Dimaprit
Histamine Agonists
Receptors, Histamine H2
Receptors, Histamine
Methylhistamines
Thiourea
Cimetidine
Histamine H2 Antagonists
Receptors, Histamine H1
Histamine
Propoxycaine
Histamine Antagonists
Pyrilamine
Betahistine
Receptors, Histamine H3
Impromidine
Histamine H1 Antagonists
Diphenhydramine
Anaphylaxis
Nitric oxide synthase inhibition by dimaprit and dimaprit analogues. (1/72)
1. The similarity in molecular structure between the histamine H2-agonist dimaprit (3-dimethylamino-propyl-isothiourea) and the endogenous nitric oxide synthase (NOS) substrate L-arginine prompted us to study the effect of dimaprit and some dimaprit analogues on NOS activity. Dimaprit and some of its analogues were tested in an in vitro assay which measures the conversion of [3H]-L-arginine to [3H]-L-citrulline. Dimaprit inhibits rat brain NOS (nNOS) concentration dependently with an IC50 of 49+/-14 microM. 2. Removal of one or both of the methyl groups from the non-isothiourea nitrogen of dimaprit improved nNOS inhibitory properties. Aminopropylisothiourea is the most potent compound (IC50 = 4.1+/-0.9 microM) of the series followed by methylaminopropylisothiourea (IC50 = 7.6 +/- microM). 3. The observed effect of aminopropylisothiourea and methylaminopropyl-isothiourea are probably not due to the compounds themselves but to the corresponding mercaptoalkylguanidines, rearrangement products formed in aqueous solutions. This hypothesis is strengthened by the finding that aminobutylisothiourea is not active since a rearrangement to mercaptobutylguanidine does not occur. 4. Remarkably, nitrosylation of the isothiourea group of dimaprit decreases nNOS inhibitory activity, while nitrosylation of the guanidine analogue of dimaprit increases the inhibition of nNOS activity. 5. The pharmacological profile of dimaprit includes inhibition of nNOS. The nNOS inhibitory activity occurs in the same concentration range as the H2-agonist and H3-agonist activity of this compound. (+info)Nalpha-methyl histamine and histamine stimulate gastrin release from rabbit G-cells via histamine H2-receptors. (2/72)
BACKGROUND: Gastrin release by Helicobacter pylori may be an important step in the pathway leading to duodenal ulceration. A histamine H3-receptor agonist was found to release gastrin from antral mucosal fragments; this was interpreted as being due to suppression of somatostatin release. H. pylori is reported to produce Nalpha-methyl histamine (NalphaMH), which is an agonist of H3 as well as other histamine receptors. H. pylori infection also recruits mast cells, which release histamine. AIM: To determine the direct effects of histamine receptor agonists on isolated gastrin cells. METHODS: Rabbit G-cells were prepared by countercurrent elutriation and cultured on 24-well plates. RESULTS: NalphaMH (10-6-10-4 M) caused a dose-dependent increase in gastrin release from a basal level of 2.3 +/- 0.2% total cell content (TCC; mean +/- S.E.M.) to a maximum of 5.1 +/- 0.7%, an increase of 117% (P < 0. 005) above basal. This was abolished by the H2-antagonist ranitidine (10-5 M), but not by immunoblockade with anti-somatostatin antibody, the H1-antagonist chlorpheniramine (10-5 M) or the H3-antagonist thioperamide (10-4 M). The histamine H2-receptor agonist dimaprit (10-6-10-4 M) increased gastrin release from 2.4 +/- 0.2% to 3.6 +/- 0.2% TCC (P < 0.001). Gastrin release was also stimulated by histamine (10-7-10-4 M) from a basal value of 3.0 +/- 0.3% to 5.4 +/- 0.5% TCC (P < 0.001). This also was inhibited by ranitidine (10-5 M) (P < 0.01). CONCLUSION: NalphaMH and histamine release gastrin from G-cells via H2-receptors; this might contribute to H. pylori-associated hypergastrinaemia. (+info)Histamine suppresses A-type potassium current in myenteric neurons from guinea pig small intestine. (3/72)
Perforated patch-clamp methods for recording ionic currents in the whole-cell configuration were used to test the hypothesis that the ionic mechanisms for the excitatory actions of histamine on enteric neurons include suppression of A-type K(+) current (I(A)). Histamine and the selective histamine H(2) receptor agonist, dimaprit, reduced the amplitude of I(A) without affecting the slope factor for I(A) steady-state inactivation curves. Suppression of I(A) was restricted to after hyperpolarization-type myenteric neurons that were immunoreactive for calbindin. The selective histamine H(2) receptor antagonist cimetidine suppressed the action of histamine and dimaprit. Elevation of intraneuronal cAMP by forskolin, a membrane-permeant analog of cAMP, and treatment with a phosphodiesterase inhibitor suppressed I(A.) The results are consistent with the hypothesis that suppression of I(A) is part of the ionic mechanism responsible for elevation of excitability during both slow synaptic excitation and slow synaptic excitation-like responses evoked by paracrine mediators, such as histamine, in after hyperpolarization-type myenteric neurons. (+info)Actions of histamine on muscle and ganglia of the guinea pig gallbladder. (4/72)
Histamine is an inflammatory mediator present in mast cells, which are abundant in the wall of the gallbladder. We examined the electrical properties of gallbladder smooth muscle and nerve associated with histamine-induced changes in gallbladder tone. Recordings were made from gallbladder smooth muscle and neurons, and responses to histamine and receptor subtype-specific compounds were tested. Histamine application to intact smooth muscle produced a concentration-dependent membrane depolarization and increased excitability. In the presence of the H(2) antagonist ranitidine, the response to histamine was potentiated. Activation of H(2) receptors caused membrane hyperpolarization and elimination of spontaneous action potentials. The H(2) response was attenuated by the ATP-sensitive K(+) (K(ATP)) channel blocker glibenclamide in intact and isolated smooth muscle. Histamine had no effect on the resting membrane potential or excitability of gallbladder neurons. Furthermore, neither histamine nor the H(3) agonist R-alpha-methylhistamine altered the amplitude of the fast excitatory postsynaptic potential in gallbladder ganglia. The mast cell degranulator compound 48/80 caused a smooth muscle depolarization that was inhibited by the H(1) antagonist mepyramine, indicating that histamine released from mast cells can activate gallbladder smooth muscle. In conclusion, histamine released from mast cells can act on gallbladder smooth muscle, but not in ganglia. The depolarization and associated contraction of gallbladder smooth muscle represent the net effect of activation of both H(1) (excitatory) and H(2) (inhibitory) receptors, with the H(2) receptor-mediated response involving the activation of K(ATP) channels. (+info)Histamine H(2) receptors mediate the inhibitory effect of histamine on human eosinophil degranulation. (5/72)
The effect of histamine on human eosinophil degranulation and the receptor mediating such effect were studied in vitro using the complement C5a-mediated eosinophil peroxidase (EPO) release model. Following pre-treatment with 5 microg ml(-1) cytochalasin B(CB), C5a induced a concentration-dependent release of EPO from eosinophils isolated from healthy donors. Histamine (0.1-50 microM), but not L-histidine, inhibited concentration-dependently C5a-induced EPO release with IC(50) (95% CI) of 0.6 microM (0.3-1.2 microM) and maximal inhibition of approximately 60%. A similar effect was seen with the selective H(2) agonists dimaprit (IC(50) (95% CI)=6.9 microM (3.2-10.6 microM)) and amthamine (IC(50) (95% CI)=0.4 microM (0.2-0.7 microM)). Neither the selective H(1) agonist 6-(2-(4-imidazolyl)ethylamino)-N-(4-trifluoromethylphenyl) heptanecarboxamide(HTMT), nor the selective H(3) agonists imetit (up to 100 microM) had any significant effect. The inhibition by histamine was reversed by cimetidine (0.1-30 microM) and other H(2) antagonists, but not the H(1) antagonist mepyramine (1.0- 100 microM), nor the H(3) antagonist thioperamide (1.0-100 microM). Cimetidine (1-30 microM) shifted to the right the dimaprit log dose-response curve, producing a pA(2) value of 5.9 and Schild's plot slope of 0.98, thus confirming simple competitive antagonism. Histamine (10-100 microM) increased intracellular level of adenosine 3',5'-cyclic monophosphate, which was completely abolished by cimetidine (30 microM), but not mepyramine or thioperamide. The cyclic AMP analogue - dibutyryl cyclic AMP - also inhibited degranulation (IC(50) approximately 300 microM). The cyclic AMP phosphodiesterase(PDE) IV inhibitor rolipram (10 microM) synergistically enhanced the inhibition of EPO release by histamine. These results suggest that histamine, via stimulation of H(2) receptors and a consequent elevation of intracellular levels of cyclic AMP, inhibits human eosinophil degranulation. (+info)Histamine induces exocytosis and IL-6 production from human lung macrophages through interaction with H1 receptors. (6/72)
Increasing evidence suggests that a continuous release of histamine from mast cells occurs in the airways of asthmatic patients and that histamine may modulate functions of other inflammatory cells such as macrophages. In the present study histamine (10(-9)-10(-6) M) increased in a concentration-dependent fashion the basal release of beta-glucuronidase (EC(50) = 8.2 +/- 3.5 x 10(-9) M) and IL-6 (EC(50) = 9.3 +/- 2.9 x 10(-8) M) from human lung macrophages. Enhancement of beta-glucuronidase release induced by histamine was evident after 30 min and peaked at 90 min, whereas that of IL-6 required 2-6 h of incubation. These effects were reproduced by the H(1) agonist (6-[2-(4-imidazolyl)ethylamino]-N-(4-trifluoromethylphenyl)heptane carboxamide but not by the H(2) agonist dimaprit. Furthermore, histamine induced a concentration-dependent increase of intracellular Ca(2+) concentrations ([Ca(2+)](i)) that followed three types of response, one characterized by a rapid increase, a second in which [Ca(2+)](i) displays a slow but progressive increase, and a third characterized by an oscillatory pattern. Histamine-induced beta-glucuronidase and IL-6 release and [Ca(2+)](i) elevation were inhibited by the selective H(1) antagonist fexofenadine (10(-7)-10(-4) M), but not by the H(2) antagonist ranitidine. Inhibition of histamine-induced beta-glucuronidase and IL-6 release by fexofenadine was concentration dependent and displayed the characteristics of a competitive antagonism (K(d) = 89 nM). These data demonstrate that histamine induces exocytosis and IL-6 production from human macrophages by activating H(1) receptor and by increasing [Ca(2+)](i) and they suggest that histamine may play a relevant role in the long-term sustainment of allergic inflammation in the airways. (+info)Phe217 regulates the transfer of allosteric information across the subunit interface of the RecA protein filament. (7/72)
BACKGROUND: ATP-mediated cooperative assembly of a RecA nucleoprotein filament activates the protein for catalysis of DNA strand exchange. RecA is a classic allosterically regulated enzyme in that ATP binding results in a dramatic increase in ssDNA binding affinity. This increase in ssDNA binding affinity results almost exclusively from an ATP-mediated increase in cooperative filament assembly rather than an increase in the inherent affinity of monomeric RecA for DNA. Therefore, certain residues at the subunit interface must play an important role in transmitting allosteric information across the filament structure of RecA. RESULTS: Using electron microscopic analysis of RecA polymer formation in the absence of DNA, we show that while wild-type RecA undergoes a slight decrease in filament length in the presence of ATP, a Phe217Tyr substitution results in a dramatic ATP-induced increase in cooperative filament assembly. Biosensor DNA binding measurements reveal that the Phe217Tyr mutation increases ATP-mediated cooperative interaction between RecA subunits by more than 250-fold. CONCLUSIONS: These studies represent the first identification of a subunit interface residue in RecA (Phe217) that plays a critical role in regulating the flow of ATP-mediated information throughout the protein filament structure. We propose a model by which conformational changes that occur upon ATP binding are propagated through the structure of a RecA monomer, resulting in the insertion of the Phe217 side chain into a pocket in the neighboring subunit. This event serves as a key step in intersubunit communication leading to ATP-mediated cooperative filament assembly and high affinity binding to ssDNA. (+info)Structure of a fast kinesin: implications for ATPase mechanism and interactions with microtubules. (8/72)
We determined the crystal structure of the motor domain of the fast fungal kinesin from Neurospora crassa (NcKin). The structure has several unique features. (i) Loop 11 in the switch 2 region is ordered and enables one to describe the complete nucleotide-binding pocket, including three inter-switch salt bridges between switch 1 and 2. (ii) Loop 9 in the switch 1 region bends outwards, making the nucleotide-binding pocket very wide. The displacement in switch 1 resembles that of the G-protein ras complexed with its guanosine nucleotide exchange factor. (iii) Loop 5 in the entrance to the nucleotide-binding pocket is remarkably long and interacts with the ribose of ATP. (iv) The linker and neck region is not well defined, indicating that it is mobile. (v) Image reconstructions of ice-embedded microtubules decorated with NcKin show that it interacts with several tubulin subunits, including a central beta-tubulin monomer and the two flanking alpha-tubulin monomers within the microtubule protofilament. Comparison of NcKin with other kinesins, myosin and G-proteins suggests that the rate-limiting step of ADP release is accelerated in the fungal kinesin and accounts for the unusually high velocity and ATPase activity. (+info)Dimaprit is not a medical condition or disease. It is actually a synthetic peptide that acts as an agonist for certain types of receptors found in the body, specifically the H2 histamine receptors. These receptors are involved in various physiological processes, such as regulating gastric acid secretion and modulating immune responses.
As a research tool, Dimaprit is used to study the functions of H2 histamine receptors and their roles in different biological systems. It is not typically used as a therapeutic agent in clinical medicine.
Histamine agonists are substances that bind to and activate histamine receptors, leading to the initiation or enhancement of various physiological responses. Histamine is a naturally occurring molecule that plays a key role in the body's immune and allergic responses, as well as in the regulation of sleep, wakefulness, and appetite.
There are four main types of histamine receptors (H1, H2, H3, and H4), each with distinct functions and signaling pathways. Histamine agonists can be selective for one or more of these receptor subtypes, depending on their pharmacological properties.
For example, H1 agonists are commonly used as decongestants and antihistamines to treat allergies, while H2 agonists are used to treat gastroesophageal reflux disease (GERD) and peptic ulcers. H3 agonists have been investigated for their potential therapeutic use in the treatment of neurological disorders such as Parkinson's disease and schizophrenia, while H4 agonists are being studied for their role in inflammation and immune regulation.
It is important to note that histamine agonists can also have adverse effects, particularly if they are not selective for a specific receptor subtype or if they are used at high doses. These effects may include increased heart rate, blood pressure, and bronchodilation (opening of the airways), as well as gastrointestinal symptoms such as nausea, vomiting, and diarrhea.
Histamine H2 receptors are a type of G protein-coupled receptor that are widely distributed throughout the body, including in the stomach, heart, and brain. They are activated by the neurotransmitter histamine, which is released by mast cells in response to an allergen or injury. When histamine binds to H2 receptors, it triggers a variety of physiological responses, such as increasing gastric acid secretion, regulating heart rate and contractility, and modulating neurotransmitter release in the brain. Histamine H2 receptor antagonists, also known as H2 blockers, are commonly used to treat gastroesophageal reflux disease (GERD) and peptic ulcers by reducing gastric acid production. Examples of H2 blockers include ranitidine (Zantac), famotidine (Pepcid), and cimetidine (Tagamet).
Histamine receptors are a type of cell surface receptor that bind to histamine, a biologically active compound involved in various physiological and pathophysiological processes in the body. There are four types of histamine receptors, designated H1, H2, H3, and H4, which are classified based on their specific responses to histamine.
Histamine receptors, Histamine (H1) are G protein-coupled receptors that are widely distributed in the body, including in the smooth muscle of blood vessels, respiratory tract, and gastrointestinal tract. When histamine binds to H1 receptors, it activates a signaling pathway that leads to the contraction of smooth muscle, increased vascular permeability, and stimulation of sensory nerve endings, resulting in symptoms such as itching, sneezing, and runny nose. Antihistamines, which are commonly used to treat allergies, work by blocking H1 receptors and preventing histamine from binding to them.
It's worth noting that while histamine has many important functions in the body, excessive or inappropriate activation of histamine receptors can lead to a range of symptoms and conditions, including allergic reactions, inflammation, and neuropsychiatric disorders.
Methylhistamines are not a recognized medical term or a specific medical condition. However, the term "methylhistamine" may refer to the metabolic breakdown product of the antihistamine drug, diphenhydramine, which is also known as N-methyldiphenhydramine or dimenhydrinate.
Diphenhydramine is a first-generation antihistamine that works by blocking the action of histamine, a chemical released during an allergic reaction. When diphenhydramine is metabolized in the body, it is converted into several breakdown products, including methylhistamines.
Methylhistamines are not known to have any specific pharmacological activity or clinical significance. However, they can be used as a marker for the presence of diphenhydramine or its metabolism in the body.
Thiourea is not a medical term, but a chemical compound. It's a colorless crystalline solid with the formula SC(NH2)2. Thiourea is used in some industrial processes and can be found in some laboratory reagents. It has been studied for its potential effects on certain medical conditions, such as its ability to protect against radiation damage, but it is not a medication or a treatment that is currently in clinical use.
Cimetidine is a histamine-2 (H2) receptor antagonist, which is a type of medication that reduces the production of stomach acid. It works by blocking the action of histamine on the H2 receptors in the stomach, which are responsible for stimulating the release of stomach acid. By blocking these receptors, cimetidine reduces the amount of stomach acid produced and can help to relieve symptoms such as heartburn, indigestion, and stomach ulcers.
Cimetidine is available by prescription in various forms, including tablets, capsules, and liquid. It is typically taken two or three times a day, depending on the specific condition being treated. Common side effects of cimetidine may include headache, dizziness, diarrhea, and constipation.
In addition to its use in treating stomach acid-related conditions, cimetidine has also been studied for its potential anti-cancer properties. Some research suggests that it may help to enhance the immune system's response to cancer cells and reduce the growth of certain types of tumors. However, more research is needed to confirm these effects and determine the optimal dosage and duration of treatment.
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).
Histamine H1 receptors are a type of G protein-coupled receptor found in various cells throughout the body, including those of the cardiovascular, gastrointestinal, and nervous systems. They are activated by the neurotransmitter histamine, which is released by mast cells and basophils in response to allergic reactions, inflammation, or immune responses.
When histamine binds to H1 receptors, it triggers a range of physiological responses that contribute to the symptoms of allergies, including vasodilation (leading to redness and warmth), increased vascular permeability (resulting in fluid leakage and swelling), and smooth muscle contraction (causing bronchoconstriction, gut cramping, and nasal congestion).
Histamine H1 receptors are also involved in the regulation of sleep-wake cycles, where they contribute to the promotion of wakefulness. Antihistamines that block H1 receptors are commonly used to treat allergies, hay fever, and other conditions associated with histamine release.
Histamine is defined as a biogenic amine that is widely distributed throughout the body and is involved in various physiological functions. It is derived primarily from the amino acid histidine by the action of histidine decarboxylase. Histamine is stored in granules (along with heparin and proteases) within mast cells and basophils, and is released upon stimulation or degranulation of these cells.
Once released into the tissues and circulation, histamine exerts a wide range of pharmacological actions through its interaction with four types of G protein-coupled receptors (H1, H2, H3, and H4 receptors). Histamine's effects are diverse and include modulation of immune responses, contraction and relaxation of smooth muscle, increased vascular permeability, stimulation of gastric acid secretion, and regulation of neurotransmission.
Histamine is also a potent mediator of allergic reactions and inflammation, causing symptoms such as itching, sneezing, runny nose, and wheezing. Antihistamines are commonly used to block the actions of histamine at H1 receptors, providing relief from these symptoms.
Propoxycaine is a local anesthetic that was previously used in medical and dental procedures for its numbing effect. It works by blocking the nerve impulses in the area where it is administered, thus reducing the sensation of pain. However, its use has become less common due to the development of safer and more effective alternatives.
The chemical name for Propoxycaine is 2-diethylamino-N-(1-methoxyprop-2-yl)butanamide. It is a derivative of procaine, another local anesthetic, with an added methoxy group to the propanolamine side chain. This modification was intended to increase its potency and duration of action compared to procaine.
Propoxycaine can be administered through various routes, including topical application, injection, or as a suppository. Its effects typically begin within a few minutes after administration and last for up to an hour. Common side effects may include localized pain, redness, or swelling at the site of injection, as well as more systemic effects such as dizziness, headache, or heart palpitations.
It is important to note that Propoxycaine is no longer widely used in clinical practice due to its association with rare but serious side effects, including allergic reactions, seizures, and cardiac arrhythmias. Therefore, its use is generally restricted to specific indications and under the close supervision of a healthcare professional.
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.
Pyrilamine is an antihistamine drug that is primarily used to relieve allergic symptoms such as sneezing, itching, watery eyes, and runny nose. It works by blocking the action of histamine, a substance naturally produced by the body during an allergic reaction. Pyrilamine may also be used to treat motion sickness and to help with tension headaches or migraines.
Pyrilamine is available in various forms, including tablets, capsules, and syrup, and it can be taken with or without food. Common side effects of pyrilamine include dizziness, dry mouth, and drowsiness. It is important to avoid activities that require mental alertness, such as driving or operating heavy machinery, until you know how pyrilamine affects you.
Like all medications, pyrilamine should be taken under the supervision of a healthcare provider, who can determine the appropriate dosage and monitor for any potential side effects or interactions with other drugs. It is essential to follow the instructions provided by your healthcare provider carefully and not exceed the recommended dose.
Betahistine is a medication that is primarily used to treat symptoms associated with Ménière's disease, which is an inner ear disorder that can cause vertigo (dizziness), tinnitus (ringing in the ears), and hearing loss. Betahistine is thought to work by improving blood flow in the inner ear and reducing the pressure in the fluid-filled compartments of the ear.
Betahistine is a histamine analogue, which means that it has a similar chemical structure to histamine, a naturally occurring compound in the body that plays a role in various physiological processes, including the regulation of blood flow and inflammation. Betahistine acts as an agonist at H1 and H3 histamine receptors and as an antagonist at H2 receptors, which leads to its therapeutic effects on the inner ear.
The medication is available in tablet form and is typically taken two or three times a day, with or without food. The dosage may vary depending on the individual's response to treatment and any underlying medical conditions. Common side effects of betahistine include gastrointestinal symptoms such as nausea, vomiting, and diarrhea, as well as headache, dizziness, and dry mouth.
It is important to note that betahistine may interact with other medications, including certain antidepressants, antihistamines, and sedatives, so it is essential to inform your healthcare provider of all the medications you are taking before starting treatment with betahistine. Additionally, individuals with asthma or a history of peptic ulcers should use caution when taking this medication, as it may exacerbate these conditions.
Histamine H3 receptors are a type of G protein-coupled receptor (GPCR) that are widely distributed throughout the central and peripheral nervous system. They are activated by the neurotransmitter histamine and function as autoreceptors, inhibiting the release of histamine from presynaptic nerve terminals. Histamine H3 receptors also modulate the activity of other neurotransmitters, such as acetylcholine, dopamine, norepinephrine, and serotonin, by regulating their synthesis, release, and uptake.
Histamine H3 receptors have been identified as potential targets for the treatment of various neurological and psychiatric disorders, including sleep disorders, attention deficit hyperactivity disorder (ADHD), schizophrenia, and drug addiction. Antagonists or inverse agonists of Histamine H3 receptors may enhance the release of neurotransmitters in the brain, leading to improved cognitive function, mood regulation, and reward processing. However, further research is needed to fully understand the therapeutic potential and safety profile of Histamine H3 receptor modulators.
I'm sorry for any confusion, but "Impromidine" is not a widely recognized or established term in medical science or pharmacology. It does not appear to be listed in standard medical dictionaries or scientific literature as a drug, diagnostic agent, or medical condition.
If you have any more context or details about where you encountered this term, I'd be happy to help you try to figure out what it might refer to!
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).
Diphenhydramine is an antihistamine medication used to relieve symptoms of allergies, such as sneezing, runny nose, and itchy or watery eyes. It works by blocking the action of histamine, a substance in the body that causes allergic reactions. Diphenhydramine can also be used to treat motion sickness, insomnia, and symptoms of the common cold.
In addition to its antihistamine effects, diphenhydramine also has anticholinergic properties, which means it can help to reduce secretions in the nose and throat, and may have a drying effect on the mouth and eyes. It is available over-the-counter in various forms, including tablets, capsules, liquid, and topical creams or ointments.
It's important to note that diphenhydramine can cause drowsiness, so it should be used with caution when operating heavy machinery or driving a vehicle. It may also interact with other medications, so it's important to speak with a healthcare provider before taking this medication.
Eye color is a characteristic determined by variations in a person's genes. The color of the eyes depends on the amount and type of pigment called melanin found in the eye's iris.
There are three main types of eye colors: brown, blue, and green. Brown eyes have the most melanin, while blue eyes have the least. Green eyes have a moderate amount of melanin combined with a golden tint that reflects light to give them their unique color.
Eye color is a polygenic trait, which means it is influenced by multiple genes. The two main genes responsible for eye color are OCA2 and HERC2, both located on chromosome 15. These genes control the production, transport, and storage of melanin in the iris.
It's important to note that eye color can change during infancy and early childhood due to the development of melanin in the iris. Additionally, some medications or medical conditions may also cause changes in eye color over time.
Metiamide is not generally considered a medical term, but it is a medication that has been used in the past. Medically, metiamide is defined as a synthetic histamine H2-receptor antagonist, which means it blocks the action of histamine at the H2 receptors in the stomach. This effect reduces gastric acid secretion and can be useful in treating gastroesophageal reflux disease (GERD), peptic ulcers, and other conditions associated with excessive stomach acid production.
However, metiamide has largely been replaced by other H2 blockers like cimetidine, ranitidine, and famotidine due to its association with a rare but serious side effect called agranulocytosis, which is a severe decrease in white blood cell count that can increase the risk of infections.
Anaphylaxis is a severe, life-threatening systemic allergic reaction that occurs suddenly after exposure to an allergen (a substance that triggers an allergic reaction) to which the person has previously been sensitized. The symptoms of anaphylaxis include rapid onset of symptoms such as itching, hives, swelling of the throat and tongue, difficulty breathing, wheezing, cough, chest tightness, rapid heartbeat, hypotension (low blood pressure), shock, and in severe cases, loss of consciousness and death. Anaphylaxis is a medical emergency that requires immediate treatment with epinephrine (adrenaline) and other supportive measures to stabilize the patient's condition.
Ranitidine is a histamine-2 (H2) blocker medication that works by reducing the amount of acid your stomach produces. It is commonly used to treat and prevent ulcers in the stomach and intestines, and to manage conditions where the stomach produces too much acid, such as Zollinger-Ellison syndrome.
Ranitidine is also used to treat gastroesophageal reflux disease (GERD) and other conditions in which acid backs up from the stomach into the esophagus, causing heartburn. Additionally, ranitidine can be used to prevent and treat upper gastrointestinal bleeding caused by stress or injury in critically ill patients.
The medication is available in both prescription and over-the-counter forms, and it comes in various forms, including tablets, capsules, and liquid solutions. As with any medication, ranitidine should be taken as directed by a healthcare professional, and its potential side effects and interactions with other medications should be carefully monitored.