha-2 Adrenergic Agonists. Class Summary. Agents in this class may decrease vasomotor tone and heart rate by stimulating ... Alpha-1 Receptor Antagonists. Class Summary. Novel pilot studies in combat veterans suggest alpha-1 antagonists have efficacy ... Prazosin is an alpha-1 adrenergic blocker that is indicated for hypertension. Studies indicate that a nighttime dose of ... Clonidine is a central alpha-adrenergic agonist that is commonly used as an antihypertensive agent. It stimulates alpha2- ...
Alpha-2 Adrenergic Agonists. Class Summary. Agents in this class may decrease vasomotor tone and heart rate by stimulating ... Alpha-1 Receptor Antagonists. Class Summary. Novel pilot studies in combat veterans suggest alpha-1 antagonists have efficacy ... Prazosin is an alpha-1 adrenergic blocker that is indicated for hypertension. Studies indicate that a nighttime dose of ... Clonidine is a central alpha-adrenergic agonist that is commonly used as an antihypertensive agent. It stimulates alpha2- ...
In previous studies we investigated the role of beta- and alpha 2-adrenergic receptors through local microinjections of various ... In this study we examined the role of alpha 1-adrenergic receptors. The alpha 1-agonist methoxamine and the alpha 1-antagonist ... Modulation of desynchronized sleep through microinjection of alpha 1-adrenergic agonists and antagonists in the dorsal pontine ... In previous studies we investigated the role of beta- and alpha 2-adrenergic receptors through local microinjections of various ...
Barsuhn C Evidence for a Central Sympathoexcitatory Action of Alpha-2 Adrenergic Antagonists The Journal Of Pharmacolocy And ... "Evidence for a Central Sympathoexcitatory Action of Alpha-2 Adrenergic Antagonists". The Journal Of Pharmacolocy And ... The effect of alpha-2 adrenergic receptor antagonists on sympathetic nerve discharge (SND) recorded from the external carotid ... "Evidence for a Central Sympathoexcitatory Action of Alpha-2 Adrenergic Antagonists" The Journal Of Pharmacolocy And ...
Alpha-1 Adrenergic Receptor Antagonists for Preventing Acute Respiratory Distress Syndrome and Death from Cytokine Storm ... Faculty & Research Working Papers Alpha-1 Adrenergic Receptor Antagonists for Preventing Acute Respiratory Distress Syndrome ... We previously demonstrated that alpha-1 adrenergic receptor (α1-AR) antagonists can prevent cytokine storm syndrome in mice. ... These results highlight the urgent need for prospective trials testing whether prophylactic use of α1-AR antagonists ...
Alpha-adrenergic agonists. Class Summary. These agents stimulate alpha-adrenoreceptors in brain stem, activating an inhibitory ... A central alpha-adrenergic agonist that suppresses peripheral release of norepinephrine, resulting in lower blood pressure; ... A pure peripheral alpha-adrenergic agonist, which causes peripheral vasoconstriction and raises blood pressure without ... H2 receptor antagonists. Class Summary. These agents are reversible competitive blockers of histamine at the H2 receptors, ...
Physiological Effects of Drugs - Adrenergic alpha-Antagonists PubMed MeSh Term *Overview. Overview. subject area of * Blockade ... Adrenergic Antagonists PubMed MeSh Term narrower concept * Physiological Effects of Drugs - Adrenergic alpha-1 Receptor ... Catecholamine responses to alpha-adrenergic blockade during exercise in women acutely exposed to altitude Journal Article ... Influence of alpha-adrenergic blockade on the catecholamine response to exercise at 4,300 meters Journal Article ...
Keywords: Adrenergic alpha-antagonists; Cholinergic antagonists; Ureteral diseases; Urinary catheterization. Publication types ...
It acts as an alpha-1 adrenergic receptor antagonist. The most common side effect is a reduction in the amount of semen ... Alpha-1 adrenergic receptor antagonists are being investigated as a means to male birth control due to their ability to inhibit ... although combination with other α1-antagonists is not well studied. Silodosin, is an alpha-adrenoreceptor antagonist. It works ... Intra operative floppy iris syndrome occurs in some people taking alpha adrenoreceptor antagonists and may lead to ...
Doxazosin tablets are an alpha 1 adrenergic antagonist indicated for: (1). *Signs and symptoms of Benign Prostatic Hyperplasia ... Doxazosin mesylate is a quinazoline compound that is a selective inhibitor of the alpha 1 subtype of alpha-adrenergic receptors ... Like other alpha 1-adrenergic blocking agents, doxazosin has a greater effect on blood pressure and heart rate in the standing ... The mechanism of action of doxazosin is selective blockade of the alpha 1 (postjunctional) subtype of adrenergic receptors. ...
Doxazosin tablets, USP are alpha 1 adrenergic antagonist indicated for: *Signs and symptoms of Benign Prostatic Hyperplasia ( ... Doxazosin mesylate is a quinazoline compound that is a selective inhibitor of the alpha 1 subtype of alpha-adrenergic receptors ... Like other alpha 1-adrenergic blocking agents, doxazosin has a greater effect on blood pressure and heart rate in the standing ... Alpha 1 antagonists, including doxazosin, have been associated with priapism (painful penile erection, sustained for hours and ...
Researchers tested the capacity of adrenergic antagonists, drugs such as alpha and beta blockers, to disrupt the receptors ... "This receptor is found in many pathogens, so we can use this knowledge to design specific antagonists to block bacterial ... an alpha blocker drug used to treat hypertension, to successfully impede signaling to the receptor. Without such signals, ... processes between microbes and humans and to the development of novel treatments of bacterial infections with antagonists to ...
Determination of Subtype Selectivity of Alpha-Adrenergic Antagonists THOMAS N. LAVIN, BRIAN B. HOFFMAN and ROBERT J. LEFKOWITZ ... Regulation of Myometrial Adrenoreceptors and Adrenergic Response by Sex Steroids JAMES M. ROBERTS, PAUL A. INSEL and ALAN ...
Add Selective Alpha Adrenergic Antagonist (e.g. Tamsulosin, Alfuzosin). *Antibiotics: First-Line (caution regarding prolonged ...
Alpha-1 Blockers(Alpha-1 Antagonists, Alpha-Adrenergic Blocking Agents) (Doxazosin, Prazosin, Terazosin) ... Peripheral Adrenergic Inhibitor (Peripheral-Acting Adrenergic Antagonist) ( Reserpine). *This drug relaxes blood vessels and ... Alpha-2 Agonists (Nervous System Inhibitors) ( Guanabenz, Clonidine, Methyldopa). *These drugs relax and widen blood vessels, ...
Selective antagonists of alpha-1 adrenergic receptors:. *. terazosin (Hytrin). *. doxazosin (Cardura). *. terazosin (Hytrin) ... Adrenergic nerve blocker/blockers that act by replacing norepinephrine (Levophed) by an inactive transmitter:. *. reserpine ( ...
Nonselective alpha-1 and alpha-2 adrenergic antagonist. Reversibly binds to alpha-1 adrenergic receptors on the iris dilator ... Phentolamine directly antagonizes mydriatic effect of an alpha-1 adrenergic agonist, and indirectly reverses mydriasis induced ... Indicated for treatment of pharmacologically-induced mydriasis produced by adrenergic agonists (eg, phenylephrine) or ... Indicated for treatment of pharmacologically-induced mydriasis produced by adrenergic agonists (eg, phenylephrine) or ...
Caution should also be exercised in patients receiving alpha adrenergic receptor antagonists such as in the treatment of ... Alpha-adrenergic agonists, as a class, may impact blood pressure. Caution in using drugs such as betablockers, anti- ... Alpha-adrenergic agonists as a class may impact blood pressure. Advise UPNEEQ patients with cardiovascular disease, orthostatic ...
The FDA considers the risk for IFIS to be a class effect for alpha-1 adrenergic receptor antagonists [8,9]. The prevalence of ... alpha1-adrenergic antagonists and floppy iris syndrome: tip of the iceberg? Ophthalmology. 2005 Dec;112(12):2059-60. PubMed - ... alpha1-adrenergic receptor antagonists and the iris: new mechanistic insights into floppy iris syndrome. Surv Ophthalmol. 2006 ... Alpha-receptor antagonist medications potentially interfere with iris muscle dilation, resulting in difficult lens removal and ...
... alpha-adrenergic blockers and angiotensin II receptor antagonists. Supplemental drugs could be used as combination therapy or ... and no trials evaluated ACE inhibitors or alpha-adrenergic blockers. It is important in this type of analysis not to include ... Review: calcium antagonists lead to a higher risk for myocardial infarction, congestive heart failure, and major cardiovascular ... A 12-month comparison of ACE inhibitor and CA antagonist therapy in mild to moderate essential hypertension - the GLANT Study. ...
Yohimbine is an alpha-2 adrenergic antagonist, and has been used in a variety of research projects. It is a veterinary drug ...
Certain drugs such as corticosteroids, beta-adrenergic agonists (eg, isoproterenol), alpha-adrenergic antagonists (eg, ...
Prostatic hyperplasia, pharmacological treatment, adrenergic alpha-Antagonists Abstract. Benign Prostatic Hyperplasia (BPH) ... Does previous treatment with 5-alpha reductase inhibitors have an impact on prostatic enucleation with holmium laser? Results ...
RAPAFLO, an alpha-1 adrenergic receptor antagonist, is indicated for the treatment of the signs and symptoms of benign ... An in vitro study examining binding affinity of silodosin to the three subtypes of the alpha-1 adrenoreceptors (alpha-1A, alpha ... RAPAFLO is the brand name for silodosin, a selective antagonist of alpha-1 adrenoreceptors. The chemical name of silodosin is 1 ... Silodosin is a selective antagonist of post-synaptic alpha-1 adrenoreceptors, which are located in the human prostate, bladder ...
Alpha-adrenergic antagonists. * Alternative medicine. * Analgesics. * Antibiotics. * Anticoagulants. * Antiepileptic drugs. * ...
These results suggest that CEC acts on two different subtypes of prejunctional alpha-2 autoreceptors; on one of them it acts as ... an antagonist and increases the electrically evoked overflow of tritium (and inhibits both the effect of UK-14,304 and ... Alternatively, one can admit that CEC is able to inhibit alpha-2 autoreceptors, which causes an increase of the transmitter ... on prejunctional alpha-2 autoreceptors of the canine saphenous vein. The effect was tested on tritium overflow evoked by ...
Affinity DataKi: 1.90nMAssay Description:Antagonist activity at human recombinant adrenergic Alpha-2C receptor expressed in CHO ... TargetAlpha-2C adrenergic receptor(Homo sapiens (Human)). Pfizer Inc. Curated by ChEMBL. ... TargetAlpha-2C adrenergic receptor(Homo sapiens (Human)). Pfizer Inc. Curated by ChEMBL. ... TargetAlpha-2B adrenergic receptor(Homo sapiens (Human)). Pfizer Inc. Curated by ChEMBL. ...
Iris morphologic changes related to alpha(1)-adrenergic receptor antagonists implications for intraoperative floppy iris ... The cause of IFIS has been identified as the intake of systemic alpha-adrenoceptor antagonists (alpha-blockers), drugs ... Handzel DM, Briesen S, Rausch S, Kälble T. Cataract surgery in patients taking alpha-1 antagonists: know the risks, avoid the ... Santaella RM, Destafeno JJ, Stinnett SS, Proia AD, Chang DF, Kim T. The effect of alpha1-adrenergic receptor antagonist ...
Urimax is an antagonist.Used for treatment of treating prostatic hyperplasia (benign) as it helps relieve symptoms, such as ... No, Urimax is an alpha-adrenergic antagonist used to treat benign prostatic hyperplasia. Tamsulosin hydrochloride is the active ... In the human prostate, tamsulosin hydrochloride, a selective alpha 1A-adrenoceptor blocking drug, shows selectivity for alpha ... Tamsulosin hydrochloride, a selective alpha 1A-adrenoceptor blocking drug, shows selectivity for alpha 1A-receptors. ...
... an alpha-adrenergic antagonist (1 microM), reduced sympathetic constriction in controls, but abolished this response in TiO2 ... The enhanced sensitivity to alpha-adrenergic receptor blockade following TiO2 exposure suggests an augmented responsiveness to ... Nanoparticle inhalation modulates arteriolar sympathetic constriction: role of nitric oxide, prostanoids, and alpha-adrenergic ...
  • Another source names recurring urinary retention, recurring urinary infections, uncontrolled macrohematuria, bladder stones, hydronephrosis, combination with other α1-antagonists or dopamine agonists, and severe renal or hepatic impairment as contraindications. (wikipedia.org)
  • Centrally-acting sympatholytic agent/agents (alpha2 adrenergic receptor agonists). (pharmacology2000.com)
  • Now a team of investigators [ 1 ] from the University of Adelaide, Australia, has undertaken a systematic review of 27 studies involving 3048 participants to assess the effects of buprenorphine versus tapered doses of methadone , alpha-2-adrenergic agonists, symptomatic medications or placebo, or different buprenorphine regimens for managing opioid withdrawal. (medscape.com)
  • In previous studies we investigated the role of beta- and alpha 2-adrenergic receptors through local microinjections of various drugs into the dorsal pontine tegmentum (DPT) of the cat. (nih.gov)
  • In this study we examined the role of alpha 1-adrenergic receptors. (nih.gov)
  • The H2 antagonists are highly selective, do not affect the H1 receptors, and are not anticholinergic agents. (medscape.com)
  • Looking at pharmacologic and pathophysiologic principles, two paths are responsible for IFIS: (1) The direct effect of alpha-blockers on iris receptors reduces the power of dilating agents and (2) ultrastructural changes lead to irreversible functional loss in the smooth muscle tissue of the iris and to chronic loss of muscular tension, with or without the presence of dilating drugs. (crstodayeurope.com)
  • In the human prostate, tamsulosin hydrochloride, a selective alpha 1A-adrenoceptor blocking drug, shows selectivity for alpha 1A-receptors. (yashodahospitals.com)
  • Nanoparticle inhalation modulates arteriolar sympathetic constriction: role of nitric oxide, prostanoids, and alpha-adrenergic receptors. (cdc.gov)
  • It belongs to the class of alpha-2 adrenergic receptor antagonists , influencing the sympathetic nervous system's activity by blocking specific receptors. (enhancedlabs.com)
  • Alpha yohimbine's primary mechanism of action centers on its interaction with alpha-2 adrenergic receptors. (enhancedlabs.com)
  • By antagonizing these receptors, alpha yohimbine potentially increases norepinephrine release, leading to heightened alertness, improved mood, and enhanced fat mobilization. (enhancedlabs.com)
  • While alpha yohimbine's influence on the alpha-2 adrenergic receptors can lead to various desirable effects, it can also trigger unwanted side effects. (enhancedlabs.com)
  • 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. (citizendium.org)
  • Drugs that act on adrenergic receptors or affect the life cycle of adrenergic transmitters. (citizendium.org)
  • These data indicate that low doses of the alpha-2 receptor antagonist piperoxane and rauwolscine act centrally to increase SND. (erowid.org)
  • It acts as an alpha-1 adrenergic receptor antagonist. (wikipedia.org)
  • Alpha-receptor antagonist medications potentially interfere with iris muscle dilation, resulting in difficult lens removal and possibly increasing complications. (urotoday.com)
  • RAPAFLO, an alpha-1 adrenergic receptor antagonist, is indicated for the treatment of the signs and symptoms of benign prostatic hyperplasia (BPH). (globalrph.com)
  • A serotonin 5-HT3 receptor antagonist used to prevent nausea and vomiting in cancer chemotherapy and postoperatively. (drugbank.com)
  • A 5HT-3 receptor antagonist used as an antiemetic in the treatment of chemotherapy-induced nausea and vomiting. (drugbank.com)
  • RAPAFLO is the brand name for silodosin, a selective antagonist of alpha-1 adrenoreceptors. (globalrph.com)
  • Silodosin is a selective antagonist of post-synaptic alpha-1 adrenoreceptors, which are located in the human prostate, bladder base, bladder neck, prostatic capsule, and prostatic urethra. (globalrph.com)
  • One week later, animals were spinally pretreated with receptor antagonists selective for opioid, serotonin or alpha-adrenoceptors, and the ability of these agents to alter spinal morphine-induced antinociception was assessed. (omeka.net)
  • A non selective beta-adrenergic antagonist used to treat mild to severe chronic heart failure, hypertension, and left ventricular dysfunction following myocardial infarction in clinically stable patients. (drugbank.com)
  • The alpha 1-agonist methoxamine and the alpha 1-antagonist prazosin were injected into the DPT of freely moving, unanaesthetized cats. (nih.gov)
  • The mechanism of its therapeutic actions is not clear, but it can act as an alpha-adrenergic antagonist and a dopamine agonist. (umassmed.edu)
  • Modulation of vestibulospinal reflexes through microinjection of an alpha 1-adrenergic antagonist in the dorsal pontine tegmentum of decerebrate cats. (architalbiol.org)
  • Researchers tested the capacity of adrenergic antagonists, drugs such as alpha and beta blockers, to disrupt the receptor's sensing ability. (sciencedaily.com)
  • The "intra-operative floppy iris syndrome" cataract surgery complication has been reported in men using alpha-blockers. (urotoday.com)
  • The risk of complicated cataract surgery was 14.9% in patients using alpha-blockers, approximately 50% higher than those not receiving this medication (9.5%) (p=0.003). (urotoday.com)
  • Four drug classes were evaluated in the trials: thiazides (21 trials), beta-adrenergic blockers (5), calcium-channel blockers (4) and angiotensin-converting-enzyme (ACE) inhibitors (1). (cmaj.ca)
  • RAPAFLO should not be used in combination with other alpha-blockers. (globalrph.com)
  • Alpha-blockers: Interactions involving concomitant use have not been determined. (globalrph.com)
  • Concomitant use of PDE5 inhibitors with alpha-blockers including Rapaflo can potentially cause symptomatic hypotension. (globalrph.com)
  • The cause of IFIS has been identified as the intake of systemic alpha-adrenoceptor antagonists (alpha-blockers), drugs prescribed in men for lower urinary tract syndromes such as benign prostatic hyperplasia. (crstodayeurope.com)
  • Include alpha-blockers in preoperative medical history. (crstodayeurope.com)
  • When general practitioners (GPs) conduct preoperative work-ups in patients taking alpha-blockers, in most cases their interest focuses on cardiovascular risks and patients' use of anticoagulants, as the connection between the intake of alpha-blockers and intraoperative cataract surgery complications is largely unknown to primary-care physicians. (crstodayeurope.com)
  • Although atropine is no longer in common use in ophthalmology because of its long duration of action, some surgeons prescribe topical use of this cycloplegic agent for 2 to 3 days prior to surgery for patients with known intake of alpha-blockers. (crstodayeurope.com)
  • α-adrenergic-antagonists (alpha blockers) are a type of drug called adrenergic antagonists. (informationautism.org)
  • Effects of 10 mg/kg 4-CMC alone or in combination with the alpha-adrenergic antagonist prazosin (Praz, 0.3 mg/kg, n = 5), the dopamine D1 antagonist SCH23390 [SCH, 0.1 mg/kg, n = 5 (except for SCH + 4CMC, n = 4)] and the ganglionic blocker chlorisondamine (chloro 1.0 mg/kg, n = 5) on BP, HR, and activity. (aspetjournals.org)
  • Blockade of these alpha-1 adrenoreceptors can cause smooth muscle in these tissues to relax, resulting in an improvement in urine flow and a reduction in BPH symptoms. (globalrph.com)
  • The enhanced sensitivity to alpha-adrenergic receptor blockade following TiO2 exposure suggests an augmented responsiveness to tonic sympathetic activity. (cdc.gov)
  • Caution is advised when alpha-adrenergic-antagonist-containing products, including JALYN®, are coadministered with PDE-5 inhibitors. (jalyn.com)
  • Alpha-adrenergic antagonists and PDE-5 inhibitors are both vasodilators that can lower blood pressure. (jalyn.com)
  • Propranolol is a nonselective beta-adrenergic receptor blocking agent. (medscape.com)
  • The effect of alpha-2 adrenergic receptor antagonists on sympathetic nerve discharge (SND) recorded from the external carotid and splanchnic nerves were studied in baroreceptor-denervated cats.Low i.v. doses of piperoxane end rauwolscine dramatically increased SND and produced a concomitant rise in mean arterial pressure and heart rate. (erowid.org)
  • These agents stimulate alpha-adrenoreceptors in brain stem, activating an inhibitory neuron, which in turn results in reduced sympathetic outflow. (medscape.com)
  • Phentolamine, an alpha-adrenergic antagonist (1 microM), reduced sympathetic constriction in controls, but abolished this response in TiO2 exposed rats (max % change -22.3+/-3.1 control, -9.7+/-2.9 TiO2). (cdc.gov)
  • In a study made available online this week and in an upcoming issue of the Proceedings of the National Academy of Sciences, researchers describe how they used phentolamine, an alpha blocker drug used to treat hypertension, to successfully impede signaling to the receptor. (sciencedaily.com)
  • In vitro binding experiments indicated that piperoxane and rauwolscine bound selectively to the alpha-2 adrenergic receptor and had little affinity for alpha-1 receptor sites. (erowid.org)
  • Silodosin has high affinity for the α1A adrenergic receptor in the prostate, the bladder, and the prostatic urethra. (wikipedia.org)
  • An in vitro study examining binding affinity of silodosin to the three subtypes of the alpha-1 adrenoreceptors (alpha-1A, alpha-1B, and alpha-1D) was conducted. (globalrph.com)
  • The results of the study demonstrated that silodosin binds with high affinity to the alpha-1A subtype. (globalrph.com)
  • citation needed] Alpha-1 adrenergic receptor antagonists are being investigated as a means to male birth control due to their ability to inhibit ejaculation but not orgasm. (wikipedia.org)
  • Alternatively, one can admit that CEC is able to inhibit alpha-2 autoreceptors, which causes an increase of the transmitter release, and to activate a nonadrenergic inhibitory receptor thus causing a reduction of the transmitter release. (unesp.br)
  • Urimax is an antagonist prescribed for treating prostatic hyperplasia (benign) as it helps relieve symptoms, such as urinary incontinence. (yashodahospitals.com)
  • No, Urimax is an alpha-adrenergic antagonist used to treat benign prostatic hyperplasia. (yashodahospitals.com)
  • Fual extended-release tablet, USP is an alpha adrenergic antagonist, indicated for the treatment of signs and symptoms of benign prostatic hyperplasia. (sdrugs.com)
  • Tamsulosin-containing products, including JALYN®, should not be coadministered with other alpha-adrenergic antagonists because of the increased risk of symptomatic hypotension. (jalyn.com)
  • Alpha-blocker medications are the first line of therapy for men with these urinary symptoms. (urotoday.com)
  • Alpha Yohimbine, also known as rauwolscine, is a compound derived from the bark of the Pausinystalia yohimbe tree. (enhancedlabs.com)
  • The Truth About Alpha Yohimbine! (enhancedlabs.com)
  • With its potential effects on weight loss and sexual health, alpha yohimbine has captured the interest of researchers and supplement enthusiasts alike. (enhancedlabs.com)
  • As an expert in the field, this article delves into the intricate details of alpha yohimbine supplements, including their mechanism of action, historical background, potential benefits, side effects, usage guidelines, and intriguing facts. (enhancedlabs.com)
  • Alpha yohimbine, scientifically termed yohimbine, is an alkaloid compound found in the bark of the Pausinystalia yohimbe tree, native to Central and West Africa. (enhancedlabs.com)
  • This makes alpha yohimbine a potentially more tolerable choice for those with pre-existing medical conditions or a predisposition to experiencing adverse reactions to stimulants. (enhancedlabs.com)
  • However, individual responses can vary, and consulting a healthcare professional is crucial when considering either alpha yohimbine or yohimbine HCl supplementation. (enhancedlabs.com)
  • Intra operative floppy iris syndrome occurs in some people taking alpha adrenoreceptor antagonists and may lead to complications during cataract surgery. (wikipedia.org)
  • To assess the frequency of cataract surgery complications arising from alpha-blocker therapy in a large patient population. (urotoday.com)
  • The purpose of this study was to assess the impact of alpha-blocker therapy on complications during cataract surgery in a large patient population. (urotoday.com)
  • This lack of information among GPs has been identified as the most salient risk factor for complications related to alpha-blocker intake, and, as a result, the number of published studies in urology, general, and family medicine journals describing IFIS outside the ophthalmic community has increased in recent years. (crstodayeurope.com)
  • If possible, alpha blocker medications should be discontinued prior to eye surgery in older patients. (urotoday.com)
  • As alpha-blocker medications are the first line of therapy for men with LUTS, these reports of IFIS led the Food and Drug Administration, American Urological Association, American Academy of Ophthalmology, and American Society of Cataract and Refractive Surgery to issue statements alerting physicians and patients to potential difficulties during cataract surgery in patients using alpha-1 blocker therapy [7,8,9]. (urotoday.com)
  • This knowledge opens the door to further understanding of the signaling processes between microbes and humans and to the development of novel treatments of bacterial infections with antagonists to these signals, Dr. Sperandio said. (sciencedaily.com)
  • Federated across two ARD cohorts, our main result shows that patients using α1-AR antagonists, as compared to nonusers, had a 40% relative risk reduction for ventilation and dying (p=0.014). (stanford.edu)
  • As with other alpha-adrenergic antagonists, orthostatic hypotension (postural hypotension, dizziness, and vertigo) may occur in patients treated with tamsulosin-containing products, including JALYN®, and can result in syncope. (jalyn.com)
  • Les variables comprenaient les données sociodémographiques, cliniques et thérapeutiques des patients pris en charge pour une urgence pénienne. (bvsalud.org)
  • Résultats : Durant cette période, 63 patients ont été pris en charge pour urgences péniennes. (bvsalud.org)
  • Injections of a beta-adrenergic antagonist in pontine reticular structures modify the gain of vestibulospinal reflexes in decerebrate cats. (architalbiol.org)
  • Injections of beta-adrenergic substances in the locus coeruleus affect the gain of vestibulospinal reflexes in decerebrate cats. (architalbiol.org)
  • These results highlight the urgent need for prospective trials testing whether prophylactic use of α1-AR antagonists ameliorates diseases associated with cytokine storm syndrome, such as COVID-19. (stanford.edu)
  • The FDA considers the risk for IFIS to be a class effect for alpha-1 adrenergic receptor antagonists [8,9]. (urotoday.com)
  • Silodosin, is an alpha-adrenoreceptor antagonist. (wikipedia.org)
  • The present study was undertaken to look for the effect of chloroethylclonidine (CEC) on prejunctional alpha-2 autoreceptors of the canine saphenous vein. (unesp.br)
  • We previously demonstrated that alpha-1 adrenergic receptor (α1-AR) antagonists can prevent cytokine storm syndrome in mice. (stanford.edu)
  • Antagonist activity at human recombinant adrenergic Alpha-2C receptor expressed in CHO cells assessed as inhibition of NE-induced calcium mobilizatio. (bindingdb.org)
  • Antagonist activity at human recombinant adrenergic alpha2B receptor expressed in CHO cells assessed as inhibition of NE-induced calcium mobilization. (bindingdb.org)