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.
An antilipemic agent which reduces both CHOLESTEROL and TRIGLYCERIDES in the blood.
A nuclear transcription factor. Heterodimerization with RETINOID X RECEPTOR GAMMA is important to metabolism of LIPIDS. It is the target of FIBRATES to control HYPERLIPIDEMIAS.
An antilipemic agent that lowers CHOLESTEROL and TRIGLYCERIDES. It decreases LOW DENSITY LIPOPROTEINS and increases HIGH DENSITY LIPOPROTEINS.
Intracellular receptors that can be found in the cytoplasm or in the nucleus. They bind to extracellular signaling molecules that migrate through or are transported across the CELL MEMBRANE. Many members of this class of receptors occur in the cytoplasm and are transported to the CELL NUCLEUS upon ligand-binding where they signal via DNA-binding and transcription regulation. Also included in this category are receptors found on INTRACELLULAR MEMBRANES that act via mechanisms similar to CELL SURFACE RECEPTORS.
Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.
A class of nongenotoxic CARCINOGENS that induce the production of hepatic PEROXISOMES and induce hepatic neoplasms after long-term administration.
Derivatives of propionic acid. Included under this heading are a broad variety of acid forms, salts, esters, and amides that contain the carboxyethane structure.
A family of 6-membered heterocyclic compounds occurring in nature in a wide variety of forms. They include several nucleic acid constituents (CYTOSINE; THYMINE; and URACIL) and form the basic structure of the barbiturates.
Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Drugs that bind to and activate dopamine receptors.
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.
Endogenous compounds and drugs that bind to and activate GAMMA-AMINOBUTYRIC ACID receptors (RECEPTORS, GABA).
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 and activate nicotinic cholinergic receptors (RECEPTORS, NICOTINIC). Nicotinic agonists act at postganglionic nicotinic receptors, at neuroeffector junctions in the peripheral nervous system, and at nicotinic receptors in the central nervous system. Agents that function as neuromuscular depolarizing blocking agents are included here because they activate nicotinic receptors, although they are used clinically to block nicotinic transmission.
Compounds that bind to and activate ADRENERGIC ALPHA-2 RECEPTORS.
Drugs that selectively bind to and activate alpha adrenergic receptors.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Compounds that bind to and stimulate PURINERGIC P1 RECEPTORS.
Drugs that bind to and activate muscarinic cholinergic receptors (RECEPTORS, MUSCARINIC). Muscarinic agonists are most commonly used when it is desirable to increase smooth muscle tone, especially in the GI tract, urinary bladder and the eye. They may also be used to reduce heart rate.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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.

Fenofibrate is a medication that belongs to the class of drugs known as fibrates. It is primarily used to lower levels of cholesterol and other fats (triglycerides) in the blood. Fenofibrate works by increasing the breakdown and elimination of these fats from the body, which can help reduce the risk of heart disease and stroke.

Fenofibrate is available in various forms, including tablets and capsules, and is typically taken once or twice a day with meals. Common side effects of fenofibrate include headache, nausea, and muscle pain. More serious side effects are rare but can include liver damage, kidney problems, and an increased risk of gallstones.

It's important to note that fenofibrate should be used in conjunction with a healthy diet, regular exercise, and other lifestyle changes to manage high cholesterol and triglyceride levels effectively. Additionally, patients taking fenofibrate should be monitored regularly by their healthcare provider to ensure that the medication is working properly and to check for any potential side effects.

PPAR-alpha (Peroxisome Proliferator-Activated Receptor alpha) is a type of nuclear receptor protein that functions as a transcription factor, regulating the expression of specific genes involved in lipid metabolism. It plays a crucial role in the breakdown of fatty acids and the synthesis of high-density lipoproteins (HDL or "good" cholesterol) in the liver. PPAR-alpha activation also has anti-inflammatory effects, making it a potential therapeutic target for metabolic disorders such as diabetes, hyperlipidemia, and non-alcoholic fatty liver disease (NAFLD).

Bezafibrate is a medication that belongs to a class of drugs called fibrates. It is primarily used to treat high cholesterol and related conditions, such as hyperlipidemia and mixed dyslipidemia. The medication works by reducing the levels of triglycerides and increasing the levels of "good" cholesterol (HDL) in the blood.

Bezafibrate achieves this effect by activating certain receptors in the body, known as peroxisome proliferator-activated receptors (PPARs), which play a role in regulating lipid metabolism. By binding to these receptors, bezafibrate helps to promote the breakdown of fats and reduce the production of cholesterol in the liver.

It is important to note that bezafibrate should be used in conjunction with lifestyle modifications, such as a healthy diet and regular exercise, to effectively manage high cholesterol and related conditions. Additionally, it may interact with other medications, so it is essential to inform your healthcare provider of all the drugs you are taking before starting bezafibrate therapy.

As with any medication, bezafibrate can cause side effects, including gastrointestinal symptoms such as nausea, diarrhea, and abdominal pain, as well as headaches, muscle cramps, and skin rashes. In rare cases, it may also cause more serious side effects, such as liver or kidney damage, so regular monitoring of liver and kidney function is recommended during treatment.

Overall, bezafibrate is a valuable tool in the management of high cholesterol and related conditions, but it should be used under the guidance and supervision of a healthcare professional to ensure safe and effective use.

Cytoplasmic receptors and nuclear receptors are two types of intracellular receptors that play crucial roles in signal transduction pathways and regulation of gene expression. They are classified based on their location within the cell. Here are the medical definitions for each:

1. Cytoplasmic Receptors: These are a group of intracellular receptors primarily found in the cytoplasm of cells, which bind to specific hormones, growth factors, or other signaling molecules. Upon binding, these receptors undergo conformational changes that allow them to interact with various partners, such as adapter proteins and enzymes, leading to activation of downstream signaling cascades. These pathways ultimately result in modulation of cellular processes like proliferation, differentiation, and apoptosis. Examples of cytoplasmic receptors include receptor tyrosine kinases (RTKs), serine/threonine kinase receptors, and cytokine receptors.
2. Nuclear Receptors: These are a distinct class of intracellular receptors that reside primarily in the nucleus of cells. They bind to specific ligands, such as steroid hormones, thyroid hormones, vitamin D, retinoic acid, and various other lipophilic molecules. Upon binding, nuclear receptors undergo conformational changes that facilitate their interaction with co-regulatory proteins and the DNA. This interaction results in the modulation of gene transcription, ultimately leading to alterations in protein expression and cellular responses. Examples of nuclear receptors include estrogen receptor (ER), androgen receptor (AR), glucocorticoid receptor (GR), thyroid hormone receptor (TR), vitamin D receptor (VDR), and peroxisome proliferator-activated receptors (PPARs).

Both cytoplasmic and nuclear receptors are essential components of cellular communication networks, allowing cells to respond appropriately to extracellular signals and maintain homeostasis. Dysregulation of these receptors has been implicated in various diseases, including cancer, diabetes, and autoimmune disorders.

Hypolipidemic agents are a class of medications that are used to lower the levels of lipids (fats) in the blood, particularly cholesterol and triglycerides. These drugs work by reducing the production or increasing the breakdown of fats in the body, which can help prevent or treat conditions such as hyperlipidemia (high levels of fats in the blood), atherosclerosis (hardening and narrowing of the arteries), and cardiovascular disease.

There are several different types of hypolipidemic agents, including:

1. Statins: These drugs block the action of an enzyme called HMG-CoA reductase, which is necessary for the production of cholesterol in the liver. By reducing the amount of cholesterol produced, statins can help lower LDL (bad) cholesterol levels and increase HDL (good) cholesterol levels.
2. Bile acid sequestrants: These drugs bind to bile acids in the intestines and prevent them from being reabsorbed into the bloodstream. This causes the liver to produce more bile acids, which requires it to use up more cholesterol, thereby lowering LDL cholesterol levels.
3. Nicotinic acid: Also known as niacin, this drug can help lower LDL and VLDL (very low-density lipoprotein) cholesterol levels and increase HDL cholesterol levels. It works by reducing the production of fatty acids in the liver.
4. Fibrates: These drugs are used to treat high triglyceride levels. They work by increasing the breakdown of fats in the body and reducing the production of VLDL cholesterol in the liver.
5. PCSK9 inhibitors: These drugs block the action of a protein called PCSK9, which helps regulate the amount of LDL cholesterol in the blood. By blocking PCSK9, these drugs can help lower LDL cholesterol levels.

It's important to note that hypolipidemic agents should only be used under the guidance and supervision of a healthcare provider, as they can have side effects and may interact with other medications.

Peroxisome proliferators are a class of synthetic compounds that can induce the proliferation (i.e., increase in number) of peroxisomes in the cells of various organisms, including mammals. These compounds include certain pharmaceuticals, industrial chemicals, and environmental pollutants.

Peroxisomes are small, membrane-bound organelles found in the cytoplasm of eukaryotic cells (cells with a true nucleus). They play a crucial role in several metabolic processes, including the breakdown of fatty acids, the detoxification of harmful substances, and the biosynthesis of certain lipids.

Peroxisome proliferators exert their effects by binding to and activating specific nuclear receptors called peroxisome proliferator-activated receptors (PPARs). PPARs are transcription factors that regulate the expression of genes involved in cellular metabolism, differentiation, and growth. Activation of PPARs by peroxisome proliferators leads to an increase in peroxisome number and altered peroxisomal functions, which can have various consequences for cellular homeostasis and overall organism health.

It is important to note that long-term exposure to certain peroxisome proliferators has been linked to increased risks of cancer and other diseases in animals, although the evidence in humans is less clear. Further research is needed to fully understand the potential health impacts of these compounds.

Propionates, in a medical context, most commonly refer to a group of medications that are used as topical creams or gels to treat fungal infections of the skin. Propionic acid and its salts, such as propionate, are the active ingredients in these medications. They work by inhibiting the growth of fungi, which causes the infection. Common examples of propionate-containing medications include creams used to treat athlete's foot, ringworm, and jock itch.

It is important to note that there are many different types of medications and compounds that contain the word "propionate" in their name, as it refers to a specific chemical structure. However, in a medical context, it most commonly refers to antifungal creams or gels.

Pyrimidines are heterocyclic aromatic organic compounds similar to benzene and pyridine, containing two nitrogen atoms at positions 1 and 3 of the six-member ring. They are one of the two types of nucleobases found in nucleic acids, the other being purines. The pyrimidine bases include cytosine (C) and thymine (T) in DNA, and uracil (U) in RNA, which pair with guanine (G) and adenine (A), respectively, through hydrogen bonding to form the double helix structure of nucleic acids. Pyrimidines are also found in many other biomolecules and have various roles in cellular metabolism and genetic regulation.

Transcription factors are proteins that play a crucial role in regulating gene expression by controlling the transcription of DNA to messenger RNA (mRNA). They function by binding to specific DNA sequences, known as response elements, located in the promoter region or enhancer regions of target genes. This binding can either activate or repress the initiation of transcription, depending on the properties and interactions of the particular transcription factor. Transcription factors often act as part of a complex network of regulatory proteins that determine the precise spatiotemporal patterns of gene expression during development, differentiation, and homeostasis in an organism.

The liver is a large, solid organ located in the upper right portion of the abdomen, beneath the diaphragm and above the stomach. It plays a vital role in several bodily functions, including:

1. Metabolism: The liver helps to metabolize carbohydrates, fats, and proteins from the food we eat into energy and nutrients that our bodies can use.
2. Detoxification: The liver detoxifies harmful substances in the body by breaking them down into less toxic forms or excreting them through bile.
3. Synthesis: The liver synthesizes important proteins, such as albumin and clotting factors, that are necessary for proper bodily function.
4. Storage: The liver stores glucose, vitamins, and minerals that can be released when the body needs them.
5. Bile production: The liver produces bile, a digestive juice that helps to break down fats in the small intestine.
6. Immune function: The liver plays a role in the immune system by filtering out bacteria and other harmful substances from the blood.

Overall, the liver is an essential organ that plays a critical role in maintaining overall health and well-being.

Messenger RNA (mRNA) is a type of RNA (ribonucleic acid) that carries genetic information copied from DNA in the form of a series of three-base code "words," each of which specifies a particular amino acid. This information is used by the cell's machinery to construct proteins, a process known as translation. After being transcribed from DNA, mRNA travels out of the nucleus to the ribosomes in the cytoplasm where protein synthesis occurs. Once the protein has been synthesized, the mRNA may be degraded and recycled. Post-transcriptional modifications can also occur to mRNA, such as alternative splicing and addition of a 5' cap and a poly(A) tail, which can affect its stability, localization, and translation efficiency.

"Cells, cultured" is a medical term that refers to cells that have been removed from an organism and grown in controlled laboratory conditions outside of the body. This process is called cell culture and it allows scientists to study cells in a more controlled and accessible environment than they would have inside the body. Cultured cells can be derived from a variety of sources, including tissues, organs, or fluids from humans, animals, or cell lines that have been previously established in the laboratory.

Cell culture involves several steps, including isolation of the cells from the tissue, purification and characterization of the cells, and maintenance of the cells in appropriate growth conditions. The cells are typically grown in specialized media that contain nutrients, growth factors, and other components necessary for their survival and proliferation. Cultured cells can be used for a variety of purposes, including basic research, drug development and testing, and production of biological products such as vaccines and gene therapies.

It is important to note that cultured cells may behave differently than they do in the body, and results obtained from cell culture studies may not always translate directly to human physiology or disease. Therefore, it is essential to validate findings from cell culture experiments using additional models and ultimately in clinical trials involving human subjects.

Dopamine agonists are a class of medications that mimic the action of dopamine, a neurotransmitter in the brain that regulates movement, emotion, motivation, and reinforcement of rewarding behaviors. These medications bind to dopamine receptors in the brain and activate them, leading to an increase in dopaminergic activity.

Dopamine agonists are used primarily to treat Parkinson's disease, a neurological disorder characterized by motor symptoms such as tremors, rigidity, bradykinesia (slowness of movement), and postural instability. By increasing dopaminergic activity in the brain, dopamine agonists can help alleviate some of these symptoms.

Examples of dopamine agonists include:

1. Pramipexole (Mirapex)
2. Ropinirole (Requip)
3. Rotigotine (Neupro)
4. Apomorphine (Apokyn)

Dopamine agonists may also be used off-label to treat other conditions, such as restless legs syndrome or certain types of dopamine-responsive dystonia. However, these medications can have significant side effects, including nausea, dizziness, orthostatic hypotension, compulsive behaviors (such as gambling, shopping, or sexual addiction), and hallucinations. Therefore, they should be used with caution and under the close supervision of a healthcare provider.

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.

GABA (gamma-aminobutyric acid) agonists are substances that bind to and activate GABA receptors in the brain, mimicking the actions of GABA, which is the primary inhibitory neurotransmitter in the central nervous system. These agents can produce various effects such as sedation, anxiolysis, muscle relaxation, and anticonvulsant activity by enhancing the inhibitory tone in the brain. They are used clinically to treat conditions such as anxiety disorders, seizures, and muscle spasticity. Examples of GABA agonists include benzodiazepines, barbiturates, and certain non-benzodiazepine hypnotics.

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 agonists are substances that bind to and activate nicotinic acetylcholine receptors (nAChRs), which are ligand-gated ion channels found in the nervous system of many organisms, including humans. These receptors are activated by the endogenous neurotransmitter acetylcholine and the exogenous compound nicotine.

When a nicotinic agonist binds to the receptor, it triggers a conformational change that leads to the opening of an ion channel, allowing the influx of cations such as calcium, sodium, and potassium. This ion flux can depolarize the postsynaptic membrane and generate or modulate electrical signals in excitable tissues, such as neurons and muscles.

Nicotinic agonists have various therapeutic and recreational uses, but they can also produce harmful effects, depending on the dose, duration of exposure, and individual sensitivity. Some examples of nicotinic agonists include:

1. Nicotine: A highly addictive alkaloid found in tobacco plants, which is the prototypical nicotinic agonist. It is used in smoking cessation therapies, such as nicotine gum and patches, but it can also lead to dependence and various health issues when consumed through smoking or vaping.
2. Varenicline: A medication approved for smoking cessation that acts as a partial agonist of nAChRs. It reduces the rewarding effects of nicotine and alleviates withdrawal symptoms, helping smokers quit.
3. Rivastigmine: A cholinesterase inhibitor used to treat Alzheimer's disease and other forms of dementia. It increases the concentration of acetylcholine in the synaptic cleft, enhancing its activity at nicotinic receptors and improving cognitive function.
4. Succinylcholine: A neuromuscular blocking agent used during surgical procedures to induce paralysis and facilitate intubation. It acts as a depolarizing nicotinic agonist, causing transient muscle fasciculations followed by prolonged relaxation.
5. Curare and related compounds: Plant-derived alkaloids that act as competitive antagonists of nicotinic receptors. They are used in anesthesia to induce paralysis and facilitate mechanical ventilation during surgery.

In summary, nicotinic agonists are substances that bind to and activate nicotinic acetylcholine receptors, leading to various physiological responses. These compounds have diverse applications in medicine, from smoking cessation therapies to treatments for neurodegenerative disorders and anesthesia. However, they can also pose risks when misused or abused, as seen with nicotine addiction and the potential side effects of certain medications.

Adrenergic alpha-2 receptor agonists are a class of medications that bind to and activate adrenergic alpha-2 receptors, which are found in the nervous system and other tissues. These receptors play a role in regulating various bodily functions, including blood pressure, heart rate, and release of certain hormones.

When adrenergic alpha-2 receptor agonists bind to these receptors, they can cause a variety of effects, such as:

* Vasoconstriction (narrowing of blood vessels), which can increase blood pressure
* Decreased heart rate and force of heart contractions
* Suppression of the release of norepinephrine (a hormone and neurotransmitter involved in the "fight or flight" response) from nerve endings
* Analgesia (pain relief)

Adrenergic alpha-2 receptor agonists are used in a variety of medical conditions, including:

* High blood pressure
* Glaucoma (to reduce pressure in the eye)
* Anesthesia (to help prevent excessive bleeding and to provide sedation)
* Opioid withdrawal symptoms (to help manage symptoms such as anxiety, agitation, and muscle aches)

Examples of adrenergic alpha-2 receptor agonists include clonidine, brimonidine, and dexmedetomidine.

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

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

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

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

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.

Purinergic P1 receptor agonists are substances that bind to and activate purinergic P1 receptors, which are a type of G protein-coupled receptor found in many tissues throughout the body. These receptors are activated by endogenous nucleotides such as adenosine and its metabolites.

Purinergic P1 receptors include four subtypes: A1, A2A, A2B, and A3. Each of these subtypes has distinct signaling pathways and physiological roles. For example, A1 receptor activation can lead to vasodilation, bradycardia, and anti-inflammatory effects, while A2A receptor activation can increase cyclic AMP levels and have anti-inflammatory effects.

Purinergic P1 receptor agonists are used in various therapeutic applications, including as cardiovascular drugs, antiplatelet agents, and anti-inflammatory agents. Some examples of purinergic P1 receptor agonists include adenosine, regadenoson, and dipyridamole.

It's important to note that the use of these substances should be under medical supervision due to their potential side effects and interactions with other medications.

Muscarinic agonists are a type of medication that binds to and activates muscarinic acetylcholine receptors, which are found in various organ systems throughout the body. These receptors are activated naturally by the neurotransmitter acetylcholine, and when muscarinic agonists bind to them, they mimic the effects of acetylcholine.

Muscarinic agonists can have a range of effects on different organ systems, depending on which receptors they activate. For example, they may cause bronchodilation (opening up of the airways) in the respiratory system, decreased heart rate and blood pressure in the cardiovascular system, increased glandular secretions in the gastrointestinal and salivary systems, and relaxation of smooth muscle in the urinary and reproductive systems.

Some examples of muscarinic agonists include pilocarpine, which is used to treat dry mouth and glaucoma, and bethanechol, which is used to treat urinary retention. It's important to note that muscarinic agonists can also have side effects, such as sweating, nausea, vomiting, and diarrhea, due to their activation of receptors in various organ systems.

... an α2A adrenergic receptor agonist. Medetomidine, an α2 adrenergic agonist. Nonspecific agonists act as agonists at both alpha- ... Media related to Alpha-adrenergic agonists at Wikimedia Commons Adrenergic+alpha-Agonists at the U.S. National Library of ... Alpha blocker Adrenergic agonist Beta-adrenergic agonist Declerck I, Himpens B, Droogmans G, Casteels R (September 1990). "The ... Alpha-adrenergic agonists have the opposite function of alpha blockers. Alpha adrenoreceptor ligands mimic the action of ...
Ephedrine Pseudoephedrine Adrenergic receptor Alpha adrenergic agonist List of adrenergic drugs Siegel, George J; et al. (2006 ... the adrenergic receptors). Directly acting adrenergic agonists act on adrenergic receptors. All adrenergic receptors are G- ... An adrenergic agonist is a drug that stimulates a response from the adrenergic receptors. The five main categories of ... Agonists of each class of receptor elicit these downstream responses. Indirectly acting adrenergic agonists affect the uptake ...
Alpha 2 adrenergic agonists can be used to manage the symptoms of acute withdrawal. Lofexidine and clonidine are also used for ... adrenergic agonists for the management of opioid withdrawal". Cochrane Database of Systematic Reviews. 2016 (5): CD002024. doi: ... "Clinical Opiate Withdrawal Scale" (PDF). Gowing, Linda; Farrell, Michael; Ali, Robert; White, Jason M (2016-05-03). "Alpha 2 - ...
Giovannitti JA, Thoms SM, Crawford JJ (2015). "Alpha-2 adrenergic receptor agonists: a review of current clinical applications ... This is because adrenergic stimulation by agonists results in normal calcium channel regulation. If these adrenergic receptors ... Adrenergic receptor Alpha blocker Beta blocker List of adrenergic drugs Propranolol Sympathetic nervous system Wiysonge, CS; ... There are few non-cardiovascular uses for adrenergic antagonists. Alpha-adrenergic antagonists are also used for treatment of ...
Important vasoactive substances are angiotensin-11, endothelin-1, and alpha-adrenergic agonists. Various vasoactive agents, ...
Alpha-adrenergic agonists work by decreasing production of fluid and increasing drainage. Brimonidine and Apraclonidine are two ... Furthermore, less selective alpha agonists such as [epinephrine] may decrease the production of aqueous humor through ... commonly prescribes alpha agonists for glaucoma treatment. Alphagan P uses a purite preservative, which is better tolerated by ...
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Another commonly used alpha-2 adrenergic agonist is dexmedetomidine, which is commonly used to provide a short term sedative ... One commonly used premedication is clonidine, an alpha-2 adrenergic agonist. It reduces postoperative shivering, postoperative ... The most volatile anesthetic has been found to be a GABAA agonist, although the site of action on the receptor remains unknown ...
Adverse effects in mammals are caused by amitraz' alpha-adrenergic agonist activity. Symptoms can include low blood pressure ... Its effectiveness is traced back on alpha-adrenergic agonist activity, interaction with octopamine receptors of the central ...
Alpha-1 adrenergic receptor agonists, Alpha-2 adrenergic receptor agonists, Imidazolines, Tert-butyl compounds, Topical ... Xylometazoline is in the decongestant and alpha-adrenergic agonist families of medication. Xylometazoline was patented in 1956 ... It binds to α1 and α2 adrenergic receptors in the nasal mucosa. Due to its sympathomimetic effects, it should not be used by ... The drug works by stimulating adrenergic receptors on the lamina propria of blood vessels in the nose. The decongestant effect ...
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Alpha-adrenergic agonists may cause urinary retention by stimulating the contraction of the urethral sphincter. Calcium channel ...
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 ... "Quantitative relationships between alpha-adrenergic activity and binding affinity of alpha-adrenoceptor agonists and ... "Electrophysiologic and hemodynamic effects of chronic oral therapy with the alpha 2-agonists clonidine and tiamenidine in ...
These adjuvants may include epinephrine (or more specific alpha-adrenergic agonists), corticosteroids, opioids, or ketamine. ... Epinephrine increases the length of analgesic duration and decreases blood flow by acting as an agonist at the α1-adrenoceptor ...
Alpha adrenergic agonists are recommended in addition to intravenous fluids to increase the blood pressure; anticholinesterase ...
Potential interaction with sympathomimetic drugs (adrenergic agonists) and sympatholytic drugs (alpha-blockers and beta- ... Nicotinic agonists, Nicotinic antagonists, Plant toxin insecticides, Pregnane X receptor agonists, Pyridine alkaloids, ... Both drugs are agonists are nicotinic cholinergic receptors ... Kishioka S, Kiguchi N, Kobayashi Y, Saika F (2014). "Nicotine ... Nicotine acts as a receptor agonist at most nicotinic acetylcholine receptors (nAChRs), except at two nicotinic receptor ...
Arnsten AF (2010). "The use of alpha-2A adrenergic agonists for the treatment of attention-deficit/hyperactivity disorder". ... Clonidine An α2A adrenergic receptor agonist has also been approved in the US. Clonidine was initially developed as a treatment ... These include the alpha-2 agonists (clonidine and guanfacine), tricyclic antidepressants (desipramine and nortriptyline), and ... In contrast, ADHD stimulants are indirect agonists of postsynaptic dopamine receptors; in other words, these stimulants ...
"Inhibition of the lipolytic action of beta-adrenergic agonists in human adipocytes by alpha-adrenergic agonists". J. Lipid Res ... Agonists 4-NEMD 7-Me-marsanidine (also I1 agonist) Agmatine (also I agonist, NMDA, 5-HT3, nicotinic antagonist and NOS ... For example, the alpha-2A adrenergic receptor subtype is post-synaptic in the prefrontal cortex and these receptors strengthen ... The alpha-2 (α2) adrenergic receptor (or adrenoceptor) is a G protein-coupled receptor (GPCR) associated with the Gi ...
Bell CC (January 1983). "Simultaneous treatment of hypertension and opiate withdrawal using an alpha 2-adrenergic agonist". ... Hydromorphone is a semi-synthetic μ-opioid agonist. As a hydrogenated ketone of morphine, it shares the pharmacologic ... Mu-opioid receptor agonists, Phenols, Semisynthetic opioids, World Health Organization essential medicines, Wikipedia medicine ...
The real purpose of 6-hydroxydopamine is to increase sensitivity to alpha- and beta-adrenergic agonists. The supersensitivity ...
Alpha-1 adrenergic receptor agonists, Alpha-2 blockers, Cyclopropyl compounds, Imidazolines, Phenol ethers, All stub articles, ... Cirazoline is a full agonist at the α1A adrenergic receptor, a partial agonist at both the α1B and α1D adrenergic receptors, ... Arnsten, A.F.T.; Jentsch, J.D. (September 1997). "The Alpha-1 Adrenergic Agonist, Cirazoline, Impairs Spatial Working Memory ... Cirazoline is an α1 adrenergic agonist and an α2 adrenergic antagonist". Journal of Pharmacology and Experimental Therapeutics ...
Another countermeasure includes administration of midodrine, which is a selective alpha-1 adrenergic agonist. Midodrine ... The use of beta-2 adrenergic agonists to increase muscle mass, and the use of essential amino acids in conjunction with ...
Alpha-adrenergic agonist medications, such as decongestants with pseudoephedrine can increase bladder outlet resistance. In ... Selective alpha-1 blockers are similar in effectiveness but have slightly different side effect profiles. Alpha blockers relax ... Effects may take longer to appear than alpha blockers, but they persist for many years. When used together with alpha blockers ... Non-selective alpha blockers such as terazosin and doxazosin may also require slow dose adjustments as they can lower blood ...
... barbiturates and Alpha-adrenergic agonists, such as clonidine. Conversely, coadministration of NMDA-antagonists with alpha-2 ... adrenergic antagonists, like yohimbine, could theoretically potentiate NAT. In the late 1980s, John Olney, a researcher ...
... s must not be used in the treatment of selective alpha-adrenergic agonist overdose. The blockade of only beta ... β1-adrenergic receptors are located mainly in the heart and in the kidneys. β2-adrenergic receptors are located mainly in the ... Newer, third-generation beta blockers can cause vasodilation through blockade of alpha-adrenergic receptors. Accordingly, ... These agents are capable of exerting low-level agonist activity at the β-adrenergic receptor while simultaneously acting as a ...
Oxyfedrine Ractopamine Reproterol Rimiterol Tretoquinol Tulobuterol Zilpaterol Zinterol Alpha-adrenergic agonist "WHAT ARE BETA ... Beta adrenergic agonists or beta agonists are medications that relax muscles of the airways, causing widening of the airways ... In general, pure beta-adrenergic agonists have the opposite function of beta blockers: beta-adrenoreceptor agonist ligands ... Adrenergic+beta-Agonists at the U.S. National Library of Medicine Medical Subject Headings (MeSH) Delbruck, Max. "The beta- ...
"Shock and Hypotension in the Newborn Medication: Alpha/Beta Adrenergic Agonists, Vasodilators, Inotropic agents, Volume ... This group includes some medications that are administered for Parkinson's disease, as well as other dopamine agonists such as ... ISBN 978-0-19-150851-6. Dopamine binds to beta-1, beta-2, alpha-1 and dopaminergic receptors Lewis RJ (2004). Sax's Dangerous ... and β2 adrenergic receptors. Side effects of dopamine include negative effects on kidney function and irregular heartbeats. The ...
... is a potent sedative drug which acts as a selective alpha-2 adrenergic agonist. It is closely related to dexmedetomidine ... Alpha-2 adrenergic receptor agonists, Imidazoles, 1-Naphthyl compounds, All stub articles, Sedative stubs). ... 1H-imidazoles on alpha 1- and alpha 2-adrenergic receptors". Journal of Medicinal Chemistry. 37 (15): 2328-33. doi:10.1021/ ... Like other alpha-2 agonists, it produces sedative and muscle relaxant effects but without producing respiratory depression. It ...
... a potent alpha 1-adrenergic receptor agonist, selective for the alpha 1A receptor subtype". J. Pharmacol. Exp. Ther. 274 (1): ... 1994). "Cloning, expression and characterization of human alpha adrenergic receptors alpha 1a, alpha 1b and alpha 1c". Biochem ... The alpha-1A adrenergic receptor (α1A adrenoreceptor), also known as ADRA1A, formerly known also as the alpha-1C adrenergic ... There are 3 alpha-1 adrenergic receptor subtypes: alpha-1A, -1B and -1D, all of which signal through the Gq/11 family of G- ...
... at higher doses may have direct alpha-adrenergic agonist and beta-1 adrenergic agonist effects. However at doses ... Alpha-1 adrenergic receptor agonists, Beta-adrenergic agonists, Cardiac stimulants, Phenylethanolamines, Phenols, Substituted ... It is an α1-adrenergic receptor agonist with some β effect. It is currently sold in its generic form by Slayback Pharma. ... McDonald M, Santucci R (2004). "Successful management of stuttering priapism using home self-injections of the alpha-agonist ...
... an α2A adrenergic receptor agonist. Medetomidine, an α2 adrenergic agonist. Nonspecific agonists act as agonists at both alpha- ... Media related to Alpha-adrenergic agonists at Wikimedia Commons Adrenergic+alpha-Agonists at the U.S. National Library of ... Alpha blocker Adrenergic agonist Beta-adrenergic agonist Declerck I, Himpens B, Droogmans G, Casteels R (September 1990). "The ... Alpha-adrenergic agonists have the opposite function of alpha blockers. Alpha adrenoreceptor ligands mimic the action of ...
Alpha/Beta Adrenergic Agonists. Class Summary. These are used in the emergency management of systemic allergic reactions or ... John M James, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Allergy Asthma and ... Delayed clinical and ex vivo response to mammalian meat in patients with IgE to galactose-alpha-1,3-galactose. J Allergy Clin ...
Alpha-2-adrenergic receptor agonists for the prevention of delirium and cognitive decline after open heart surgery ( ... Alpha-2-adrenergic receptor agonists for the prevention of delirium and cognitive decline after open heart surgery ( ... The alpha-2-adrenergic receptor agonist dexmedetomidine shows promise as prophylaxis and treatment for delirium in intensive ... However, dexmedetomidine, a parenterally administered alpha-2-adrenergic receptor agonist that attenuates sympathetic nervous ...
John M James, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Allergy Asthma and ... Delayed clinical and ex vivo response to mammalian meat in patients with IgE to galactose-alpha-1,3-galactose. J Allergy Clin ...
Oximetazolina una agonistas alfa-adrenérgicos, simpaticomiméticos de acción directa utilizada como vasoconstrictor para aliviar la congestión nasal La acción simpaticomimética de oximetazolina contrae las arteriolas más pequeñas de las fosas nasales, produciendo un prolongado (hasta 12 horas), el efecto suave y descongestión. Oximetazolina provoca alivio de la hiperemia conjuntival por la vasoconstricción causa de la conjuntiva superficial los vasos sanguíneos. Acción de la droga se ha demostrado en la conjuntivitis alérgica aguda y en la industria química (cloro) conjuntivitis ...
Alpha-adrenergic Agonists for the Management of Opioid Withdrawal MATTHEW ROYALL, KATHRYN K. GARNER, SUSAN HILL, MATTHEW BARNES ... Alpha-adrenergic agonists were more efficacious than placebo in the management of opioid withdrawal, but are best reserved as ...
Auvi-Q™ Alpha and Beta Adrenergic Agonist Epinephrine 0.3 mg Injection Prefilled Auto-Injector 0.3 mL ... Auvi-Q™ Alpha and Beta Adrenergic Agonist Epinephrine 0.15 mg Injection Prefilled Auto-Injector 0.15 mL ... Adrenalin® Alpha and Beta Adrenergic Agonist Epinephrine 1 mg / mL (1:1000) Injection Single-Use Vial 1 mL ... Alpha and Beta Adrenergic Agonist Epinephrine 0.15 mg (1:2000) Injection Prefilled Auto-Injector 0.3 mL ...
Adrenergic alpha-Agonists / adverse effects * Adrenergic alpha-Agonists / therapeutic use* * Aging / psychology ...
Scientific Rationale for the Use of Alpha-Adrenergic Agonists and Glucocorticoids in the Therapy of Pediatric Stridor. Gustavo ...
Brimonidine is in a class of drugs called alpha adrenergic agonists. Brimonidine works by decreasing the amount of fluid in the ...
Clonidine, an alpha agonist, formally prescribed in clinical medicine as antihypertensive medication, is currently being used ... Clonidine is an alpha-2 adrenergic agonist. It is non-selective in the sense that it binds to alpha-2A, B and C subtypes [1] ( ... Clonidine is a non-selective alpha-2 adrenergic agonist that has been used in psychiatric practice in panoply of clinical ... Alpha-2 adrenergic receptors are present in high concentrations in the prefrontal cortex (PFC) but only in low concentrations ...
alpha-Adrenergic Agonists. Strength : 0.2 / 0.5%. Pack Size (Form) : 5ML OPHTHALMIC SOLUTION (BOTTLE) ...
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Guanfacine is a selective central alpha2A-adrenergic receptor agonist in that it has a 15-20 times higher affinity for this ... INTUNIV® is a central alpha2A-adrenergic receptor agonist indicated for the treatment of Attention Deficit Hyperactivity ... Guanfacine is a central alpha2A-adrenergic receptor agonist. Guanfacine is not a central nervous system (CNS) stimulant. The ... By stimulating central alpha2A-adrenergic receptors, guanfacine reduces sympathetic nerve impulses from the vasomotor center to ...
ATX vs alpha-adrenergic agonists. There are no head-to-head trials comparing ATX with alpha-adrenergic agonist medications like ... In comparing risks of ATX vs alpha-agonists, remember that alpha drugs can cause hypotension, rebound hypertension, sedation, ... CCPR Verdict: For usual ADHD treatment, we place ATX slightly behind the central alpha-agonists in the group of medications to ... There is indirect evidence that alpha-agonists may be more effective than ATX, and they are generally considered next in line ...
... belongs to a class of medicines known as alpha-adrenergic agonists. Iopidine is an eye drop used in conjunction with other ...
Choi, Y., Novak, J., Hillier, A.J., Votolato, N. (2006). The Effect of Alpha-2 Adrenergic Agonists on Memory and Cognitive ...
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 ... Caution should also be exercised in patients receiving alpha adrenergic receptor antagonists such as in the treatment of ...
Sympathomimetic amine that directly acts as an agonist at alpha- and beta-adrenergic receptors and indirectly causes the ... Alpha-adrenergic antagonists, beta-adrenergic receptor antagonists, reserpine, or quinidine may antagonize the vasopressor ... Stimulates alpha-adrenergic receptors of smooth muscle cells in the bladder (increases resistance to urinary outflow) ... Comment: If additional adrenergic drugs are to be administered by any route, they should be used with caution because the ...
The effects of medetomidine, an alpha 2-adrenergic agonist, on ventilatory drive in the dog.﻽. Bloor BC, Abdul-Rasool I, Temp J ...
Alpha-adrenergic agonists decrease the rate of fluid production. They can be used alone or in combination with other anti- ...
07215 alpha-Adrenergic receptor agonists/antagonists. 07214 beta-Adrenergic receptor agonists/antagonists. 07213 Dopamine ... 07211 Serotonin receptor agonists/antagonists. 07228 Eicosanoid receptor agonists/antagonists. 07224 Opioid receptor agonists/ ... 00592 alpha-Linolenic acid metabolism. 01040 Biosynthesis of unsaturated fatty acids. Nucleotide metabolism 00230 Purine ... 04261 Adrenergic signaling in cardiomyocytes. 04270 Vascular smooth muscle contraction. Digestive system 04970 Salivary ...
Cirazoline is an alpha-1 adrenergic agonist and an alpha-2 adrenergic antagonist. R R Ruffolo and J E Waddell ... Cirazoline is an alpha-1 adrenergic agonist and an alpha-2 adrenergic antagonist. R R Ruffolo and J E Waddell ... Correlation between phosphatidylinositol labeling and contraction in rabbit aorta: effect of alpha-1 adrenergic activation. R ... Correlation between phosphatidylinositol labeling and contraction in rabbit aorta: effect of alpha-1 adrenergic activation. R ...
and Sowers, J. R. Alcohol withdrawal syndrome: clinical and hormonal responses to alpha 2-adrenergic agonist treatment. Alcohol ... Balldin, J. and Bokstrom, K. Treatment of alcohol abstinence symptoms with the alpha 2-agonist clonidine. Acta Psychiatr.Scand ... A randomized, double-blind, placebo-controlled, clinical trial of D-alpha-tocopheryl acetate (vitamin E), as add-on therapy, ...
Shire claims that this unscheduled drug is the first selective alpha-2A adrenergic receptor agonist approved for this ...
Contain brimonidine, a selective alpha-2 adrenergic agonist that decreases aqueous humor production. ...
... alpha-two adrenergic agonists, and antiparkinsonian drugs. Levetiracetam was reported helpful in one study (Casa & Bosio, 2005 ... Medications such as the benzodiazepines are agonists at this site, and so would be expected to reduce the symptoms of HPPD if ...
Very potent beta adrenergic receptor agonists with minimal effects on alpha adrenergic receptors:. *. ? propranolol (Inderal) ... beta-adrenergic receptor activation relaxes gastrointestinal smooth muscle. *. ? alpha-2 agonists act indirectly by reducing ... Alpha -- 2 adrenergic receptors inhibit lipolysis. *. ? Hepatic catecholamine effects our mediated mainly by beta adrenergic ... alpha -adrenergic receptor activation relaxes gastrointestinal smooth muscle. *. ? ...
Mehrotra S, Gupta S, Villalón CM et al (2007) Rat carotid artery responses to alpha-adrenergic receptor agonists and 5-HT after ... used meta-chlorophenylpiperazine (m-CCP), a 5-HT receptor agonist, to evaluate the involvement of 5-HT receptor in the ... Chen Z, Yuhanna IS, Galcheva-Gargova Z et al (1999) Estrogen receptor alpha mediates the nongenomic activation of endothelial ... In addition to the effects on neurons, sex hormones modulate vasoconstriction mediated by α2 receptor agonists, inducing a ...
  • The alpha-adrenergic receptor has two subclasses α1 and α2. (wikipedia.org)
  • amitraz Detomidine[citation needed] Lofexidine, an α2A adrenergic receptor agonist. (wikipedia.org)
  • The alpha-2-adrenergic receptor agonist dexmedetomidine shows promise as prophylaxis and treatment for delirium in intensive care units (ICU) and postoperative settings. (bmj.com)
  • Adenylate cyclase and beta adrenergic receptor development in the mouse heart. (aspetjournals.org)
  • Shire claims that this unscheduled drug is the first selective alpha-2A adrenergic receptor agonist approved for this indication. (genengnews.com)
  • Brimonidine is in a class of drugs called alpha adrenergic agonists. (medlineplus.gov)
  • Contain brimonidine, a selective alpha-2 adrenergic agonist that decreases aqueous humor production. (nasemsd.org)
  • Alpha adrenoreceptor ligands mimic the action of epinephrine and norepinephrine signaling in the heart, smooth muscle and central nervous system, with norepinephrine being the highest affinity. (wikipedia.org)
  • Xylometazoline Oxymetazoline Apraclonidine[citation needed] Cirazoline Epinephrine The following agents are also listed as agonists by MeSH. (wikipedia.org)
  • Alpha-adrenergic agonists are a class of sympathomimetic agents that selectively stimulates alpha adrenergic receptors. (wikipedia.org)
  • Alpha 2 receptors are associated with sympatholytic properties. (wikipedia.org)
  • Nonspecific agonists act as agonists at both alpha-1 and alpha-2 receptors. (wikipedia.org)
  • ergotamine etilefrine indanidine mephentermine metaraminol methoxamine mivazerol naphazoline norfenefrine octopamine phenylpropanolamine propylhexedrine rilmenidine romifidine synephrine talipexole Alpha-adrenergic agonists, more specifically the auto receptors of alpha 2 neurons, are used in the treatment of glaucoma by decreasing the production of aqueous fluid by the ciliary bodies of the eye and also by increasing uveoscleral outflow. (wikipedia.org)
  • It specifically targets alpha-2 receptors in the brainstem vasomotor centre, decreasing presynaptic Ca levels and release of NE. (karger.com)
  • Alpha-2 adrenergic receptors are present in high concentrations in the prefrontal cortex (PFC) but only in low concentrations in the nucleus accumbens. (karger.com)
  • Alpha-2B receptors are located mainly in thalamus associated with sedation. (karger.com)
  • There is strong evidence that obesity leads to increased sympathetic modulation and a decreased vagal tone leading to a lack of autonomic control (characterized by reduction of heart rate variability) that can bring about changes in the renin-angiotensin-aldosterone system in alpha agonists and central alpha 2-1 and beta-adrenergic receptors. (bvsalud.org)
  • Comment: Tricyclic antidepressants increase or decrease effects of sympathomimetics, by blocking reuptake of NE, or blocking uptake of indirect sympathomimetics into the adrenergic neuron. (medscape.com)
  • Many of the ergot alkaloids act as alpha-adrenergic antagonists. (bvsalud.org)
  • Clonidine, an alpha agonist, formally prescribed in clinical medicine as antihypertensive medication, is currently being used more frequently to address a multitude of psychiatric entities. (karger.com)
  • Clonidine is a non-selective alpha-2 adrenergic agonist that has been used in psychiatric practice in panoply of clinical indications. (karger.com)
  • Clonidine is an alpha-2 adrenergic agonist. (karger.com)
  • It is non-selective in the sense that it binds to alpha-2A, B and C subtypes [ 1 ] (cf. guanfacine, which is more selective to alpha-2A). (karger.com)
  • Atomoxetine (ATX, Strattera) was approved by the FDA for ADHD treatment in 2002, and since then has become a second- or third-line option (after stimulants and sometimes after central alpha-agonists) for ADHD in both children and adults. (thecarlatreport.com)
  • Iopidine (apraclonidine hydrochloride) belongs to a class of medicines known as alpha-adrenergic agonists. (mydr.com.au)
  • Alpha-adrenergic agonists decrease the rate of fluid production. (optometrists.org)
  • Alpha-adrenergic agonists were more efficacious than placebo in the management of opioid withdrawal, but are best reserved as an alternative to methadone. (aafp.org)
  • We will test this hypothesis via three specific aims: Aim 1: Establish how agents that specifically target TNF-alpha, IL-6, and IL-8 modulate dust extract-induced lung inflammation in vivo. (cdc.gov)
  • The reduction of the stress response caused by alpha 2 agonists were theorised to be beneficial peri operatively by reducing cardiac complications, however this has shown not to be clinically effective as there was no reduction in cardiac events or mortality but there was an increased incidence of hypotension and bradycardia. (wikipedia.org)
  • Aim 2: Determine how agents that augment PKA, especially therapeutic beta-adrenergic agonists, dampen dust extract-induced PKC isoform activation and attenuate lung inflammation in vitro and in vivo. (cdc.gov)
  • treatment may include Comprehensive Behavioral Intervention for Tics and alpha-adrenergic agonists or antipsychotics. (msdmanuals.com)
  • Norepinephrine modulates the motility of resting and activated microglia via different adrenergic receptors. (nih.gov)
  • Analysis of adrenergic receptor expression with quantitative PCR indicated that resting microglia primarily express β2 receptors but switch expression to α2A receptors under proinflammatory conditions modeled by LPS treatment. (nih.gov)
  • The use of subtype-selective receptor agonists and antagonists confirmed the involvement of β2 receptors in mediating microglial process dynamics in resting cells and α2A receptors in activated cells. (nih.gov)
  • Clonidine works by stimulating alpha-2 receptors in the brain, which results in a decrease in the release of norepinephrine, a hormone that constricts blood vessels and increases blood pressure. (redcrossdc.org)
  • By stimulating alpha-2 adrenergic receptors in the brain, it helps to relax and widen blood vessels, effectively reducing blood pressure and improving blood flow. (redcrossdc.org)
  • An agent that selectively binds to and activates adrenergic receptors. (mcw.edu)
  • Co-application of NE with ATP to resting microglia blocked the ATP-induced process extension and migration in isolated microglia, and β2 receptor antagonists prolonged ATP effects in brain slice tissues, suggesting the presence of cross-talk between adrenergic and purinergic signaling in microglia. (nih.gov)
  • There are no FDA-approved agents to reverse xylazine effects in humans, although veterinary adrenergic antagonists have been used for emergency treatment of accidental xylazine injection. (nih.gov)
  • Propranolol is a nonselective beta-adrenergic receptor blocking agent. (medscape.com)
  • Xylazine is an alpha-2 adrenergic receptor agonist with sedative and analgesic properties that is FDA-approved for veterinary use. (nih.gov)
  • Atipamezole, a potent alpha-2 adrenergic antagonist, is widely used in veterinary medicine for reversing the sedative effects of alpha-2 adrenergic agonists like medetomidine and xylazine. (openpr.com)
  • Midodrine is in a class of medications called alpha-adrenergic agonists. (medlineplus.gov)
  • Midodrine: Alpha adrenergic agonist leading to vasoconstriction. (uab.edu)
  • Xylazine may also affect the clinical presentation of opioid withdrawal as adrenergic withdrawal somewhat resembles opioid withdrawal symptoms, and xylazine has a very short pharmacological half-life (in animals). (nih.gov)
  • It's in a class of drugs called alpha-adrenergic agonists, and it works by reducing fluid levels in the eye. (healthline.com)
  • Clonidine is a medication that belongs to the class of drugs known as alpha-2 adrenergic agonists. (redcrossdc.org)
  • Brimonidine topical gel, 0.33% is an alpha adrenergic agonist indicated for the topical treatment of persistent (nontransient) facial erythema of rosacea in adults 18 years of age or older. (nih.gov)
  • Adrenergic therapies are used to treat opioid withdrawal syndrome, and so it is uncertain whether prolonged xylazine exposure will affect SUD treatment protocols and / or the therapeutics employed. (nih.gov)
  • Intrathecal injection of clonidine and dexmedetomidine produce behavioral analgesia by an alpha 2-adrenergic mechanism. (nih.gov)
  • A retrospective review of clinic records was undertaken to determine the efficacy and adverse effects of the centrally acting adrenergic agonists methyldopa and clonidine, the alpha-1 antagonist prazosin, and the direct vasodilator hydralazine in patients with mild and moderate hypertension. (nih.gov)
  • Publications] Uawabe, K.: 'Rationale for the use of alpha-blockers in the treatment of benign prostatic hyperplasia (BPH)' Int.J.Urol. (nii.ac.jp)
  • Selective Alpha Adrenergic Agonists. (toprx.com)
  • Pseudoephedrine: non selective alpha and beta receptor agonist. (uab.edu)
  • Publications] Moriyama, N: 'Evaluation of alpha_1-adrenoceptor subtypes in human hypertrohied prostate using [^3H] YM617, an alpha_1-selective antagonist' Acta Histochem Cytochem.27. (nii.ac.jp)
  • Similar declines in blood pressure levels occurred when hydralazine was used with an alpha-2 adrenergic agonist or beta-adrenoceptor blocking agent. (nih.gov)
  • The use of asthma medication, such as beta-agonists, is primarily to relax and expand the airways to support easy breathing. (digitales.com.au)
  • The clinical implications of these characters of alpha_1-adrenergic receptor of the prostate warrant further studies. (nii.ac.jp)
  • These results indicate that alpha_1-adrenergic receptor is little affected by endocrionological and thermal interventions. (nii.ac.jp)
  • Endocrinological and thermal effects on alpha_1-adrenergic-receptor-mediated contraction of the prostate. (nii.ac.jp)
  • The contraction of the prostate induced by alpha_1-adrenergic receptor agonist was examined in regards to the possible changes in properties when exposed to endocrinological and thermal stimuli. (nii.ac.jp)
  • Thermal effects by laser irradiation induced little changes in contraction force and Kd and Bmax of alpha_1-adrenergic receptor of the human prostate. (nii.ac.jp)
  • Publications] Moriyama,N.: 'Age-related changes in alpha_1-adrenoceptores in rat prostate. (nii.ac.jp)
  • Publications] Moriyama, N.: 'Effect of bunnazosin, alpha_1-adrenoceptor blocker, on multidirectional contractilc response and localization of bunazosin binding sites in human hypertrophied prostate' Gen.Pharmac.26. (nii.ac.jp)
  • Alpha-2 adrenergic agonists can lower blood pressure. (nih.gov)
  • A large body of experimental data has shown that lead raises blood pressure and increases responsiveness to alpha-adrenergic agonists in rats and pigeons. (nih.gov)
  • Tizanidine tablet is a central alpha-2-adrenergic agonist indicated for the management of spasticity. (nih.gov)
  • ages .According to the vision of the Italian Association of Dia - Prolactin cialis agonists alpha-adrenergic.the central [14].with and without the treaty relationship, on average, tocologico.the basis ofta in male subjects suffering from type 2 diabetesterazioni of the vascular system, strengthens the need for. (ericamulherin.com)