Drugs that bind to but do not activate CHOLINERGIC RECEPTORS, thereby blocking the actions of ACETYLCHOLINE or cholinergic agonists.
An alkaloid from SOLANACEAE, especially DATURA and SCOPOLIA. Scopolamine and its quaternary derivatives act as antimuscarinics like ATROPINE, but may have more central nervous system effects. Among the many uses are as an anesthetic premedication, in URINARY INCONTINENCE, in MOTION SICKNESS, as an antispasmodic, and as a mydriatic and cycloplegic.
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 mimic the effects of parasympathetic nervous system activity. Included here are drugs that directly stimulate muscarinic receptors and drugs that potentiate cholinergic activity, usually by slowing the breakdown of acetylcholine (CHOLINESTERASE INHIBITORS). Drugs that stimulate both sympathetic and parasympathetic postganglionic neurons (GANGLIONIC STIMULANTS) are not included here.
An alkaloid, originally from Atropa belladonna, but found in other plants, mainly SOLANACEAE. Hyoscyamine is the 3(S)-endo isomer of atropine.
A nicotinic antagonist that is well absorbed from the gastrointestinal tract and crosses the blood-brain barrier. Mecamylamine has been used as a ganglionic blocker in treating hypertension, but, like most ganglionic blockers, is more often used now as a research tool.
Drugs that bind to and activate cholinergic receptors.
Agents that inhibit the actions of the parasympathetic nervous system. The major group of drugs used therapeutically for this purpose is the MUSCARINIC ANTAGONISTS.
A high-affinity muscarinic antagonist commonly used as a tool in animal and tissue studies.
Cell surface proteins that bind acetylcholine with high affinity and trigger intracellular changes influencing the behavior of cells. Cholinergic receptors are divided into two major classes, muscarinic and nicotinic, based originally on their affinity for nicotine and muscarine. Each group is further subdivided based on pharmacology, location, mode of action, and/or molecular biology.
A slowly hydrolyzed CHOLINERGIC AGONIST that acts at both MUSCARINIC RECEPTORS and NICOTINIC RECEPTORS.
A neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.
One of the two major classes of cholinergic receptors. Muscarinic receptors were originally defined by their preference for MUSCARINE over NICOTINE. There are several subtypes (usually M1, M2, M3....) that are characterized by their cellular actions, pharmacology, and molecular biology.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Abrupt changes in the membrane potential that sweep along the CELL MEMBRANE of excitable cells in response to excitation stimuli.
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.
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 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.
Drugs that bind to but do not activate GABA RECEPTORS, thereby blocking the actions of endogenous GAMMA-AMINOBUTYRIC ACID and GABA RECEPTOR AGONISTS.
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 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.
Drugs that bind to but do not activate histamine receptors, thereby blocking the actions of histamine or histamine agonists. Classical antihistaminics block the histamine H1 receptors only.
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.
Compounds that selectively bind to and block the activation of ADENOSINE A2 RECEPTORS.
Drugs that bind to and block the activation of ADRENERGIC ALPHA-1 RECEPTORS.
Compounds that bind to and block the stimulation of PURINERGIC P2 RECEPTORS.
Drugs that bind to but do not activate SEROTONIN 5-HT3 RECEPTORS, thereby blocking the actions of SEROTONIN or SEROTONIN 5-HT3 RECEPTOR AGONISTS.
Drugs that bind to but do not activate SEROTONIN 5-HT2 RECEPTORS, thereby blocking the actions of SEROTONIN or SEROTONIN 5-HT2 RECEPTOR AGONISTS. Included under this heading are antagonists for one or more specific 5-HT2 receptor subtypes.
Compounds that bind to and block the stimulation of ADENOSINE A1 RECEPTORS.
A class of drugs designed to prevent leukotriene synthesis or activity by blocking binding at the receptor level.
Agents that antagonize ANGIOTENSIN RECEPTORS. Many drugs in this class specifically target the ANGIOTENSIN TYPE 1 RECEPTOR.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
Drugs that bind to and block the activation of ADRENERGIC ALPHA-2 RECEPTORS.
Drugs that bind to but do not activate ADRENERGIC RECEPTORS. Adrenergic antagonists block the actions of the endogenous adrenergic transmitters EPINEPHRINE and NOREPINEPHRINE.
Drugs that bind to but do not activate GABA-A RECEPTORS thereby blocking the actions of endogenous or exogenous GABA-A RECEPTOR AGONISTS.
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 selectively bind to but do not activate HISTAMINE H3 RECEPTORS. They have been used to correct SLEEP WAKE DISORDERS and MEMORY DISORDERS.
Quantitative determination of receptor (binding) proteins in body fluids or tissue using radioactively labeled binding reagents (e.g., antibodies, intracellular receptors, plasma binders).
Cell-surface proteins that bind SEROTONIN and trigger intracellular changes which influence the behavior of cells. Several types of serotonin receptors have been recognized which differ in their pharmacology, molecular biology, and mode of action.
Cell surface proteins that bind ENDOTHELINS with high affinity and trigger intracellular changes which influence the behavior of cells.
Drugs that bind to and block the activation of ADRENERGIC BETA-2 RECEPTORS.
A class of ionotropic glutamate receptors characterized by affinity for N-methyl-D-aspartate. NMDA receptors have an allosteric binding site for glycine which must be occupied for the channel to open efficiently and a site within the channel itself to which magnesium ions bind in a voltage-dependent manner. The positive voltage dependence of channel conductance and the high permeability of the conducting channel to calcium ions (as well as to monovalent cations) are important in excitotoxicity and neuronal plasticity.
The interaction of two or more substrates or ligands with the same binding site. The displacement of one by the other is used in quantitative and selective affinity measurements.
Drugs that bind to but do not activate SEROTONIN 5-HT1 RECEPTORS, thereby blocking the actions of SEROTONIN 5-HT1 RECEPTOR AGONISTS. Included under this heading are antagonists for one or more of the specific 5-HT1 receptor subtypes.
A class of drugs that act by selective inhibition of calcium influx through cellular membranes.
A potent noncompetitive antagonist of the NMDA receptor (RECEPTORS, N-METHYL-D-ASPARTATE) used mainly as a research tool. The drug has been considered for the wide variety of neurodegenerative conditions or disorders in which NMDA receptors may play an important role. Its use has been primarily limited to animal and tissue experiments because of its psychotropic effects.
A common name used for the genus Cavia. The most common species is Cavia porcellus which is the domesticated guinea pig used for pets and biomedical research.
Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.
Compounds that selectively bind to and block the activation of ADENOSINE A3 RECEPTORS.
A subtype of endothelin receptor found predominantly in the VASCULAR SMOOTH MUSCLE. It has a high affinity for ENDOTHELIN-1 and ENDOTHELIN-2.
Compounds with BENZENE fused to AZEPINES.
Biphenyl compounds are organic substances consisting of two phenyl rings connected by a single covalent bond, and can exhibit various properties and uses, including as intermediates in chemical synthesis, components in plastics and dyes, and as additives in fuels.
Compounds which inhibit or antagonize the action or biosynthesis of estrogenic compounds.
Derivative of noroxymorphone that is the N-cyclopropylmethyl congener of NALOXONE. It is a narcotic antagonist that is effective orally, longer lasting and more potent than naloxone, and has been proposed for the treatment of heroin addiction. The FDA has approved naltrexone for the treatment of alcohol dependence.
The action of a drug that may affect the activity, metabolism, or toxicity of another drug.
Piperazines are a class of heterocyclic organic compounds containing a seven-membered ring with two nitrogen atoms at positions 1 and 4, often used in pharmaceuticals as smooth muscle relaxants, antipsychotics, antidepressants, and antihistamines, but can also be found as recreational drugs with stimulant and entactogen properties.
A group of compounds that contain the structure SO2NH2.
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.
A specific opiate antagonist that has no agonist activity. It is a competitive antagonist at mu, delta, and kappa opioid receptors.
Endogenous compounds and drugs that bind to and activate SEROTONIN RECEPTORS. Many serotonin receptor agonists are used as ANTIDEPRESSANTS; ANXIOLYTICS; and in the treatment of MIGRAINE DISORDERS.

Cholinergic and GABAergic regulation of nitric oxide synthesis in the guinea pig ileum. (1/496)

Nitric oxide (NO) synthesis was examined in intact longitudinal muscle-myenteric plexus preparations of the guinea pig ileum by determining the formation of [3H]citrulline during incubation with [3H]arginine. Spontaneous [3H]citrulline production after 30 min was 80-90 dpm/mg, which constituted approximately 1% of the tissue radioactivity. Electrical stimulation (10 Hz) led to a threefold increase in [3H]citrulline formation. Removal of calcium from the medium or addition of NG-nitro-L-arginine strongly inhibited both spontaneous and electrically induced production of [3H]citrulline. TTX reduced the electrically induced but not spontaneous [3H]citrulline formation. The electrically induced formation of [3H]citrulline was diminished by (+)-tubocurarine and mecamylamine and enhanced by scopolamine, which suggests that endogenous ACh inhibits, via muscarinic receptors, and stimulates, via nicotinic receptors, the NO synthesis in the myenteric plexus. The GABAA receptor agonist muscimol and GABA also reduced the electrically evoked formation of [3H]citrulline, whereas baclofen was without effect. Bicuculline antagonized the inhibitory effect of GABA. It is concluded that nitrergic myenteric neurons are equipped with GABAA receptors, which mediate inhibition of NO synthesis.  (+info)

Cholinergic blockade inhibits gastro-oesophageal reflux and transient lower oesophageal sphincter relaxation through a central mechanism. (2/496)

BACKGROUND: Atropine, an anticholinergic agent with central and peripheral actions, reduces gastro-oesophageal reflux (GOR) in normal subjects and patients with gastro-oesophageal reflux disease (GORD) by inhibiting the frequency of transient lower oesophageal sphincter relaxation (TLOSR). AIMS: To compare the effect of methscopolamine bromide (MSB), a peripherally acting anticholinergic agent, with atropine on the rate and mechanism of GOR in patients with GORD. METHODS: Oesophageal motility and pH were recorded for 120 minutes in 10 patients with GORD who were studied on three separate occasions. For the first two recording periods, either atropine (15 microg/kg bolus, 4 microg/kg/h infusion) or saline were infused intravenously. MSB (5 mg orally, four times daily) was given for three days prior to the third recording period. RESULTS: Atropine significantly reduced basal LOS pressure (12.6 (0.17) mm Hg to 7.9 (0.17) mm Hg), and the number of TLOSR (8.1 (0.56) to 2.8 (0. 55)) and reflux episodes (7.0 (0.63) to 2.0 (0.43)) (p<0.005 for all comparisons). MSB reduced basal LOS pressure (12.6 (0.17) to 8.7 (0. 15) mm Hg, p<0.005), but had no effect on the frequency of TLOSR (8. 1 (0.56) to 7.5 (0.59)) and reflux episodes (7.0 (0.63) to 4.9 (0. 60)) (p>0.05). CONCLUSION: In contrast to atropine, MSB has no effect on the rate of TLOSR or GOR in patients with GORD. Atropine induced inhibition of TLOSR and GOR is most likely mediated through a central cholinergic blockade.  (+info)

Cardiovascular phenotype and temperature control in mice lacking thyroid hormone receptor-beta or both alpha1 and beta. (3/496)

We have used a telemetry system to record heart rate, body temperature, electrocardiogram (ECG), and locomotor activity in awake, freely moving mice lacking thyroid hormone receptor (TR)-beta or TR-alpha1 and -beta (TR-alpha1/beta). The TR-alpha1/beta-deficient mice had a reduced heart rate compared with wild-type controls. The TR-beta-deficient mice showed an elevated heart rate, which, however, was unresponsive to thyroid hormone treatment regardless of hormonal serum levels. ECG revealed that the TR-beta-deficient mice had a shortened Q-Tend time in contrast to the TR-alpha1/beta-deficient mice, which exhibited prolonged P-Q and Q-Tend times. Mental or pharmacological stimulation of the sympathetic nervous system resulted in a parallel increase in heart rate in all animals. A single injection of a nonselective beta-adrenergic-receptor blocker resulted in a parallel decrease in all mice. The TR-alpha1/beta-deficient mice also had a 0.4 degrees C lower body temperature than controls, whereas no difference was observed in locomotor activity between the different strains of mice. Our present and previous results support the hypothesis that TR-alpha1 has a major role in determining heart rate under baseline conditions and body temperature and that TR-beta mediates a hormone-induced increase in heart rate.  (+info)

Activation of nicotinic acetylcholine receptors patterns network activity in the rodent hippocampus. (4/496)

1. Intracellular and extracellular recordings from area CA3 of rat and mouse hippocampal slices revealed two distinct modes of synchronous network activity in response to continuous application of muscarinic acetylcholine receptor (mAChR) agonists. At low concentrations (e.g. 0.1-1 microM oxotremorine-M), 'burst-mode' activity comprised regular individual AMPA receptor-mediated depolarizing events, each generating several action potentials. At higher concentrations (5-50 microM), 'theta-mode' prevailed in which ordered clusters of depolarizing theta-frequency oscillations occurred. 2. Whilst theta-mode activity was abolished by the mAChR antagonist atropine (5 microM), the nicotinic acetylcholine receptor (nAChR) antagonists tubocurarine (100 microM), mecamylamine (100-500 microM) and dihydro-beta-erythroidine (250 microM) converted this mode of activity to burst-mode. 3. Likewise, disruption of synaptically available ACh using inhibitors of choline uptake (hemicholinium-3; 20-50 microM) or vesicular ACh transport (vesamicol; 50 microM) converted theta-mode into burst-mode activity. 4. Hippocampal slices prepared 2-3 weeks after transection of the primary cholinergic efferent pathway from the medial septum exhibited reduced vesicular ACh transporter immunoreactivity but still supported nAChR-dependent theta-mode activity suggesting that ACh released from this pathway was not critical for the activation of these receptors. 5. In summary, ACh-mediated activation of nAChRs tailors the pattern of network activity into theta-frequency depolarizing episodes as opposed to synchronized individual events at much lower frequencies.  (+info)

Pharmacokinetic and pharmacodynamic characterization of OROS and immediate-release amitriptyline. (5/496)

AIMS: To characterize the pharmacokinetics of amitriptyline and its metabolite nortriptyline following OROS and IR treatments, and to correlate them with anticholinergic side-effects. METHODS: The pharmacokinetics and safety of amitriptyline following administration of an osmotic controlled release tablet (OROS and an immediate release (IR) tablet were evaluated in 14 healthy subjects. In this randomized, open label, three-way crossover feasibility study, the subjects received a single 75 mg OROS tablet, three 25 mg IR tablets administered every 8 h, or 3x25 mg IR tablets administered at nighttime. In each treatment arm serial blood samples were collected for a period of 84 h after dosing. The plasma samples were analysed by gas chromatography for amitriptyline and its metabolite nortriptyline. Anticholinergic effects such as saliva output, visual acuity, and subject-rated drowsiness and dry mouth were measured on a continuous scale during each treatment period. RESULTS: Following dosing with OROS (amitriptyline hydrochloride), the mean maximal plasma amitriptyline concentration Cmax (15.3 ng ml-1 ) was lower and the mean tmax (25.7 h) was longer than that associated with the equivalent IR dose administered at nighttime (26.8 ng ml-1 and 6.3 h, respectively). The bioavailability of amitriptyline following OROS dosing was 95% relative to IR every 8 h dosing, and 89% relative to IR nighttime dosing. The metabolite-to-drug ratios after the three treatment periods were similar, suggesting no change in metabolism between treatments. The relationships between plasma amitriptyline concentration and anticholinergic effects (e.g. reduced saliva weight, dry mouth, and drowsiness) were similar with all three treatments. Of the anticholinergic effects, only decreased saliva weight and dry mouth correlated well with plasma amitriptyline concentrations; drowsiness did not. There was no apparent correlation between anticholinergic effects and the plasma nortriptyline concentration. CONCLUSIONS: The bioavailability of OROS (amitriptyline hydrochloride) was similar to that of the IR treatments and the pharmacokinetics of amitriptyline after OROS dosing may decrease the incidence of anticholinergic effects compared with that seen with nighttime dosing of the IR formulation. Therefore, this controlled-release formulation of amitriptyline may be appropriate for single daily administration.  (+info)

Venous hydrostatic indifference point as a marker of postnatal adaptation to orthostasis in swine. (6/496)

The postulate that venous adaptation assists postural baroreflex regulation by shifting the hydrostatic indifference point (HIP) toward the heart was investigated in eight midazolam-sedated newborn piglets. Whole body head-up (+15, +30, and +45 degrees ) and head-down (-15 and -30 degrees ) tilt provided a physiological range of orthostatic strain. HIP for all positive tilts shifted toward the heart (P < 0.05), +45 degrees HIP shifted most [6.7 +/- 0.3, 5.9 +/- 0.5, and 3.6 +/- 0.3 (SE) cm caudal to right atrium on days 1, 3, and 6, respectively]. HIP for negative tilts (3.0 +/- 0.2 cm caudal to right atrium) did not shift with postnatal age. Euthanasia on day 6 caused 2.1 +/- 0.3-cm caudal displacement of HIP for positive and negative tilts (P < 0.05). HIP proximity to right atrium was not altered by alpha-, beta-adrenoceptor and cholinoceptor blockade on day 5. It is concluded that early HIP migration reflects enhancement of venous pressure control to head-up orthostatic strain. The effect is independent of baroreflex-mediated adrenoceptor and cholinoceptor mechanisms.  (+info)

Blockage of mouse muscle nicotinic receptors by serotonergic compounds. (7/496)

Xenopus laevis oocytes were used to analyse the effects of serotonin (5-hydroxytryptamine, 5-HT) and serotonergic agents on ionic currents elicited by the activation of mammalian muscle nicotinic acetylcholine receptors (AChRs). 5-HT as well as other serotonergic agents, such as ketanserin, 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), methysergide, spiperone, or fluoxetine alone (up to 1 mM), did not elicit membrane currents in Xenopus oocytes expressing AChRs, but they reversibly reduced the current elicited by acetylcholine (ACh-current). Serotonin was applied before, together with or after ACh application, and its effects were examined on desensitizing and non-desensitizing ACh-currents. 5-HT reduced the amplitude and accelerated the desensitization of the desensitizing currents. In contrast, non-desensitizing currents were reduced in amplitude but their time course was not significantly affected. With the same concentration of 5-HT the inhibition was stronger on desensitizing than on non-desensitizing ACh-currents. For example, 100 microM 5-HT reduced the peak of a desensitizing ACh-current to 0. 48 +/- 0.06 (peak current ratio) and after 40 s the current was reduced to a ratio of 0.25 +/- 0.04, whereas a non-desensitizing ACh-current was reduced to a ratio of 0.66 +/- 0.01. All the serotonergic agents tested inhibited the ACh-currents rapidly and reversibly, suggesting that they are acting directly on the AChRs. The half-inhibitory concentration, IC50, of 5-HT acting on non-desensitizing currents elicited by 250 nM ACh was 247 +/- 26 microM and the Hill coefficient was 0.88, suggesting a single site for the interaction of 5-HT with the receptor. It appears that 5-HT inhibits AChRs non-competitively because neither the half-effective concentration of ACh, EC50, for ACh-current nor the Hill coefficient were affected by 5-HT. Furthermore, the extent of inhibition of 5-HT on AChRs did not depend on the nicotinic agonist (suberyldicholine, ACh or nicotine). The inhibition of AChRs by serotonergic agents was voltage-dependent. The electrical distance of the binding site for 5-HT was 0.75, whereas for the other serotonergic agents tested it was 0.22, suggesting that ketanserin, 8-OH-DPAT, methysergide, spiperone and fluoxetine act within the ion channel, but at a site more external than that for 5-HT. These substances inhibited the ACh-current more potently than 5-HT. We conclude that 5-HT and serotonergic agents inhibit, in a non-competitive manner, the ACh-current in muscle AChRs by blocking the open receptor-channel complex. Moreover, 5-HT appears to promote the desensitized state of the receptor when the current is elicited by high ACh concentrations.  (+info)

Acute effect of pretreatment with single conventional dose of salmeterol on dose-response curve to oxitropium bromide in chronic obstructive pulmonary disease. (8/496)

BACKGROUND: An earlier study documented that, in patients with chronic obstructive pulmonary disease (COPD), addition of ipratropium bromide at the clinically recommended dose (40 microg) does not produce any further bronchodilation than that achieved with salmeterol 50 microg alone. However, the dose of ipratropium bromide needed to produce near maximal bronchodilation is several times higher than the customary dosage. The full therapeutic potential of combined salmeterol plus an anticholinergic drug can therefore only be established using doses higher than those currently recommended in the marketing of these agents. A study was undertaken to examine the possible acute effects of higher than conventional doses of an anticholinergic agent on the single dose salmeterol induced bronchodilation in patients with stable and partially reversible COPD. METHODS: Thirty two outpatients received 50 microg salmeterol or placebo. Two hours after inhalation a dose-response curve to inhaled oxitropium bromide (100 microg/puff) or placebo was constructed using one puff, one puff, two puffs, and two puffs-that is, a total cumulative dose of 600 microg oxitropium bromide. Dose increments were given at 20 minute intervals with measurements being made 15 minutes after each dose. On four separate days all patients received one of the following: (1) 50 microg salmeterol + 600 microg oxitropium bromide; (2) 50 microg salmeterol + placebo; (3) placebo + 600 microg oxitropium bromide; (4) placebo + placebo. RESULTS: Salmeterol induced a good bronchodilation (mean increase 0.272 l; 95% CI 0.207 to 0.337) two hours after its inhalation. Oxitropium bromide elicited an evident dose-dependent increase in forced expiratory volume in one second (FEV(1)) and this occurred also after pretreatment with salmeterol with a further mean maximum increase of 0.152 l (95% CI of differences 0.124 to 0.180). CONCLUSIONS: This study shows that acute pretreatment with 50 microg salmeterol does not block the possibility of inducing more bronchodilation with an anticholinergic agent when a higher than normal dosage of the muscarinic antagonist is used.  (+info)

Cholinergic antagonists, also known as anticholinergics or parasympatholytics, are a class of drugs that block the action of the neurotransmitter acetylcholine in the nervous system. They achieve this by binding to and blocking the activation of muscarinic acetylcholine receptors, which are found in various organs throughout the body, including the eyes, lungs, heart, gastrointestinal tract, and urinary bladder.

The blockade of these receptors results in a range of effects depending on the specific organ system involved. For example, cholinergic antagonists can cause mydriasis (dilation of the pupils), cycloplegia (paralysis of the ciliary muscle of the eye), tachycardia (rapid heart rate), reduced gastrointestinal motility and secretion, urinary retention, and respiratory tract smooth muscle relaxation.

Cholinergic antagonists are used in a variety of clinical settings, including the treatment of conditions such as Parkinson's disease, chronic obstructive pulmonary disease (COPD), asthma, gastrointestinal disorders, and urinary incontinence. Some common examples of cholinergic antagonists include atropine, scopolamine, ipratropium, and oxybutynin.

It's important to note that cholinergic antagonists can have significant side effects, particularly when used in high doses or in combination with other medications that affect the nervous system. These side effects can include confusion, memory impairment, hallucinations, delirium, and blurred vision. Therefore, it's essential to use these drugs under the close supervision of a healthcare provider and to follow their instructions carefully.

Scopolamine hydrobromide is a synthetic anticholinergic drug, which means it blocks the action of acetylcholine, a neurotransmitter in the nervous system. It is primarily used for its anti-motion sickness and anti-nausea effects. It can also be used to help with symptoms of Parkinson's disease, such as muscle stiffness and tremors.

In medical settings, scopolamine hydrobromide may be administered as a transdermal patch, which is placed behind the ear to allow for slow release into the body over several days. It can also be given as an injection or taken orally in the form of tablets or liquid solutions.

It's important to note that scopolamine hydrobromide can have various side effects, including dry mouth, blurred vision, dizziness, and drowsiness. It may also cause confusion, especially in older adults, and should be used with caution in patients with glaucoma, enlarged prostate, or certain heart conditions.

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.

Parasympathomimetics are substances or drugs that mimic the actions of the parasympathetic nervous system. The parasympathetic nervous system is one of the two branches of the autonomic nervous system, which regulates involuntary physiological functions. It is responsible for the "rest and digest" response, and its neurotransmitter is acetylcholine.

Parasympathomimetic drugs work by either directly stimulating muscarinic receptors or increasing the availability of acetylcholine in the synaptic cleft. These drugs can have various effects on different organs, depending on the specific receptors they target. Some common effects include decreasing heart rate and contractility, reducing respiratory rate, constricting pupils, increasing glandular secretions (such as saliva and sweat), stimulating digestion, and promoting urination and defecation.

Examples of parasympathomimetic drugs include pilocarpine, which is used to treat dry mouth and glaucoma; bethanechol, which is used to treat urinary retention and neurogenic bladder; and neostigmine, which is used to treat myasthenia gravis and reverse the effects of non-depolarizing muscle relaxants.

Atropine is an anticholinergic drug that blocks the action of the neurotransmitter acetylcholine in the central and peripheral nervous system. It is derived from the belladonna alkaloids, which are found in plants such as deadly nightshade (Atropa belladonna), Jimson weed (Datura stramonium), and Duboisia spp.

In clinical medicine, atropine is used to reduce secretions, increase heart rate, and dilate the pupils. It is often used before surgery to dry up secretions in the mouth, throat, and lungs, and to reduce salivation during the procedure. Atropine is also used to treat certain types of nerve agent and pesticide poisoning, as well as to manage bradycardia (slow heart rate) and hypotension (low blood pressure) caused by beta-blockers or calcium channel blockers.

Atropine can have several side effects, including dry mouth, blurred vision, dizziness, confusion, and difficulty urinating. In high doses, it can cause delirium, hallucinations, and seizures. Atropine should be used with caution in patients with glaucoma, prostatic hypertrophy, or other conditions that may be exacerbated by its anticholinergic effects.

Mecamylamine is a non-competitive antagonist at nicotinic acetylcholine receptors. It is primarily used in the treatment of hypertension (high blood pressure) that is resistant to other medications, although it has been largely replaced by newer drugs with fewer side effects.

Mecamylamine works by blocking the action of acetylcholine, a neurotransmitter that activates nicotinic receptors and plays a role in regulating blood pressure. By blocking these receptors, mecamylamine can help to reduce blood vessel constriction and lower blood pressure.

It is important to note that mecamylamine can have significant side effects, including dry mouth, dizziness, blurred vision, constipation, and difficulty urinating. It may also cause orthostatic hypotension (a sudden drop in blood pressure when standing up), which can increase the risk of falls and fractures in older adults. As a result, mecamylamine is typically used as a last resort in patients with severe hypertension who have not responded to other treatments.

Cholinergic agonists are substances that bind to and activate cholinergic receptors, which are neuroreceptors that respond to the neurotransmitter acetylcholine. These agents can mimic the effects of acetylcholine in the body and are used in medical treatment to produce effects such as pupil constriction, increased gastrointestinal motility, bronchodilation, and improved cognition. Examples of cholinergic agonists include pilocarpine, bethanechol, and donepezil.

Parasympatholytics are a type of medication that blocks the action of the parasympathetic nervous system. The parasympathetic nervous system is responsible for the body's rest and digest response, which includes slowing the heart rate, increasing intestinal and glandular activity, and promoting urination and defecation.

Parasympatholytics work by selectively binding to muscarinic receptors, which are found in various organs throughout the body, including the heart, lungs, and digestive system. By blocking these receptors, parasympatholytics can cause a range of effects, such as an increased heart rate, decreased glandular secretions, and reduced intestinal motility.

Some common examples of parasympatholytics include atropine, scopolamine, and ipratropium. These medications are often used to treat conditions such as bradycardia (slow heart rate), excessive salivation, and gastrointestinal cramping or diarrhea. However, because they can have significant side effects, parasympatholytics are typically used only when necessary and under the close supervision of a healthcare provider.

Quinuclidinyl benzilate is a synthetic chemical compound that acts as a potent anticholinergic drug. Its chemical formula is C18H26N2O2. It is an odorless, white crystalline powder that is slightly soluble in water and more soluble in organic solvents.

Quinuclidinyl benzilate is a deliriant drug, which means it can cause delirium, confusion, hallucinations, and other altered mental states. It works by blocking the action of acetylcholine, a neurotransmitter in the brain that is involved in memory, attention, and perception.

This compound has been used in research as a tool to study the nervous system and has also been explored for its potential use as a chemical weapon. It is classified as a Schedule II controlled substance in the United States due to its high potential for abuse and the risk of severe psychological harm.

Cholinergic receptors are a type of receptor in the body that are activated by the neurotransmitter acetylcholine. Acetylcholine is a chemical that nerve cells use to communicate with each other and with muscles. There are two main types of cholinergic receptors: muscarinic and nicotinic.

Muscarinic receptors are found in the heart, smooth muscle, glands, and the central nervous system. They are activated by muscarine, a type of alkaloid found in certain mushrooms. When muscarinic receptors are activated, they can cause changes in heart rate, blood pressure, and other bodily functions.

Nicotinic receptors are found in the nervous system and at the junction between nerves and muscles (the neuromuscular junction). They are activated by nicotine, a type of alkaloid found in tobacco plants. When nicotinic receptors are activated, they can cause the release of neurotransmitters and the contraction of muscles.

Cholinergic receptors play an important role in many physiological processes, including learning, memory, and movement. They are also targets for drugs used to treat a variety of medical conditions, such as Alzheimer's disease, Parkinson's disease, and myasthenia gravis (a disorder that causes muscle weakness).

Carbachol is a cholinergic agonist, which means it stimulates the parasympathetic nervous system by mimicking the action of acetylcholine, a neurotransmitter that is involved in transmitting signals between nerves and muscles. Carbachol binds to both muscarinic and nicotinic receptors, but its effects are more pronounced on muscarinic receptors.

Carbachol is used in medical treatments to produce miosis (pupil constriction), lower intraocular pressure, and stimulate gastrointestinal motility. It can also be used as a diagnostic tool to test for certain conditions such as Hirschsprung's disease.

Like any medication, carbachol can have side effects, including sweating, salivation, nausea, vomiting, diarrhea, bradycardia (slow heart rate), and bronchoconstriction (narrowing of the airways in the lungs). It should be used with caution and under the supervision of a healthcare professional.

Acetylcholine is a neurotransmitter, a type of chemical messenger that transmits signals across a chemical synapse from one neuron (nerve cell) to another "target" neuron, muscle cell, or gland cell. It is involved in both peripheral and central nervous system functions.

In the peripheral nervous system, acetylcholine acts as a neurotransmitter at the neuromuscular junction, where it transmits signals from motor neurons to activate muscles. Acetylcholine also acts as a neurotransmitter in the autonomic nervous system, where it is involved in both the sympathetic and parasympathetic systems.

In the central nervous system, acetylcholine plays a role in learning, memory, attention, and arousal. Disruptions in cholinergic neurotransmission have been implicated in several neurological disorders, including Alzheimer's disease, Parkinson's disease, and myasthenia gravis.

Acetylcholine is synthesized from choline and acetyl-CoA by the enzyme choline acetyltransferase and is stored in vesicles at the presynaptic terminal of the neuron. When a nerve impulse arrives, the vesicles fuse with the presynaptic membrane, releasing acetylcholine into the synapse. The acetylcholine then binds to receptors on the postsynaptic membrane, triggering a response in the target cell. Acetylcholine is subsequently degraded by the enzyme acetylcholinesterase, which terminates its action and allows for signal transduction to be repeated.

Muscarinic receptors are a type of G protein-coupled receptor (GPCR) that bind to the neurotransmitter acetylcholine. They are found in various organ systems, including the nervous system, cardiovascular system, and respiratory system. Muscarinic receptors are activated by muscarine, a type of alkaloid found in certain mushrooms, and are classified into five subtypes (M1-M5) based on their pharmacological properties and signaling pathways.

Muscarinic receptors play an essential role in regulating various physiological functions, such as heart rate, smooth muscle contraction, glandular secretion, and cognitive processes. Activation of M1, M3, and M5 muscarinic receptors leads to the activation of phospholipase C (PLC) and the production of inositol trisphosphate (IP3) and diacylglycerol (DAG), which increase intracellular calcium levels and activate protein kinase C (PKC). Activation of M2 and M4 muscarinic receptors inhibits adenylyl cyclase, reducing the production of cAMP and modulating ion channel activity.

In summary, muscarinic receptors are a type of GPCR that binds to acetylcholine and regulates various physiological functions in different organ systems. They are classified into five subtypes based on their pharmacological properties and signaling pathways.

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.

An action potential is a brief electrical signal that travels along the membrane of a nerve cell (neuron) or muscle cell. It is initiated by a rapid, localized change in the permeability of the cell membrane to specific ions, such as sodium and potassium, resulting in a rapid influx of sodium ions and a subsequent efflux of potassium ions. This ion movement causes a brief reversal of the electrical potential across the membrane, which is known as depolarization. The action potential then propagates along the cell membrane as a wave, allowing the electrical signal to be transmitted over long distances within the body. Action potentials play a crucial role in the communication and functioning of the nervous system and muscle tissue.

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.

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.

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.

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.

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.

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.

Histamine antagonists, also known as histamine blockers or H1-blockers, are a class of medications that work by blocking the action of histamine, a substance in the body that is released during an allergic reaction. Histamine causes many of the symptoms of an allergic response, such as itching, sneezing, runny nose, and hives. By blocking the effects of histamine, these medications can help to relieve or prevent allergy symptoms.

Histamine antagonists are often used to treat conditions such as hay fever, hives, and other allergic reactions. They may also be used to treat stomach ulcers caused by excessive production of stomach acid. Some examples of histamine antagonists include diphenhydramine (Benadryl), loratadine (Claritin), and famotidine (Pepcid).

It's important to note that while histamine antagonists can be effective at relieving allergy symptoms, they do not cure allergies or prevent the release of histamine. They simply block its effects. It's also worth noting that these medications can have side effects, such as drowsiness, dry mouth, and dizziness, so it's important to follow your healthcare provider's instructions carefully when taking them.

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.

Adenosine A2 receptor antagonists are a class of pharmaceutical compounds that block the action of adenosine at A2 receptors. Adenosine is a naturally occurring molecule in the body that acts as a neurotransmitter and has various physiological effects, including vasodilation and inhibition of heart rate.

Adenosine A2 receptor antagonists work by binding to A2 receptors and preventing adenosine from activating them. This results in the opposite effect of adenosine, leading to vasoconstriction and increased heart rate. These drugs are used for a variety of medical conditions, including asthma, chronic obstructive pulmonary disease (COPD), and heart failure.

Examples of Adenosine A2 receptor antagonists include theophylline, caffeine, and some newer drugs such asistradefylline and tozadenant. These drugs have different pharmacological properties and are used for specific medical conditions. It is important to note that adenosine A2 receptor antagonists can have side effects, including restlessness, insomnia, and gastrointestinal symptoms, and should be used under the guidance of a healthcare professional.

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.

Purinergic P2 receptor antagonists are pharmaceutical agents that block the activity of P2 receptors, which are a type of cell surface receptor that binds extracellular nucleotides such as ATP and ADP. These receptors play important roles in various physiological processes, including neurotransmission, inflammation, and platelet aggregation.

P2 receptors are divided into two main subfamilies: P2X and P2Y. The P2X receptors are ligand-gated ion channels that allow the flow of ions across the cell membrane upon activation, while the P2Y receptors are G protein-coupled receptors that activate intracellular signaling pathways.

Purinergic P2 receptor antagonists are used in clinical medicine to treat various conditions, such as chronic pain, urinary incontinence, and cardiovascular diseases. For example, the P2X3 receptor antagonist gefapixant is being investigated for the treatment of refractory chronic cough, while the P2Y12 receptor antagonists clopidogrel and ticagrelor are used to prevent thrombosis in patients with acute coronary syndrome.

Overall, purinergic P2 receptor antagonists offer a promising therapeutic approach for various diseases by targeting specific receptors involved in pathological processes.

Serotonin 5-HT3 receptor antagonists are a class of medications that work by blocking the serotonin 5-HT3 receptors, which are found in the gastrointestinal tract and the brain. These receptors play a role in regulating nausea and vomiting, among other functions.

When serotonin binds to these receptors, it can trigger a series of events that lead to nausea and vomiting, particularly in response to chemotherapy or surgery. By blocking the 5-HT3 receptors, serotonin cannot bind to them and therefore cannot trigger these events, which helps to reduce nausea and vomiting.

Examples of 5-HT3 receptor antagonists include ondansetron (Zofran), granisetron (Kytril), palonosetron (Aloxi), and dolasetron (Anzemet). These medications are commonly used to prevent and treat nausea and vomiting associated with chemotherapy, radiation therapy, and surgery.

Serotonin 5-HT2 receptor antagonists are a class of drugs that block the action of serotonin, a neurotransmitter, at 5-HT2 receptors. These receptors are found in the central and peripheral nervous systems and are involved in various physiological functions such as mood regulation, cognition, appetite control, and vasoconstriction.

By blocking the action of serotonin at these receptors, serotonin 5-HT2 receptor antagonists can produce a range of effects depending on the specific receptor subtype that they target. For example, some serotonin 5-HT2 receptor antagonists are used to treat psychiatric disorders such as schizophrenia and depression, while others are used to treat migraines or prevent nausea and vomiting associated with chemotherapy.

Some common examples of serotonin 5-HT2 receptor antagonists include risperidone, olanzapine, and paliperidone (used for the treatment of schizophrenia), mirtazapine (used for the treatment of depression), sumatriptan (used for the treatment of migraines), and ondansetron (used to prevent nausea and vomiting).

Adenosine A1 receptor antagonists are a class of pharmaceutical compounds that block the action of adenosine at A1 receptors. Adenosine is a naturally occurring purine nucleoside that acts as a neurotransmitter and modulator of various physiological processes, including cardiovascular function, neuronal excitability, and immune response.

Adenosine exerts its effects by binding to specific receptors on the surface of cells, including A1, A2A, A2B, and A3 receptors. The activation of A1 receptors leads to a variety of physiological responses, such as vasodilation, negative chronotropy (slowing of heart rate), and negative inotropy (reduced contractility) of the heart, as well as inhibition of neurotransmitter release in the brain.

Adenosine A1 receptor antagonists work by binding to and blocking the action of adenosine at A1 receptors, thereby preventing or reducing its effects on these physiological processes. These drugs have been investigated for their potential therapeutic uses in various conditions, such as heart failure, cardiac arrest, and neurological disorders.

Examples of adenosine A1 receptor antagonists include:

* Dipyridamole: a vasodilator used to treat peripheral arterial disease and to prevent blood clots.
* Caffeine: a natural stimulant found in coffee, tea, and chocolate, which acts as a weak A1 receptor antagonist.
* Rolofylline: an experimental drug that has been investigated for its potential use in treating acute ischemic stroke and traumatic brain injury.
* KW-3902: another experimental drug that has been studied for its potential therapeutic effects in heart failure, cardiac arrest, and neurodegenerative disorders.

It's important to note that adenosine A1 receptor antagonists may have side effects and potential risks, and their use should be monitored and managed by healthcare professionals.

Leukotriene antagonists are a class of medications that work by blocking the action of leukotrienes, which are chemicals released by the immune system in response to an allergen or irritant. Leukotrienes cause airway muscles to tighten and inflammation in the airways, leading to symptoms such as wheezing, shortness of breath, and coughing. By blocking the action of leukotrienes, leukotriene antagonists can help relieve these symptoms and improve lung function. These medications are often used to treat asthma and allergic rhinitis (hay fever). Examples of leukotriene antagonists include montelukast, zafirlukast, and pranlukast.

Angiotensin receptor antagonists (ARAs), also known as angiotensin II receptor blockers (ARBs), are a class of medications used to treat hypertension, heart failure, and protect against kidney damage in patients with diabetes. They work by blocking the action of angiotensin II, a potent vasoconstrictor and hormone that increases blood pressure and promotes tissue fibrosis. By blocking the binding of angiotensin II to its receptors, ARAs cause relaxation of blood vessels, decreased sodium and water retention, and reduced cardiac remodeling, ultimately leading to improved cardiovascular function and reduced risk of organ damage. Examples of ARAs include losartan, valsartan, irbesartan, and candesartan.

"Wistar rats" are a strain of albino rats that are widely used in laboratory research. They were developed at the Wistar Institute in Philadelphia, USA, and were first introduced in 1906. Wistar rats are outbred, which means that they are genetically diverse and do not have a fixed set of genetic characteristics like inbred strains.

Wistar rats are commonly used as animal models in biomedical research because of their size, ease of handling, and relatively low cost. They are used in a wide range of research areas, including toxicology, pharmacology, nutrition, cancer, cardiovascular disease, and behavioral studies. Wistar rats are also used in safety testing of drugs, medical devices, and other products.

Wistar rats are typically larger than many other rat strains, with males weighing between 500-700 grams and females weighing between 250-350 grams. They have a lifespan of approximately 2-3 years. Wistar rats are also known for their docile and friendly nature, making them easy to handle and work with in the laboratory setting.

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.

Adrenergic antagonists, also known as beta blockers or sympatholytic drugs, are a class of medications that block the effects of adrenaline and noradrenaline (also known as epinephrine and norepinephrine) on the body. These neurotransmitters are part of the sympathetic nervous system and play a role in the "fight or flight" response, increasing heart rate, blood pressure, and respiratory rate.

Adrenergic antagonists work by binding to beta-adrenergic receptors in the body, preventing the neurotransmitters from activating them. This results in a decrease in heart rate, blood pressure, and respiratory rate. These medications are used to treat various conditions such as hypertension, angina, heart failure, arrhythmias, glaucoma, and anxiety disorders.

There are two types of adrenergic antagonists: beta blockers and alpha blockers. Beta blockers selectively bind to beta-adrenergic receptors, while alpha blockers bind to alpha-adrenergic receptors. Some medications, such as labetalol, have both beta and alpha blocking properties.

It is important to note that adrenergic antagonists can interact with other medications and may cause side effects, so it is essential to use them under the guidance of a healthcare professional.

GABA-A receptor antagonists are pharmacological agents that block the action of gamma-aminobutyric acid (GABA) at GABA-A receptors. GABA is the primary inhibitory neurotransmitter in the central nervous system, and it exerts its effects by binding to GABA-A receptors, which are ligand-gated chloride channels. When GABA binds to these receptors, it opens the chloride channel, leading to an influx of chloride ions into the neuron and hyperpolarization of the membrane, making it less likely to fire.

GABA-A receptor antagonists work by binding to the GABA-A receptor and preventing GABA from binding, thereby blocking the inhibitory effects of GABA. This can lead to increased neuronal excitability and can result in a variety of effects depending on the specific antagonist and the location of the receptors involved.

GABA-A receptor antagonists have been used in research to study the role of GABA in various physiological processes, and some have been investigated as potential therapeutic agents for conditions such as anxiety, depression, and insomnia. However, their use is limited by their potential to cause seizures and other adverse effects due to excessive neuronal excitation. Examples of GABA-A receptor antagonists include picrotoxin, bicuculline, and flumazenil.

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).

Histamine H3 antagonists, also known as inverse agonists, are a class of drugs that block the activity of histamine at the H3 receptor. Histamine is a naturally occurring neurotransmitter and autacoid involved in various physiological functions, including the modulation of wakefulness and arousal, regulation of food intake, and control of blood pressure and fluid balance.

The H3 receptor is primarily located in the central nervous system (CNS) and acts as an auto-receptor on histamine-containing neurons to regulate the release of histamine. By blocking the activity of these receptors, histamine H3 antagonists increase the release of histamine in the CNS, which can lead to increased wakefulness and arousal.

Histamine H3 antagonists have been studied for their potential therapeutic use in various neurological and psychiatric disorders, including narcolepsy, attention deficit hyperactivity disorder (ADHD), and Alzheimer's disease. However, further research is needed to fully understand the clinical benefits and safety of these drugs.

A radioligand assay is a type of in vitro binding assay used in molecular biology and pharmacology to measure the affinity and quantity of a ligand (such as a drug or hormone) to its specific receptor. In this technique, a small amount of a radioactively labeled ligand, also known as a radioligand, is introduced to a sample containing the receptor of interest. The radioligand binds competitively with other unlabeled ligands present in the sample for the same binding site on the receptor. After allowing sufficient time for binding, the reaction is stopped, and the amount of bound radioligand is measured using a technique such as scintillation counting. The data obtained from this assay can be used to determine the dissociation constant (Kd) and maximum binding capacity (Bmax) of the receptor-ligand interaction, which are important parameters in understanding the pharmacological properties of drugs and other ligands.

Serotonin receptors are a type of cell surface receptor that bind to the neurotransmitter serotonin (5-hydroxytryptamine, 5-HT). They are widely distributed throughout the body, including the central and peripheral nervous systems, where they play important roles in regulating various physiological processes such as mood, appetite, sleep, memory, learning, and cognition.

There are seven different classes of serotonin receptors (5-HT1 to 5-HT7), each with multiple subtypes, that exhibit distinct pharmacological properties and signaling mechanisms. These receptors are G protein-coupled receptors (GPCRs) or ligand-gated ion channels, which activate intracellular signaling pathways upon serotonin binding.

Serotonin receptors have been implicated in various neurological and psychiatric disorders, including depression, anxiety, schizophrenia, and migraine. Therefore, selective serotonin receptor agonists or antagonists are used as therapeutic agents for the treatment of these conditions.

Endothelin receptors are a type of G protein-coupled receptor that bind to endothelin, a potent vasoconstrictor peptide. There are two main types of endothelin receptors: ETA and ETB. ETA receptors are found in vascular smooth muscle cells and activate phospholipase C, leading to an increase in intracellular calcium and subsequent contraction of the smooth muscle. ETB receptors are found in both endothelial cells and vascular smooth muscle cells. In endothelial cells, ETB receptor activation leads to the release of nitric oxide and prostacyclin, which cause vasodilation. In vascular smooth muscle cells, ETB receptor activation causes vasoconstriction through a mechanism that is not fully understood.

Endothelin receptors play important roles in regulating blood flow, vascular remodeling, and the development of cardiovascular diseases such as hypertension and heart failure. They are also involved in the regulation of cell growth, differentiation, and apoptosis in various tissues.

Adrenergic beta-2 receptor antagonists, also known as beta-2 adrenergic blockers or beta-2 antagonists, are a class of medications that block the action of epinephrine (adrenaline) and other catecholamines at beta-2 adrenergic receptors. These receptors are found in various tissues throughout the body, including the lungs, blood vessels, and skeletal muscles.

Beta-2 adrenergic receptor antagonists are primarily used to treat respiratory conditions such as asthma and chronic obstructive pulmonary disease (COPD). They work by relaxing the smooth muscle in the airways, which helps to reduce bronchoconstriction and improve breathing.

Some examples of beta-2 adrenergic receptor antagonists include:

* Butoxamine
* ICI 118,551
* Salbutamol (also a partial agonist)
* Terbutaline (also a partial agonist)

It's important to note that while these medications are called "antagonists," some of them can also act as partial agonists at beta-2 receptors, meaning they can both block the action of catecholamines and stimulate the receptor to some degree. This property can make them useful in certain clinical situations, such as during an asthma attack or preterm labor.

N-Methyl-D-Aspartate (NMDA) receptors are a type of ionotropic glutamate receptor, which are found in the membranes of excitatory neurons in the central nervous system. They play a crucial role in synaptic plasticity, learning, and memory processes. NMDA receptors are ligand-gated channels that are permeable to calcium ions (Ca2+) and other cations.

NMDA receptors are composed of four subunits, which can be a combination of NR1, NR2A-D, and NR3A-B subunits. The binding of the neurotransmitter glutamate to the NR2 subunit and glycine to the NR1 subunit leads to the opening of the ion channel and the influx of Ca2+ ions.

NMDA receptors have a unique property in that they require both agonist binding and membrane depolarization for full activation, making them sensitive to changes in the electrical activity of the neuron. This property allows NMDA receptors to act as coincidence detectors, playing a critical role in synaptic plasticity and learning.

Abnormal functioning of NMDA receptors has been implicated in various neurological disorders, including Alzheimer's disease, Parkinson's disease, epilepsy, and chronic pain. Therefore, NMDA receptors are a common target for drug development in the treatment of these conditions.

"Competitive binding" is a term used in pharmacology and biochemistry to describe the behavior of two or more molecules (ligands) competing for the same binding site on a target protein or receptor. In this context, "binding" refers to the physical interaction between a ligand and its target.

When a ligand binds to a receptor, it can alter the receptor's function, either activating or inhibiting it. If multiple ligands compete for the same binding site, they will compete to bind to the receptor. The ability of each ligand to bind to the receptor is influenced by its affinity for the receptor, which is a measure of how strongly and specifically the ligand binds to the receptor.

In competitive binding, if one ligand is present in high concentrations, it can prevent other ligands with lower affinity from binding to the receptor. This is because the higher-affinity ligand will have a greater probability of occupying the binding site and blocking access to the other ligands. The competition between ligands can be described mathematically using equations such as the Langmuir isotherm, which describes the relationship between the concentration of ligand and the fraction of receptors that are occupied by the ligand.

Competitive binding is an important concept in drug development, as it can be used to predict how different drugs will interact with their targets and how they may affect each other's activity. By understanding the competitive binding properties of a drug, researchers can optimize its dosage and delivery to maximize its therapeutic effect while minimizing unwanted side effects.

Serotonin 5-HT1 receptor antagonists are a class of pharmaceutical drugs that block the activation of serotonin 5-HT1 receptors. Serotonin, also known as 5-hydroxytryptamine (5-HT), is a neurotransmitter that plays a role in various physiological functions, including mood regulation, appetite control, and sensory perception. The 5-HT1 receptor family includes several subtypes (5-HT1A, 5-HT1B, 5-HT1D, 5-HT1E, and 5-HT1F) that are widely distributed throughout the central and peripheral nervous systems.

When serotonin binds to these receptors, it triggers a series of intracellular signaling events that can have excitatory or inhibitory effects on neuronal activity. By blocking the interaction between serotonin and 5-HT1 receptors, antagonists modulate the downstream consequences of receptor activation.

Serotonin 5-HT1 receptor antagonists are used in various clinical contexts to treat or manage a range of conditions:

1. Migraine prevention: Some 5-HT1B/1D receptor antagonists, such as sumatriptan and rizatriptan, are highly effective in aborting migraine attacks by constricting dilated cranial blood vessels and reducing the release of pro-inflammatory neuropeptides.
2. Nausea and vomiting: Certain 5-HT3 receptor antagonists, like ondansetron and granisetron, are used to prevent chemotherapy-induced nausea and vomiting by blocking the activation of emetic circuits in the brainstem.
3. Psychiatric disorders: Although not widely used, some 5-HT1A receptor antagonists have shown promise in treating depression and anxiety disorders due to their ability to modulate serotonergic neurotransmission.
4. Neuroprotection: Preclinical studies suggest that 5-HT1A receptor agonists may have neuroprotective effects in various neurological conditions, such as Parkinson's disease and stroke. However, further research is needed to establish their clinical utility.

In summary, serotonin 5-HT1 receptor antagonists are a diverse group of medications with applications in migraine prevention, nausea and vomiting management, psychiatric disorders, and potential neuroprotection. Their unique pharmacological profiles enable them to target specific pathophysiological mechanisms underlying various conditions, making them valuable tools in modern therapeutics.

Calcium channel blockers (CCBs) are a class of medications that work by inhibiting the influx of calcium ions into cardiac and smooth muscle cells. This action leads to relaxation of the muscles, particularly in the blood vessels, resulting in decreased peripheral resistance and reduced blood pressure. Calcium channel blockers also have anti-arrhythmic effects and are used in the management of various cardiovascular conditions such as hypertension, angina, and certain types of arrhythmias.

Calcium channel blockers can be further classified into two main categories based on their chemical structure: dihydropyridines (e.g., nifedipine, amlodipine) and non-dihydropyridines (e.g., verapamil, diltiazem). Dihydropyridines are more selective for vascular smooth muscle and have a greater effect on blood pressure than heart rate or conduction. Non-dihydropyridines have a more significant impact on cardiac conduction and contractility, in addition to their vasodilatory effects.

It is important to note that calcium channel blockers may interact with other medications and should be used under the guidance of a healthcare professional. Potential side effects include dizziness, headache, constipation, and peripheral edema.

Dizocilpine maleate is a chemical compound that is commonly known as an N-methyl-D-aspartate (NMDA) receptor antagonist. It is primarily used in research settings to study the role of NMDA receptors in various physiological processes, including learning and memory.

The chemical formula for dizocilpine maleate is C16H24Cl2N2O4·C4H4O4. The compound is a white crystalline powder that is soluble in water and alcohol. It has potent psychoactive effects and has been investigated as a potential treatment for various neurological and psychiatric disorders, although it has not been approved for clinical use.

Dizocilpine maleate works by blocking the action of glutamate, a neurotransmitter that plays a key role in learning and memory, at NMDA receptors in the brain. By doing so, it can alter various cognitive processes and has been shown to have anticonvulsant, analgesic, and neuroprotective effects in animal studies. However, its use is associated with significant side effects, including hallucinations, delusions, and memory impairment, which have limited its development as a therapeutic agent.

I must clarify that the term "Guinea Pigs" is not typically used in medical definitions. However, in colloquial or informal language, it may refer to people who are used as the first to try out a new medical treatment or drug. This is known as being a "test subject" or "in a clinical trial."

In the field of scientific research, particularly in studies involving animals, guinea pigs are small rodents that are often used as experimental subjects due to their size, cost-effectiveness, and ease of handling. They are not actually pigs from Guinea, despite their name's origins being unclear. However, they do not exactly fit the description of being used in human medical experiments.

I'm sorry for any confusion, but "Pyridines" is not a medical term. It is a chemical term that refers to a class of organic compounds with the chemical structure of a six-membered ring containing one nitrogen atom and five carbon atoms (heterocyclic aromatic compound).

In a biological or medical context, pyridine derivatives can be found in various natural and synthetic substances. For example, some medications contain pyridine rings as part of their chemical structure. However, "Pyridines" itself is not a medical term or condition.

Adenosine A3 receptor antagonists are a class of pharmaceutical compounds that block the action of adenosine at the A3 receptor. Adenosine is a naturally occurring purine nucleoside that acts as a neurotransmitter and modulator of various physiological processes, including cardiovascular function, immune response, and neuromodulation.

The A3 receptor is one of four subtypes of adenosine receptors (A1, A2A, A2B, and A3) that are widely distributed throughout the body. The activation of A3 receptors has been implicated in a variety of pathological conditions, including inflammation, pain, ischemia-reperfusion injury, and cancer.

Adenosine A3 receptor antagonists have been investigated as potential therapeutic agents for various diseases, such as rheumatoid arthritis, chronic pain, ischemic heart disease, and cancer. These compounds work by preventing the binding of adenosine to its receptor, thereby blocking its downstream signaling pathways.

Some examples of Adenosine A3 receptor antagonists include:

* MRS1523
* MRE-2029F20
* LUF5834
* VUF5574
* OT-7962

It is important to note that while Adenosine A3 receptor antagonists have shown promise in preclinical studies, their clinical efficacy and safety profile are still being evaluated in ongoing research.

Endothelin A (ETA) receptor is a type of G protein-coupled receptor that is activated by the peptide hormone endothelin-1, endothelin-2, and endothelin-3. It is widely expressed in various tissues and organs, including vascular smooth muscle cells, cardiac myocytes, fibroblasts, and kidney cells. Activation of ETA receptor leads to vasoconstriction, increased cell proliferation, and fibrosis, which contribute to the development of hypertension, heart failure, and chronic kidney disease. Therefore, ETA receptor antagonists have been developed as potential therapeutic agents for these conditions.

Benzazepines are a class of heterocyclic compounds that contain a benzene fused to a diazepine ring. In the context of pharmaceuticals, benzazepines refer to a group of drugs with various therapeutic uses, such as antipsychotics and antidepressants. Some examples of benzazepine-derived drugs include clozapine, olanzapine, and loxoprofen. These drugs have complex mechanisms of action, often involving multiple receptor systems in the brain.

Biphenyl compounds, also known as diphenyls, are a class of organic compounds consisting of two benzene rings linked by a single carbon-carbon bond. The chemical structure of biphenyl compounds can be represented as C6H5-C6H5. These compounds are widely used in the industrial sector, including as intermediates in the synthesis of other chemicals, as solvents, and in the production of plastics and dyes. Some biphenyl compounds also have biological activity and can be found in natural products. For example, some plant-derived compounds that belong to this class have been shown to have anti-inflammatory, antioxidant, and anticancer properties.

Estrogen antagonists, also known as antiestrogens, are a class of drugs that block the effects of estrogen in the body. They work by binding to estrogen receptors and preventing the natural estrogen from attaching to them. This results in the inhibition of estrogen-mediated activities in various tissues, including breast and uterine tissue.

There are two main types of estrogen antagonists: selective estrogen receptor modulators (SERMs) and pure estrogen receptor downregulators (PERDS), also known as estrogen receptor downregulators (ERDs). SERMs, such as tamoxifen and raloxifene, can act as estrogen agonists or antagonists depending on the tissue type. For example, they may block the effects of estrogen in breast tissue while acting as an estrogen agonist in bone tissue, helping to prevent osteoporosis.

PERDS, such as fulvestrant, are pure estrogen receptor antagonists and do not have any estrogen-like activity. They are used primarily for the treatment of hormone receptor-positive breast cancer in postmenopausal women.

Overall, estrogen antagonists play an important role in the management of hormone receptor-positive breast cancer and other conditions where inhibiting estrogen activity is beneficial.

Naltrexone is a medication that is primarily used to manage alcohol dependence and opioid dependence. It works by blocking the effects of opioids and alcohol on the brain, reducing the euphoric feelings and cravings associated with their use. Naltrexone comes in the form of a tablet that is taken orally, and it has no potential for abuse or dependence.

Medically, naltrexone is classified as an opioid antagonist, which means that it binds to opioid receptors in the brain without activating them, thereby blocking the effects of opioids such as heroin, morphine, and oxycodone. It also reduces the rewarding effects of alcohol by blocking the release of endorphins, which are natural chemicals in the brain that produce feelings of pleasure.

Naltrexone is often used as part of a comprehensive treatment program for addiction, along with counseling, behavioral therapy, and support groups. It can help individuals maintain abstinence from opioids or alcohol by reducing cravings and preventing relapse. Naltrexone is generally safe and well-tolerated, but it may cause side effects such as nausea, headache, dizziness, and fatigue in some people.

It's important to note that naltrexone should only be used under the supervision of a healthcare provider, and it is not recommended for individuals who are currently taking opioids or who have recently stopped using them, as it can cause withdrawal symptoms. Additionally, naltrexone may interact with other medications, so it's important to inform your healthcare provider of all medications you are taking before starting naltrexone therapy.

A drug interaction is the effect of combining two or more drugs, or a drug and another substance (such as food or alcohol), which can alter the effectiveness or side effects of one or both of the substances. These interactions can be categorized as follows:

1. Pharmacodynamic interactions: These occur when two or more drugs act on the same target organ or receptor, leading to an additive, synergistic, or antagonistic effect. For example, taking a sedative and an antihistamine together can result in increased drowsiness due to their combined depressant effects on the central nervous system.
2. Pharmacokinetic interactions: These occur when one drug affects the absorption, distribution, metabolism, or excretion of another drug. For example, taking certain antibiotics with grapefruit juice can increase the concentration of the antibiotic in the bloodstream, leading to potential toxicity.
3. Food-drug interactions: Some drugs may interact with specific foods, affecting their absorption, metabolism, or excretion. An example is the interaction between warfarin (a blood thinner) and green leafy vegetables, which can increase the risk of bleeding due to enhanced vitamin K absorption from the vegetables.
4. Drug-herb interactions: Some herbal supplements may interact with medications, leading to altered drug levels or increased side effects. For instance, St. John's Wort can decrease the effectiveness of certain antidepressants and oral contraceptives by inducing their metabolism.
5. Drug-alcohol interactions: Alcohol can interact with various medications, causing additive sedative effects, impaired judgment, or increased risk of liver damage. For example, combining alcohol with benzodiazepines or opioids can lead to dangerous levels of sedation and respiratory depression.

It is essential for healthcare providers and patients to be aware of potential drug interactions to minimize adverse effects and optimize treatment outcomes.

Piperazines are a class of heterocyclic organic compounds that contain a seven-membered ring with two nitrogen atoms at positions 1 and 4. They have the molecular formula N-NRR' where R and R' can be alkyl or aryl groups. Piperazines have a wide range of uses in pharmaceuticals, agrochemicals, and as building blocks in organic synthesis.

In a medical context, piperazines are used in the manufacture of various drugs, including some antipsychotics, antidepressants, antihistamines, and anti-worm medications. For example, the antipsychotic drug trifluoperazine and the antidepressant drug nefazodone both contain a piperazine ring in their chemical structure.

However, it's important to note that some piperazines are also used as recreational drugs due to their stimulant and euphoric effects. These include compounds such as BZP (benzylpiperazine) and TFMPP (trifluoromethylphenylpiperazine), which have been linked to serious health risks, including addiction, seizures, and death. Therefore, the use of these substances should be avoided.

Sulfonamides are a group of synthetic antibacterial drugs that contain the sulfonamide group (SO2NH2) in their chemical structure. They are bacteriostatic agents, meaning they inhibit bacterial growth rather than killing them outright. Sulfonamides work by preventing the bacteria from synthesizing folic acid, which is essential for their survival.

The first sulfonamide drug was introduced in the 1930s and since then, many different sulfonamides have been developed with varying chemical structures and pharmacological properties. They are used to treat a wide range of bacterial infections, including urinary tract infections, respiratory tract infections, skin and soft tissue infections, and ear infections.

Some common sulfonamide drugs include sulfisoxazole, sulfamethoxazole, and trimethoprim-sulfamethoxazole (a combination of a sulfonamide and another antibiotic called trimethoprim). While sulfonamides are generally safe and effective when used as directed, they can cause side effects such as rash, nausea, and allergic reactions. It is important to follow the prescribing physician's instructions carefully and to report any unusual symptoms or side effects promptly.

"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.

Naloxone is a medication used to reverse the effects of opioids, both illicit and prescription. It works by blocking the action of opioids on the brain and restoring breathing in cases where opioids have caused depressed respirations. Common brand names for naloxone include Narcan and Evzio.

Naloxone is an opioid antagonist, meaning that it binds to opioid receptors in the body without activating them, effectively blocking the effects of opioids already present at these sites. It has no effect in people who have not taken opioids and does not reverse the effects of other sedatives or substances.

Naloxone can be administered via intranasal, intramuscular, intravenous, or subcutaneous routes. The onset of action varies depending on the route of administration but generally ranges from 1 to 5 minutes when given intravenously and up to 10-15 minutes with other methods.

The duration of naloxone's effects is usually shorter than that of most opioids, so multiple doses or a continuous infusion may be necessary in severe cases to maintain reversal of opioid toxicity. Naloxone has been used successfully in emergency situations to treat opioid overdoses and has saved many lives.

It is important to note that naloxone does not reverse the effects of other substances or address the underlying causes of addiction, so it should be used as part of a comprehensive treatment plan for individuals struggling with opioid use disorders.

Serotonin receptor agonists are a class of medications that bind to and activate serotonin receptors in the body, mimicking the effects of the neurotransmitter serotonin. These drugs can have various effects depending on which specific serotonin receptors they act upon. Some serotonin receptor agonists are used to treat conditions such as migraines, cluster headaches, and Parkinson's disease, while others may be used to stimulate appetite or reduce anxiety. It is important to note that some serotonin receptor agonists can have serious side effects, particularly when taken in combination with other medications that affect serotonin levels, such as selective serotonin reuptake inhibitors (SSRIs) or monoamine oxidase inhibitors (MAOIs). This can lead to a condition called serotonin syndrome, which is characterized by symptoms such as agitation, confusion, rapid heart rate, high blood pressure, and muscle stiffness.

Trospium is a non-selective muscarinic antagonist that does not cross into the CNS and reduces peripheral cholinergic side ... "Muscarinic Cholinergic Receptor Agonist and Peripheral Antagonist for Schizophrenia". The New England Journal of Medicine. 384 ... However, cholinergic-mediated side effects prevented advancement of xanomeline into phase 3 trials. Xanomeline was licensed to ... an M1/M4 preferring muscarinic cholinergic receptor agonist, produces antipsychotic-like activity in rats and mice". ...
"Muscarinic Cholinergic Receptor Agonist and Peripheral Antagonist for Schizophrenia". The New England Journal of Medicine. 384 ... Trospium is a non-CNS penetrant non-selective muscarinic antagonist to quell peripheral muscarinic agonist-dependent side ... Further development was enabled through a novel co-formulation strategy with the peripherally restricted muscarinic antagonist ... May 2000). "Xanomeline, an M(1)/M(4) preferring muscarinic cholinergic receptor agonist, produces antipsychotic-like activity ...
Cholinergic Agonists and Muscarinic Receptor Antagonists. St. Louis, Missouri: Elsevier. pp. 82-97. ISBN 978-0-323-39307-2. ... β-receptor antagonist) Metoprolol (β-receptor antagonist) Atenolol (β1 antagonist) Prazosin (α1 antagonist) Oxymetazoline ( ... For a cholinergic agent, the following criteria describe the structure activity relationship: Ing's Rule of 5: there should be ... A parasympathomimetic drug, sometimes called a cholinomimetic drug or cholinergic receptor stimulating agent, is a substance ...
Antimuscarinic agents are muscarinic antagonists and they bind to muscarinic cholinergic receptors postsynaptically without ... in synapses of the cholinergic nervous system. They block acetylcholine from binding to cholinergic receptors, namely the ... Cholinergic blocking drugs are a group of drugs that block the action of acetylcholine (ACh), a neurotransmitter, ... According to their site of actions, cholinergic blocking drugs can be classified into two general types - antimuscarinic and ...
Stanton T, Bolden-Watson C, Cusack B, Richelson E (1993). "Antagonism of the five cloned human muscarinic cholinergic receptors ... Certain muscarinic antagonists can be classified into either long-acting muscarinic receptor antagonists (LAMAs) or short- ... Effects of Muscarinic Antagonist Atropine (Muscarinic Receptor Antagonist), Cardiovascular Pharmacology Concepts, Richard E. ... and muscarinic receptor antagonists work to prevent this transmission from occurring. Notably, muscarinic antagonists reduce ...
... is a competitive cholinergic receptor antagonist, selective for the M3 receptor subtype. The binding of ... July 2001). "Effects of YM905, a Novel Muscarinic M3-Receptor Antagonist, on Experimental Models of Bowel Dysfunction In Vivo ... Muscarinic antagonists, 3-Quinuclidinyl esters, Wikipedia medicine articles ready to translate, Tetrahydroisoquinolines). ...
Henderson CG, Ungar A (April 1978). "Effect of cholinergic antagonists on sympathetic ganglionic transmission of vasomotor ... In insects, the cholinergic system is limited to the central nervous system. The nicotinic receptors are considered cholinergic ... Nicotinic antagonists that block the receptor include mecamylamine, dihydro-β-erythroidine, and hexamethonium. In muscle-type ... Thus, for example, nicotinic receptor antagonists interfere with the baroreflex that normally corrects changes in blood ...
... a Cholinergic antagonist, to this end, she observed instead a change in the cells' spontaneous synaptic activity. This activity ... This was unusual, as the Aplysia response she was researching was cholinergic and was not expected to change with the addition ... From this data Kehoe determined that both the adrenergic and cholinergic responses she observed involved the same receptor. She ...
... prolonged REM cycles can be reduced by using a cholinergic antagonist (atropine). One study found that auditory stimulation ... Within the pedunculopontine tegmentum region, in the brainstem, reduced GABA imbibition of cholinergic neurons acts again in ... This change is mediated by cholinergic neurons as stressed animals' ... stressors act similarly by inhibiting the cholinergic reduction of REM sleep. Chronic mildly stressed rats display a reduction ...
"Synthesis and autoradiographic localization of muscarinic cholinergic antagonist (+)N-[11C]methyl-3-piperidyl benzilate as a ... Muscarinic antagonists, Benzilate esters, Piperidines, Tertiary alcohols, All stub articles, Hallucinogen stubs). ...
Caffeine also has an excitatory effect on mesocortical cholinergic neurons by acting as an antagonist on adenosine receptors ... The actions of A1 and A2A receptors oppose each other but are both inhibited by caffeine due to its function as an antagonist. ... Caffeine has been proven to act as an antagonist on adenosine receptors, which acts as a stimulant and therefore fulfills this ... Caffeine acts as an antagonist of adenosine A1 and A2A receptors. Adenosine is a normal neuromodulator that activates adenosine ...
5-HT7 Autoreceptor Catecholamines Cholinergic agonists and antagonists Heteroreceptor Imidazoline receptor Neuromuscular ... β3 Cholinergic: Muscarinic: M1, M2, M3, M4, M5 Nicotinic: muscle, neuronal (α-bungarotoxin-insensitive), neuronal (α- ...
... can be broadly categorized as a cholinergic physiological antagonist, because it reduces the apparent activity of ... February 2013). "Inhibition of cholinergic signaling causes apoptosis in human bronchioalveolar carcinoma" (PDF). Cancer ... cholinergic neurons, but does not act at the postsynaptic ACh receptor. Vesamicol causes a non-competitive and reversible block ...
The study showed that a pyridine moiety that is part of the telithromycin molecule acts as an antagonist on cholinergic ... do not contain the pyridine moiety and do not antagonize these cholinergic receptors significantly. Telithromycin prevents ...
5-alpha-reductase inhibitor ACE inhibitor Alpha-adrenergic agonist Angiotensin II receptor antagonist Beta blocker Cholinergic ... For receptors, these activities include agonist, antagonist, inverse agonist, or modulator. Enzyme target mechanisms include ...
... a shorter-acting cholinergic antagonist) or phenylephrine (an α-adrenergic agonist) is preferred as an aid to ophthalmic ...
... 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. ... As all cholinergic fibers contain high concentrations of ACh and AChE at their terminals, inhibition of AChE can impair their ... Cholinergic nerves play an important role in the normal function of the central nervous, endocrine, neuromuscular, ...
They can also block noradrenergic, cholinergic, and histaminergic activity. Benperidol binds D2 and some serotonin receptors. ... A dopamine antagonist, also known as an anti-dopaminergic and a dopamine receptor antagonist (DRA), is a type of drug which ... Several other dopamine antagonists are antiemetics used in the treatment of nausea and vomiting. Dopamine receptors are all G ... Dopamine+antagonists at the U.S. National Library of Medicine Medical Subject Headings (MeSH) (CS1: long volume value, Articles ...
"In vivo muscarinic cholinergic mediated effects of Lu 25-109, a M1 agonist and M2/M3 antagonist in vitro". Psychopharmacology. ... Alvameline (Lu 25-109) is a M1 receptor agonist and M2/M3 receptor antagonist that was under investigation for the treatment of ...
... quetiapine Cholinergic agents such as acetylcholine Acetylcholinesterase inhibitors Serotonin antagonists, such as Ondansetron ...
Some different classes of GABAergic drugs include agonists, antagonists, modulators, reuptake inhibitors and enzymes. ... Adenosinergic Adrenergic Cannabinoidergic Cholinergic Dopaminergic Glycinergic Histaminergic Melatonergic Monoaminergic ...
5-HT3 antagonists (e.g. ondansetron) Dopamine antagonists (e.g. domperidone) Anti-cholinergic antihistamines (e.g. ... when an antagonist (e.g., naloxone) or an agonist-antagonist (e.g., pentazocine) is administered. Physical dependence is a ... Dezocine-agonist/antagonist Pentazocine-agonist/antagonist Phenazocine Buprenorphine-partial agonist Dihydroetorphine Etorphine ... These competitive antagonists bind to the opioid receptors with higher affinity than agonists but do not activate the receptors ...
Adenosinergic Adrenergic Cannabinoidergic Cholinergic Dopaminergic GABAergic Glycinergic Histaminergic Monoaminergic ... Examples include melatonin receptor agonists and melatonin receptor antagonists. ...
Like the tropanes, it acts on cholinergic neurons, but with the opposite effect (it is an agonist as opposed to an antagonist ... They can reverse cholinergic poisoning, which can be caused by overexposure to organophosphate insecticides and chemical ...
Adenosinergic Adrenergic Cannabinoidergic Cholinergic Dopaminergic GABAergic Histaminergic Melatonergic Monoaminergic ... Examples include glycine receptor agonists, glycine receptor antagonists, and glycine reuptake inhibitors. ...
... that are much more selective for peripheral H1 receptors as opposed to the central nervous system H1 receptors and cholinergic ... H2-receptor antagonist H3-receptor antagonist Leurs R, Church MK, Taglialatela M (April 2002). "H1-antihistamines: inverse ... H1 antagonists, also called H1 blockers, are a class of medications that block the action of histamine at the H1 receptor, ... Virtually all H1-antihistamines function as inverse agonists at the histamine H1-receptor, as opposed to neutral antagonists, ...
It is a selective M1 muscarinic acetylcholine receptor antagonist. Benzatropine partially blocks cholinergic activity in the ... Drugs that decrease cholinergic transmission may impair storage of new information into long-term memory. Anticholinergic ... "Preclinical efficacy of N-substituted benztropine analogs as antagonists of methamphetamine self-administration in rats". The ...
... cholinergic and GABA). Degeneration of histaminergic neurons in AD doesn't correlate to H3R expressions since a large portion ... H1-receptor antagonist H2-receptor antagonist Yoneyama H, Shimoda A, Araki L, et al. (March 2008). "Efficient approaches to S- ... A general structural pattern that is necessary for the antagonist affinity for H3R has been described. An H3R antagonist needs ... Consequently, unlike the H1 antagonist antihistamines which are sedating, H3 antagonists have stimulant and nootropic effects, ...
Muscarinic agonist Muscarinic antagonist Nicotinic acetylcholine receptor Nicotinic agonist Nicotinic antagonist Vagal escape ... Very few parts of the sympathetic system use cholinergic receptors. In sweat glands the receptors are of the muscarinic type. ... For example, the drug pirenzepine is a muscarinic antagonist (decreases the effect of ACh), which is much more potent at M1 ... ISBN 978-81-8061-187-2. if nothing else mentioned in table Smith RS, Araneda RC (December 2010). "Cholinergic modulation of ...
"Reversal of a cholinergic-induced deficit in a rodent model of recognition memory by the selective 5-HT6 receptor antagonist, ... receptor antagonist Ro 04-6790 attenuates psychotomimetic effects of the NMDA receptor antagonist MK-801". Behavioural Brain ... It acts as a potent and selective receptor antagonist for the 5-HT6 serotonin receptor subtype, with little or no affinity at ... receptor antagonist, Ro 04-6790, in the Novel Object Discrimination task". Psychopharmacology. 202 (1-3): 111-23. doi:10.1007/ ...
Ellis, J.L.; Farmer, S.G. 1988: Effects of vip antagonists and vip and phi antisera on non adrenergic non cholinergic tracheal ... Sanghvi, I.S. 1967: Effects of cholinergic and adrenergic agents and their antagonists at the neuromuscular junction of the cat ... Dren, A.T.; Domino, E.F. 1968: Cholinergic and adrenergic activating agents as antagonists of the EEG effects of hemicholinium- ... Narioka, J.; Ohashi, Y. 2007: Effects of adrenergic and cholinergic antagonists on diameter of nasolacrimal drainage system ...
Founded in 2006, Affinity Biosciences is committed to providing the best quality primary antibody|secondary antibody|peptide|reagent kit|inhibitor|antibody customization|antibody query for the world, the phosphorylated antibody has become the name card of the affinity brand. - Affinity Biosciences,Cell Signal Transduction Research
... is used as a bronchodilator in the management of cholinergic-mediated bronchospasm associated with chronic obstructive ...
Antihistamines (histamine1-receptor antagonists): Terfenadine, astemizole, diphenhydramine, hydroxyzine [9] * Cholinergic ... Beta-adrenergic antagonists at maximally tolerated doses are used as a first-line long-term therapy in congenital long QT ...
Cholinergic Antagonists / therapeutic use * Drug Therapy, Combination * Exercise Therapy * Forced Expiratory Volume ...
Keywords: Adrenergic alpha-antagonists; Cholinergic antagonists; Ureteral diseases; Urinary catheterization. Publication types ...
Alpha2-adrenergic receptor antagonists. Class Summary. Reduce IOP.. Apraclonidine HCl (Iopidine). Decreases IOP by reducing ... Cholinergic parasympathomimetic agents. Class Summary. Pilocarpine is a miotic agent. It reduces IOP, decreases pupillary ...
Antihistamines (histamine1-receptor antagonists): Terfenadine, astemizole, diphenhydramine, hydroxyzine [9] * Cholinergic ... Beta-adrenergic antagonists at maximally tolerated doses are used as a first-line long-term therapy in congenital long QT ...
Cholinergic antagonists. Cystic fibrosis/therapy. Lung volume measurements. Plethysmography. Respiratory function tests. ...
Trospium is a non-selective muscarinic antagonist that does not cross into the CNS and reduces peripheral cholinergic side ... "Muscarinic Cholinergic Receptor Agonist and Peripheral Antagonist for Schizophrenia". The New England Journal of Medicine. 384 ... However, cholinergic-mediated side effects prevented advancement of xanomeline into phase 3 trials. Xanomeline was licensed to ... an M1/M4 preferring muscarinic cholinergic receptor agonist, produces antipsychotic-like activity in rats and mice". ...
Any cholinergic antagonist that inhibits the actions of the parasympathetic nervous system. The major group of drugs used ... Any cholinergic antagonist that inhibits the actions of the parasympathetic nervous system. The major group of drugs used ... therapeutically for this purpose is the muscarinic antagonists.. neuroprotective agent Any compound that can be used for the ... therapeutically for this purpose is the muscarinic antagonists.. mouse metabolite Any mammalian metabolite produced during a ...
Cholinergic Receptors Antagonists - Belladonna alkaloids. Derived from plants; Atropa belladonna (the deadly night shade) ... ... Cholinergic Receptor Drugs - Belladonna Alkaloids. Atropine, scopolamine. Isolated from plants ... Belladonna Alkaloids. ...
239000000812 cholinergic antagonist Substances 0.000 description 2 * 229960001265 ciclosporin Drugs 0.000 description 2 ... Pharmacologically, ketamine classified as an NMDA antagonist. The present inventor used this in thousands of case as ...
Clozapine also acts as an antagonist at adrenergic, cholinergic, histaminergic and other dopaminergic and serotonergic ... 5.20 Recurrence of Psychosis and Cholinergic Rebound after Abrupt Discontinuation of Clozapine 6 ADVERSE REACTIONS 6.1 Clinical ... Recurrence of Psychosis and Cholinergic Rebound after Abrupt Discontinuation [see Warnings and Precautions (5.20)] ... Monitor all patients carefully for the recurrence of psychotic symptoms and symptoms related to cholinergic rebound such as ...
Drugs approved for other indications, such as cholinergic compounds or NMDA receptor antagonists, should be tested for their ... Theres increasing interest in the cholinergic hypothesis, and the study of cholinergic drugs in the prevention and treatment ... Cholinergic deficiency can interfere with anti-inflammatory pathways, and this sequence has been proposed as a possible ... an Alzheimers drug that increases cholinergic activity, for treatment of delirium, but it didnt work; he added that European ...
Keywords: Reaction time, cholinergic antagonists, oxybutynin, tolterodine DOI: 10.3233/NRE-2010-0590 ...
Therapy for exposed patients should be guided by clinical toxicity and includes atropine, a muscarinic cholinergic antagonist. ... Although cholinergic toxicity is common after exposure to anticholinesterase pesticides, cholinergic symptoms are unexpected in ... Of these, 20 presented to EDs with signs and symptoms consistent with cholinergic toxidrome, although the specific findings for ... who had manifestations consistent with the cholinergic toxidrome, which is not characteristic of poisoning by the anticoagulant ...
L 4: Cholinergic antagonists por College of Pharmacy University of Sulaimani. L 4: Cholinergic antagonists. College of Pharmacy ...
... or a reduced sensitivity to cholinergic antagonists. Using a dilute agonist such as pilocarpine 0.0625% (Idiaquez et al., 1994 ... Central cholinergic depletion results in upregulation of peripheral receptors and thus hypersensitivity to cholinergic agonists ... Given that cholinergic neurotransmission is altered in AD, this might result in a change in the pupils response to light. ... As impaired nerve growth factor retrograde transport has been linked to cholinergic neurodegeneration in AD (Aloe et al., 2012 ...
Effects of acute administration of nicotinic and muscarinic cholinergic agonists and antagonists on performance in different ...
Cholinergic Antagonists. Posted on February 10, 2022. Cholinergic Antagonists. This is nearly a five hour stream in which Dr ... Posted in KevinTagged Acetylcholine, Cholinergic Antagonists, Dr Kevin McCairn, Neuroscience, neurotoxins, nicotine, sarin, ... A nicotinic antagonist is a type of anticholinergic drug that inhibits the action of acetylcholine (ACh) at nicotinic ... A cholinergic drug is any of various drugs that inhibit, enhance, or mimic the action of the neurotransmitter acetylcholine, ...
... anti-cholinergic effects, antioxidant, virus antagonists, anti-inflammatory as well as having profound effects on bacterial ...
The cholinergic receptor antagonists, atropine and methylatropine were used to reversibly inhibit cholinergic transmission. ... The centrally active cholinergic receptor antagonist atropine also caused significant impairment in radial arm maze behavior, ... Irreversible impairment in central cholinergic function was achieved by central administration of the cholinergic-specific ... The relative effects of cholinotoxin and receptor antagonist treatment on short-term (working) memory and long-term (reference ...
Steen KH, Reeh PW: Actions of cholinergic agonists and antagonists on sensory nerve endings in rat skin, in vitro. J ... Therefore, H2 receptor antagonists have been combined with H1 receptor antagonists in the treatment of chronic urticaria20and ... antagonist of histamine and serotonin), pizotifen (antagonist of histamine and serotonin), cholestyramine aspirin, interferon ... Nalbuphine, a μ agonist-antagonist,5,70has also been used to prevent pruritus, but it has been associated with drowsiness.5 ...
Behavioural effects of cholinergic agonists and antagonists. Psychopharmacology (Berl), 78(2),150-155. Tente links no:* Google ...
Cholinergic Antagonists. Opioids Analgesic & Antagonists. Hormonal Agents Conditions. *Antibiotics, Antibacterials. Antiviral ...
Cholinergic Antagonists; Hypnotics and Sedatives; Pharmacists; Deprescribing; Geriatrics ...
Cholinergic Agonists 5: Cholinergic Antagonists 6: Adrenergic Agonists & ... Cholinergic Agonists 5: Cholinergic Antagonists 6: Adrenergic Agonists & ... Cholinergic Agonists 5: Cholinergic Antagonists 6: Adrenergic Agonists & ... Cholinergic Agonists 5: Cholinergic Antagonists 6: Adrenergic Agonists & ...
Cholinergic Antagonists 76% * Cough 65% * Effects of Exercise and Self-Management Interventions on Use of Analgesics and Health ...
  • The cholinergic receptor antagonists, atropine and methylatropine were used to reversibly inhibit cholinergic transmission. (tmc.edu)
  • The centrally active cholinergic receptor antagonist atropine also caused significant impairment in radial arm maze behavior, while equivalent doses of methylatropine were without effect. (tmc.edu)
  • The relative effects of cholinotoxin and receptor antagonist treatment on short-term (working) memory and long-term (reference) memory in radial arm maze behavior were examined. (tmc.edu)
  • Differences observed between atropine and hyoscine with regard to their modifying effects on withdrawal symptoms may be explained on the basis that the drugs may be acting on the different subpopulations of the muscarinic receptor or through non-cholinergic systems. (lml.com.ly)
  • Furthermore, all ACh-induced cellular and network changes were blocked by muscarinic, but not nicotinic receptor antagonists. (springer.com)
  • There has been increasing interest in the antidepressant effects of the muscarinic cholinergic receptor antagonist scopolamine. (ox.ac.uk)
  • Pretreatment with CP-99994, a neurokinin type 1 receptor antagonist, partially abolished the O(3)-induced reactivity to cholinergic agonists and electrical field stimulation. (cdc.gov)
  • Using selective receptor antagonists, we identified that CRF receptor 2 was involved in mediating this effect. (mcmaster.ca)
  • These findings suggest that CRF, via CRF receptor 2, acts on cholinergic nerves to induce epithelial barrier dysfunction. (mcmaster.ca)
  • Effects of acute administration of nicotinic and muscarinic cholinergic agonists and antagonists on performance in different cost-benefit decision making tasks in rats. (ufl.edu)
  • Selective breeding for diisopropyl fluorophosphatesensitivity: Behavioural effects of cholinergic agonists and antagonists. (bvsalud.org)
  • The enhanced flux was inhibited by the cholinergic muscarinic antagonist atropine and the nicotinic antagonist hexamethonium. (mcmaster.ca)
  • A muscarinic antagonist used to study binding characteristics of muscarinic cholinergic receptors. (nih.gov)
  • Cholinergic receptors? (github.io)
  • One visually striking pattern is that of the 9 ictogenic tricyclic compounds, 8 target cholinergic receptors. (github.io)
  • Furthermore, clomipramine also likely exhibits anti-cholinergic effects [ 1 , 2 , 3 ] , which would mean all 9 ictogenic tricyclic compounds bind to cholinergic receptors. (github.io)
  • I have not confirmed this, but I believe these compounds are all antagonists of cholinergic receptors. (github.io)
  • Drugs that target receptors are classified as agonists or antagonists. (msdmanuals.com)
  • Antagonist drugs block the access or attachment of the body's natural agonists, usually neurotransmitters, to their receptors and thereby prevent or reduce cell responses to natural agonists. (msdmanuals.com)
  • Considerable evidence suggests that central cholinergic neurons participate in either acquisition, storage or retrieval of information. (tmc.edu)
  • Release of substance P and the effects of specific antagonists would be used to determine the synaptic coupling to down stream cholinergic or vasoactive intestinal peptide-immunoreactive neurons. (usda.gov)
  • Irreversible impairment in central cholinergic function was achieved by central administration of the cholinergic-specific neurotoxins, N-ethyl-choline aziridinium (ECA) and N-ethyl-acetylcholine aziridinium (EACA). (tmc.edu)
  • When cholinesterases are inhibited, the action of endogenously released acetylcholine at cholinergic synapses is potentiated. (bvsalud.org)
  • Mice treated with either ECA or EACA showed behavioral deficits associated with cholinergic dysfunction. (tmc.edu)
  • Ipratropium bromide, a synthetic ammonium compound structurally similar to atropine, is used as a bronchodilator in the management of cholinergic-mediated bronchospasm associated with chronic obstructive pulmonary disease and in the treatment of rhinorrhea associated with the common cold or with allergic or nonallergic seasonal rhinitis. (pharmacycode.com)
  • The major group of drugs used therapeutically for this purpose is the muscarinic antagonists. (ebi.ac.uk)
  • Agonist and antagonist drugs can be used together in people with asthma. (msdmanuals.com)
  • The neuroleptic-induced TD with those who did serotonin-dopamine antagonist hypothesis not develop it under comparatively similar maintains that drugs which have a high conditions. (who.int)
  • Experiments were designed to evaluate information processing in mice following either reversible or irreversible impairment in central cholinergic activity. (tmc.edu)
  • Trospium is a non-selective muscarinic antagonist that does not cross into the CNS and reduces peripheral cholinergic side effects associated with xanomeline. (wikipedia.org)
  • However, cholinergic-mediated side effects prevented advancement of xanomeline into phase 3 trials. (wikipedia.org)
  • In addition, 5 mM EtOH also increased the frequency and amplitude of dopaminergic neuron transients in mouse brain nucleus accumbens slices, that were blocked by the α6*-nAChR antagonist, α-conotoxin MII, suggesting a role for native α6*-nAChRs in low-dose EtOH effects. (arizona.edu)
  • Of these, 20 presented to EDs with signs and symptoms consistent with cholinergic toxidrome, although the specific findings for each patient varied. (cdc.gov)
  • Reactivity of isolated tracheal smooth muscle to cholinergic agonists was significantly increased after O(3) exposure, as were contractions to electrical field stimulation at 10 Hz. (cdc.gov)
  • The cholinergic component was greater in tissues from MS versus NS pups, suggesting that increased cholinergic activity was responsible for the MS elevated permeability. (mcmaster.ca)
  • Cholinergic antagonists are used in the treatment of Parkinson's. (trc-p.nl)
  • The role of cholinergic systems in the expression of morphine withdrawal. (lml.com.ly)
  • A los 7 y 21 días la mejoría fue similar en los tres brazos. (nih.gov)
  • What are the 2 types of nicotinic antagonists and what do they do? (brainscape.com)
  • What are some examples of Nicotinic Antagonists? (brainscape.com)
  • Nicotinic antagonists that block the receptor include mecamylamine, dihydro-β-erythroidine, and hexamethonium . (wikipedia.org)
  • Drevets WC, Zarate CA Jr, Furey ML. Antidepressant effects of the muscarinic cholinergic receptor antagonist scopolamine: a review. (jamanetwork.com)
  • These drugs may be classified as: α 2 adrenergic antagonists, D 2 dopaminergic antagonists, H 1 and H 2 histaminergic antagonists, M 1 muscarinic cholinergic antagonists, ENK enkephalinergic mixed agonists/antagonists, and 5-HT 3 serotonergic antagonists. (vin.com)
  • It has a role as a non-narcotic analgesic, an antiemetic, a sedative, a cholinergic antagonist, a dopaminergic antagonist and a first generation antipsychotic. (pharmakb.com)
  • ln our laboratory we have developed two sublines of Sprague-Dawley rats , selectively bred for high-(HY) and lowyawning (LY) frequency, and it bas been shown that they differ in their responses to cholinergic and dopaminergic drugs as well as in emotional reactivity and hierarchical composition of grooming elements. (baillement.com)
  • Cholinergic muscarinic antagonist + cholinesterase reactivator. (empr.com)
  • For instance, the muscarinic receptor antagonists atropine and scopolamine can specifically antagonized, in a dose-dependent manner, ACTH-induced grooming. (baillement.com)
  • Trospium is a non-selective muscarinic antagonist that does not cross into the CNS and reduces peripheral cholinergic side effects associated with xanomeline. (wikipedia.org)
  • [5] Trospium is a non-CNS penetrant non-selective muscarinic antagonist to quell peripheral muscarinic agonist-dependent side effects. (cloudfront.net)
  • [12] Further development was enabled through a novel co-formulation strategy with the peripherally restricted muscarinic antagonist, trospium, to quell the peripheral cholinergic side effects. (cloudfront.net)
  • To conclude, this study showed that, at least partly, the ET-1 potentiation of cholinergic nerve-mediated contraction is normally mediated by tachykinin discharge, suggesting that furthermore to nerves, many kind of cells, such as for example airway DCC-2036 smooth muscles cell, may participate to neuropeptide creation. (conferencedequebec.org)
  • nevertheless, our data additional showed that, at least partly, the ET-1 potentiation of cholinergic nerve-induced contraction is normally mediated by tachykinin discharge. (conferencedequebec.org)
  • Thus, for example, nicotinic receptor antagonists interfere with the baroreflex [9] that normally corrects changes in blood pressure by sympathetic and parasympathetic stimulation of the heart. (wikipedia.org)
  • The fact that the prior administration of naloxone, a nonselective opioid antagonist, and other neurotransmitter substances prevent environmental or pharmacological induced grooming, suggests a complex interaction among several neural systems. (baillement.com)
  • Spontaneous and drug-induced yawning have also been related to a cholinergic influence, especially to an excitatory action by the administration of cholinomimetic substances. (baillement.com)
  • The cholinergic hypothesis was initially presented over 20 years ago and suggests that a dysfunction of acetylcholine containing neurons in the brain contributes substantially to the cognitive decline observed in those with advanced age and Alzheimer's disease (AD). (nih.gov)
  • Characterizing the Access of Cholinergic Antagonists to Efferent Synapses in the Inner Ear. (rochester.edu)
  • When cholinesterases are inhibited, the action of endogenously released acetylcholine at cholinergic synapses is potentiated. (umassmed.edu)
  • The most recent new classification of anti-emetic agents are the neurokinin NK 1 antagonists. (vin.com)
  • The results of both post mortem and antemortem studies in aged humans and AD patients, as well as animal experiments suggest that a host of cholinergic abnormalities including alterations in choline transport, acetylcholine release, nicotinic and muscarinic receptor expression, neurotrophin support, and perhaps axonal transport may all contribute to cognitive abnormalities in aging and AD. (nih.gov)
  • actually a capsaicin pretreatment which depletes sensory nerves of tachykinins, leads to a significant decrease in cholinergic response both and in guinea-pig airways DCC-2036 (Stretton (Aizawa control 285% of EFS30 respectively] (Amount 2). (conferencedequebec.org)
  • The mammalian efferent vestibular system utilizes cholinergic mechanisms to excite primary vestibular afferents. (rochester.edu)
  • The onset of differentiation intensified the adverse effects on DNA synthesis and changed the rank order in keeping with a shift away from noncholinergic mechanisms and toward cholinergic mechanisms. (nih.gov)
  • 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. (bvsalud.org)
  • 14. Pharmacological study of cholinergic system on cardiovascular regulation in the cuneiform nucleus of rat. (nih.gov)
  • This is because most pharmacological studies have focused ou the ability of cholinergic antagonists to reverse grooming induced by neuropeptides. (baillement.com)
  • The dysfunction of the central cholinergic system causes cognitive deficits witnessed in neurodegenerative and associated disorders. (hindawi.com)
  • The cholinergic neurotransmitter system is critically linked to cognitive functions including attention. (imtlucca.it)
  • Reactivated acetylcholinesterase hydrolyzes excess acetylcholine resulting from organophosphorus poisoning to help restore impaired cholinergic neural function. (empr.com)
  • Botulinum neurotoxin type A (BoNTA) is a well-known cholinergic antagonist widely used in a number of approved neurological and esthetic indications. (edu.au)
  • These challenges, primarily based on assays of post mortem enzyme activity, should be taken in perspective and evaluated within the wide range of cholinergic abnormalities known to exist in both aging and AD. (nih.gov)
  • A nicotinic antagonist used primarily as a ganglionic blocker in animal research. (drugcentral.org)
  • In 2002, a novel class of antipsychotics arose with the FDA approval of aripiprazole (Abilify), a very potent D 2 antagonist with intrinsic D 2 partial agonism. (psychiatrictimes.com)
  • And exacerbation of the, the dramatic development of the overt cholinergic and adrenergic antagonist properties can cause myocardial depression. (revivemedicalny.com)
  • Molecular and functional changes to postsynaptic cholinergic signaling in the vestibular sensory organs of aging C57BL/6 mice. (rochester.edu)
  • [1] In insects , the cholinergic system is limited to the central nervous system . (wikipedia.org)
  • 1. Effect of the cholinergic system of the lateral periaqueductal gray (lPAG) on blood pressure and heart rate in normal and hydralazine hypotensive rats. (nih.gov)
  • Various neuromodulators and neurotransmitters, including acetylcholine, nitric oxide, γ -aminobutyric acid (GABA), and endogenous antioxidants, among others, play essential roles in the central cholinergic system [ 4 ]. (hindawi.com)
  • Of these, 20 presented to EDs with signs and symptoms consistent with cholinergic toxidrome, although the specific findings for each patient varied. (cdc.gov)
  • Finally, all of the toxicants shifted the transmitter fate of the cells away from the cholinergic phenotype and toward the catecholaminergic phenotype. (nih.gov)
  • 5. Effect of MK-801, an antagonist of NMDA receptor in the pedunculopontine tegmental nucleus, on cardiovascular parameters in normotensive and hydralazine hypotensive rats. (nih.gov)
  • A prior injection of muscarinic antagonists also suppressed the effect of bombesin-stimulated grooming. (baillement.com)
  • These results indicate that animals showing a definitive sign of tolerance to OP administration (subsensitivity to a cholinergic agonist) were also functionally impaired on both the mnemonic and motoric demands of a working memory task. (unboundmedicine.com)