A slowly hydrolyzing muscarinic agonist with no nicotinic effects. Bethanechol is generally used to increase smooth muscle tone, as in the GI tract following abdominal surgery or in urinary retention in the absence of obstruction. It may cause hypotension, HEART RATE changes, and BRONCHIAL SPASM.
Bethanechol compounds are parasympathomimetic agents that directly stimulate muscarinic receptors, primarily used to treat urinary retention and nonobstructive bladder dysfunction by increasing bladder contractility and decreasing post-void residual volume.
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.
Drugs that bind to and activate muscarinic cholinergic receptors (RECEPTORS, MUSCARINIC). Muscarinic agonists are most commonly used when it is desirable to increase smooth muscle tone, especially in the GI tract, urinary bladder and the eye. They may also be used to reduce heart rate.
One of the MUSCARINIC ANTAGONISTS with pharmacologic action similar to ATROPINE and used mainly as an ophthalmic parasympatholytic or mydriatic.
Complete or severe loss of the subjective sense of taste, frequently accompanied by OLFACTION DISORDERS.
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 synthetic pentapeptide that has effects like gastrin when given parenterally. It stimulates the secretion of gastric acid, pepsin, and intrinsic factor, and has been used as a diagnostic aid.
An alkaloid, originally from Atropa belladonna, but found in other plants, mainly SOLANACEAE. Hyoscyamine is the 3(S)-endo isomer of atropine.
Hydrochloric acid present in GASTRIC JUICE.
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.
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.
An antimuscarinic agent that inhibits gastric secretion at lower doses than are required to affect gastrointestinal motility, salivary, central nervous system, cardiovascular, ocular, and urinary function. It promotes the healing of duodenal ulcers and due to its cytoprotective action is beneficial in the prevention of duodenal ulcer recurrence. It also potentiates the effect of other antiulcer agents such as CIMETIDINE and RANITIDINE. It is generally well tolerated by patients.
A histamine H2 receptor antagonist that is used as an anti-ulcer agent.
Any drug used for its actions on cholinergic systems. Included here are agonists and antagonists, drugs that affect the life cycle of ACETYLCHOLINE, and drugs that affect the survival of cholinergic neurons. The term cholinergic agents is sometimes still used in the narrower sense of MUSCARINIC AGONISTS, although most modern texts discourage that usage.
A subclass of muscarinic receptor that mediates cholinergic-induced contraction in a variety of SMOOTH MUSCLES.
A group of amylolytic enzymes that cleave starch, glycogen, and related alpha-1,4-glucans. (Stedman, 25th ed) EC 3.2.1.-.
Those persons legally qualified by education and training to engage in the practice of pharmacy.
The giving of drugs, chemicals, or other substances by mouth.
Time schedule for administration of a drug in order to achieve optimum effectiveness and convenience.
An organ of digestion situated in the left upper quadrant of the abdomen between the termination of the ESOPHAGUS and the beginning of the DUODENUM.
NATIONAL LIBRARY OF MEDICINE service for health professionals and consumers. It links extensive information from the National Institutes of Health and other reviewed sources of information on specific diseases and conditions.
It is a form of protection provided by law. In the United States this protection is granted to authors of original works of authorship, including literary, dramatic, musical, artistic, and certain other intellectual works. This protection is available to both published and unpublished works. (from Circular of the United States Copyright Office, 6/30/2008)
Patient health knowledge related to medications including what is being used and why as well as instructions and precautions.
Services providing pharmaceutic and therapeutic drug information and consultation.
Societies whose membership is limited to pharmacists.
Advanced programs of training to meet certain professional requirements in fields other than medicine or dentistry, e.g., pharmacology, nutrition, nursing, etc.
I'm sorry for any confusion, but the term "Maryland" is not a recognized medical term with a specific definition in the medical field. It refers to a state in the United States. If you have any questions about a medical condition or treatment, I would be happy to try and help answer those!

Muscarinic stimulation of calcium/calmodulin-dependent protein kinase II in isolated rat pancreatic acini. (1/144)

AIM: To study whether M3 receptor occupation would lead to activation of calcium/calmodulin-dependent protein kinase II (CaM kinase II). METHODS: In this study, we isolated rat pancreatic acini by collagenase digestion; measured the Ca2+/calmodulin-independent activity of autophosphorylated form of the CaM kinase II both before and after stimulation of the acini with muscarinic secretagogue bethanechol (Bet). RESULTS: Bet stimulated the activation of, or generation of Ca(2+)-independent activity of, this kinase, in a concentration (0.0001-1 mmol.L-1) and time (5-300 s)-dependent manner; with Bet of 100 mumol.L-1, Ca(2+)-independent activity increased from an unstimulated level of 4.5 +/- 0.3 (n = 4) to 8.9 +/- 1.3 (n = 4, P < 0.05) at 5 s. Another Ca2+ mobilizing secretagogue cholecystokinin (CCK) also activated the kinase; at 1 mumol.L-1, CCK increased Ca(2+)-independent kinase activity to 12.9 +/- 0.5 (n = 6, P < 0.05). Vasoactive intestinal peptide (VIP) at 1 mumol.L-1 did not produce significant Ca(2+)-independent kinase activity (from control 3.90 +/- 0.28 to 4.53 +/- 0.47, n = 6, P > 0.05). Atropine completely blocked Bet activation of the kinase. CONCLUSION: CaM kinase II plays a pivotal role in digestive enzyme secretion, especially during the initial phase of amylase secretion.  (+info)

Myogenic mechanism for peristalsis in the cat esophagus. (2/144)

A myogenic control system (MCS) is a fundamental determinant of peristalsis in the stomach, small bowel, and colon. In the esophagus, attention has focused on neuronal control, the potential for a MCS receiving less attention. The myogenic properties of the cat esophagus were studied in vitro with and without nerves blocked by 1 microM TTX. Muscle contraction was recorded, while electrical activity was monitored by suction electrodes. Spontaneous, nonperistaltic, electrical, and mechanical activity was seen in the longitudinal muscle and persisted after TTX. Spontaneous circular muscle activity was minimal, and peristalsis was not observed without pharmacological activation. Direct electrical stimulation (ES) in the presence of bethanechol or tetraethylammonium chloride (TEA) produced slow-wave oscillations and spike potentials accompanying smooth muscle contraction that progressed along the esophagus. Increased concentrations of either drug in the presence of TTX produced slow waves and spike discharges, accompanied by peristalsis in 5 of 8 TEA- and 2 of 11 bethanechol-stimulated preparations without ES. Depolarization of the muscle by increasing K(+) concentration also produced slow waves but no peristalsis. We conclude that the MCS in the esophagus requires specific activation and is manifest by slow-wave oscillations of the membrane potential, which appear to be necessary, but are not sufficient for myogenic peristalsis. In vivo, additional control mechanisms are likely supplied by nerves.  (+info)

Cholinergic effects on human gastric motility. (3/144)

BACKGROUND: Cholinergic regulation of chronotropic (frequency) and inotropic (force) aspects of antral contractility and how these impact on gastric emptying are not well delineated. AIMS: To determine the effects of cholinergic stimulation and inhibition on myoelectric, contractile, and emptying parameters of gastric motility. METHODS: Ten normal subjects underwent three studies each, using simultaneous electrogastrography (EGG), antroduodenal manometry, and gastric emptying with dynamic antral scintigraphy (DAS). After 30 minutes of baseline fasting manometry and EGG, subjects received saline intravenously, atropine (0.6 mg then 0.25 mg/hour intravenously), or bethanechol (5 mg subcutaneously). This was followed by another 30 minutes' recording and by three hours of postprandial recording after ingestion of a technetium-99m labelled solid meal. RESULTS: During fasting, atropine decreased, whereas bethanechol increased, the antral manometric motility index and EGG power. Postprandially, atropine decreased the amplitude of antral contractions by DAS, decreased the postprandial antral manometric motility index, and slowed gastric emptying. Atropine caused a slight increase in postprandial frequency of antral contractions by DAS and gastric myoelectrical activity by EGG. Bethanechol slightly increased the amplitude, but slightly decreased the frequency of antral contractions by DAS and decreased the frequency of gastric myoelectrical activity by EGG, with no significant increase in the motility index or gastric emptying. CONCLUSIONS: Cholinergic antagonism with atropine reduces antral contractility and slows gastric emptying. Cholinergic stimulation with bethanechol increases antral contractility, but decreases the frequency of antral contractions, without altering the antral motility index or gastric emptying.  (+info)

Time course of isolated rat fundus response to muscarinic agonists: a measure of intrinsic efficacy. (4/144)

The establishment of a dose-response relationship and its quantification is the usual procedure for analysing drug action on an isolated organ. However, the time course of the effect seems to be an inherent characteristic of the agonist which produces it. In our study, we have analyzed the time-response curves of four cholinergic agonists (acetylcholine, methacholine, carbachol and bethanechol) which produce tonic contractions of the isolated rat gastric fundus. The order of affinity of agonists to muscarinic receptors on the rat fundus were carbachol > bethanechol > methacholine > acetylcholine (K(A) values: 46 +/- 12, 84 +/- 21, 380 +/- 110 and 730 +/- 120 nM, respectively). The effective concentrations which produced 60% of the maximal response (EC60) were used for establishing the time-response curves. The time-response curves were also recorded after partial alkylation of muscarinic receptors with phenoxybenzamine, after exposure of the isolated rat fundus to physostigmine and after addition of supramaximal concentrations of the agonists. The experimental time-response curve for acetylcholine was on the extreme left, followed by curves for methacholine, bethanechol and carbachol, respectively. Phenoxybenzamine and supramaximal doses of the agonists did not change the order of response development in time, but supramaximal doses shifted all curves to the left and phenoxybenzamine shifted all time-response curves to the right. Only physostigmine shifted the time-response curve for methacholine to the right. The results of our study suggest that the response rate of the isolated rat gastric fundus to cholinergic agonists depends on the intrinsic activity of these agents, but not on their affinity for muscarinic receptors.  (+info)

Topical diltiazem and bethanechol decrease anal sphincter pressure without side effects. (5/144)

BACKGROUND: Topical nitrates lower anal sphincter pressure and heal anal fissures, but a majority of patients experience headache. The internal anal sphincter has a calcium dependent mechanism to maintain tone, and also receives an inhibitory extrinsic cholinergic innervation. It may therefore be possible to lower anal sphincter pressure using calcium channel blockers and cholinergic agonists without side effects. AIMS: To investigate the effect of oral and topical calcium channel blockade and a topical cholinomimetic on anal sphincter pressure. METHODS: Three studies were conducted, each involving 10 healthy volunteers. In the first study subjects were given oral 60 mg diltiazem or placebo on separate occasions. They were then given diltiazem once or twice daily for four days. In the second and third studies diltiazem and bethanechol gels of increasing concentration were applied topically to lower anal pressure. RESULTS: A single dose of 60 mg diltiazem lowered the maximum resting anal sphincter pressure (MRP) by a mean of 21%. Once daily diltiazem produced a clinically insignificant effect but a twice daily regimen reduced anal pressure by a mean of 17%. Diltiazem and bethanechol gel produced a dose dependent reduction of the anal pressure; 2% diltiazem produced a maximal 28% reduction, and 0.1% bethanechol a maximal 24% reduction, the effect lasting three to five hours. CONCLUSIONS: Topical diltiazem and bethanechol substantially reduce anal sphincter pressure for a prolonged period, and represent potential low side effect alternatives to topical nitrates for the treatment of anal fissures.  (+info)

Intracellular divalent cation release in pancreatic acinar cells during stimulus-secretion coupling. I. Use of chlorotetracycline as fluorescent probe. (6/144)

Stimulus-secretion coupling in pancreatic exocrine cells was studied using dissociated acini, prepared from mouse pancreas, and chlorotetracycline (CTC), a fluorescent probe which forms highly fluorescent complexes with Ca2+ and Mg2+ ions bound to membranes. Acini, preloaded by incubation with CTC (100 microM), displayed a fluorescence having spectral properties like that of CTC complexed to calcium (excitation and emission maxima at 398 and 527 nm, respectively). Stimulation with either bethanechol or caerulein resulted in a rapid loss of fluorescence intensity and an increase in outflux of CTC from the acini. After 5 min of stimulation, acini fluorescence had been reduced by 40% and appeared to be that of CTC complexed to Mg2+ (excitation and emission maxima at 393 and 521 nm, respectively). The fluorescence loss induced by bethanechol was blocked by atropine and was seen at all agonist concentrations that elicited amylase release. Maximal fluorescence loss, however, required a bethanechol concentration three times greater than that needed for maximal amylase release. In contrast, acini preloaded with ANS or oxytetracycline, probes that are relatively insensitive to membrane-bound divalent cations, displayed no secretagogue-induced fluorescence changes. These results are consistent with the hypothesis that CTC is able to probe some set of intracellular membranes which release calcium during secretory stimulation and that this release results in dissociation of Ca(2+)-complexed CTC.  (+info)

Signaling mechanisms for muscarinic receptor-mediated coronary vasoconstriction in isolated rat hearts. (7/144)

Signaling mechanisms for muscarinic receptor-mediated vasoconstriction in coronary resistance arteries were studied in potassium-arrested isolated rat hearts perfused at a constant flow rate. The cholinergic agonist bethanechol was given by bolus injection or constant infusion. Perfusion pressure was monitored as an indicator of coronary vascular resistance. Bolus injection of bethanechol evoked a phasic vasoconstriction in a dose-dependent manner, whereas infusion of bethanechol evoked a tonic vasoconstriction without producing tachyphylaxis. Bethanechol-induced phasic vasoconstriction was eliminated by perfusion with a Ca(2+)-free buffer. The L-type voltage-operated Ca(2+) channel blocker nifedipine decreased the maximal constrictor response to bethanechol by 59 +/- 2% (n = 4, P <.001), whereas the putative receptor-operated Ca(2+) channel blocker SK&F 96365 converted this vasoconstriction into vasodilation that was not mediated by nitric oxide. The protein kinase C inhibitor chelerythrine reduced the maximal phasic vasoconstrictor response to bethanechol by 78 +/- 2% (n = 6, P <.001) Bethanechol-induced tonic vasoconstriction was rapidly converted to a sustained vasodilation during infusion of SK&F 96365 or nifedipine, whereas infusion of chelerythrine gradually attenuated the tonic response to bethanechol. Results from other experiments do not support a role for phospholipase A(2)-dependent mediators in generating coronary vasoconstrictor responses to bethanechol. It is concluded that voltage-independent receptor-operated Ca(2+) channels, voltage-operated Ca(2+) channels, and protein kinase C are major signaling components for muscarinic receptor-mediated contraction of rat coronary resistance arteries.  (+info)

Parasympathetic non-adrenergic, non-cholinergic-induced protein synthesis and mitogenic activity in rat parotid glands. (8/144)

Electrical stimulation of the parasympathetic auriculo-temporal nerve (40 Hz, 30 min), in the anaesthetized rat under - and -adrenoceptor blockade, increased [3H]thymidine and [3H]leucine uptake into the parotid glands by 80 and 263 %, respectively. The increase in response to parasympathetic stimulation was almost the same ([3H]thymidine 82 % and [3H]leucine 283 %) when atropine (2 mg kg-1 I.P. or I.V.) was included in the pretreatment. Neither intravenous infusion of vasoactive intestinal peptide (0.5-20 mg kg-1 min-1, 30 min) nor of bethanechol (10 mg kg-1 min-1, 30 min), under adrenoceptor blockade, increased the uptake of [3H]thymidine into the glands. However, these drugs increased [3H]leucine uptake, and in combination they interacted positively. Whereas vasoactive intestinal peptide is likely to be involved in the parasympathetic nerve-evoked protein synthesis, the nature of the non-adrenergic, non-cholinergic component(s) involved in the mitogenic response is presently unknown.  (+info)

Bethanechol is a parasympathomimetic drug, which means it stimulates the parasympathetic nervous system. This system is responsible for regulating many automatic functions in the body, including digestion and urination. Bethanechol works by causing the smooth muscles of the bladder to contract, which can help to promote urination in people who have difficulty emptying their bladder completely due to certain medical conditions such as surgery, spinal cord injury, or multiple sclerosis.

The medical definition of 'Bethanechol' is:

A parasympathomimetic agent that stimulates the muscarinic receptors of the autonomic nervous system, causing contraction of smooth muscle and increased secretion of exocrine glands. It is used to treat urinary retention and associated symptoms, such as those caused by bladder-neck obstruction due to prostatic hypertrophy or neurogenic bladder dysfunction. Bethanechol may also be used to diagnose urinary tract obstruction and to test the integrity of the bladder's innervation.

Bethanechol compounds are a type of cholinergic agent used in medical treatment. They are parasympathomimetic drugs, which means they mimic the actions of the neurotransmitter acetylcholine at muscarinic receptors. Specifically, bethanechol compounds stimulate the muscarinic receptors in the smooth muscle of the bladder and gastrointestinal tract, increasing tone and promoting contractions.

Bethanechol is primarily used to treat urinary retention and associated symptoms, such as those that can occur after certain types of surgery or with conditions like spinal cord injury or multiple sclerosis. It works by helping the bladder muscle contract, which can promote urination.

It's important to note that bethanechol should be used with caution, as it can have various side effects, including sweating, increased salivation, flushed skin, and gastrointestinal symptoms like nausea, vomiting, or diarrhea. It may also interact with other medications, so it's crucial to discuss any potential risks with a healthcare provider before starting this treatment.

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.

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

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

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

Tropicamide is a muscarinic antagonist, which is a type of drug that blocks the action of acetylcholine in the body. In particular, it blocks the muscarinic receptors found in the eye, which results in pupil dilation (mydriasis) and paralysis of the ciliary muscle (cycloplegia).

Tropicamide is commonly used in ophthalmology as a diagnostic aid during eye examinations. It is often instilled into the eye to dilate the pupil, which allows the eye care professional to more easily examine the back of the eye and assess conditions such as cataracts, glaucoma, or retinal disorders. The cycloplegic effect of tropicamide also helps to relax the accommodation reflex, making it easier to measure the refractive error of the eye and determine the appropriate prescription for eyeglasses or contact lenses.

It is important to note that tropicamide can cause temporary blurring of vision and sensitivity to light, so patients should be advised not to drive or operate heavy machinery until the effects of the medication have worn off.

Ageusia is a medical term that refers to the complete loss of taste. It can affect a person's ability to detect sweet, salty, sour, bitter, and savory flavors. Ageusia can be caused by various factors such as damage to the nerves responsible for transmitting taste signals to the brain, exposure to certain chemicals or radiation therapy, and some medical conditions like diabetes, hypertension, and upper respiratory infections. In some cases, ageusia may be temporary, while in others, it can be permanent. It is important to consult a healthcare professional if experiencing a loss of taste, as it could be a sign of an underlying health issue.

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.

Pentagastrin is a synthetic polypeptide hormone that stimulates the release of gastrin and hydrochloric acid from the stomach. It is used diagnostically to test for conditions such as Zollinger-Ellison syndrome, a rare disorder in which tumors in the pancreas or duodenum produce excessive amounts of gastrin, leading to severe ulcers and other digestive problems.

Pentagastrin is typically administered intravenously, and its effects are monitored through blood tests that measure gastric acid secretion. It is a potent stimulant of gastric acid production, and its use is limited to diagnostic purposes due to the risk of adverse effects such as nausea, flushing, and increased heart rate.

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.

Gastric acid, also known as stomach acid, is a digestive fluid produced in the stomach. It's primarily composed of hydrochloric acid (HCl), potassium chloride (KCl), and sodium chloride (NaCl). The pH of gastric acid is typically between 1.5 and 3.5, making it a strong acid that helps to break down food by denaturing proteins and activating digestive enzymes.

The production of gastric acid is regulated by the enteric nervous system and several hormones. The primary function of gastric acid is to initiate protein digestion, activate pepsinogen into the active enzyme pepsin, and kill most ingested microorganisms. However, an excess or deficiency in gastric acid secretion can lead to various gastrointestinal disorders such as gastritis, ulcers, and gastroesophageal reflux disease (GERD).

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.

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.

Pirenzepine is a medication that belongs to a class of drugs called anticholinergics or parasympatholytics. It works by blocking the action of acetylcholine, a neurotransmitter in the body, on certain types of muscarinic receptors.

Pirenzepine is primarily used to treat peptic ulcers and gastroesophageal reflux disease (GERD) by reducing the production of stomach acid. It may also be used to manage symptoms of irritable bowel syndrome, such as abdominal pain and diarrhea.

The medication is available in the form of tablets or gel for topical application. Side effects of pirenzepine may include dry mouth, blurred vision, constipation, dizziness, and difficulty urinating. It should be used with caution in people with glaucoma, benign prostatic hyperplasia, or other conditions that may be exacerbated by anticholinergic drugs.

It is important to note that this definition is for informational purposes only and should not be taken as medical advice. Always consult with a healthcare professional before starting any new medication.

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.

Cholinergic agents are a class of drugs that mimic the action of acetylcholine, a neurotransmitter in the body that is involved in the transmission of nerve impulses. These agents work by either increasing the amount of acetylcholine in the synapse (the space between two neurons) or enhancing its action on receptors.

Cholinergic agents can be classified into two main categories: direct-acting and indirect-acting. Direct-acting cholinergic agents, also known as parasympathomimetics, directly stimulate muscarinic and nicotinic acetylcholine receptors. Examples of direct-acting cholinergic agents include pilocarpine, bethanechol, and carbamate.

Indirect-acting cholinergic agents, on the other hand, work by inhibiting the enzyme acetylcholinesterase, which is responsible for breaking down acetylcholine in the synapse. By inhibiting this enzyme, indirect-acting cholinergic agents increase the amount of acetylcholine available to stimulate receptors. Examples of indirect-acting cholinergic agents include physostigmine, neostigmine, and edrophonium.

Cholinergic agents are used in the treatment of a variety of medical conditions, including myasthenia gravis, Alzheimer's disease, glaucoma, and gastrointestinal disorders. However, they can also have significant side effects, such as bradycardia, bronchoconstriction, and increased salivation, due to their stimulation of muscarinic receptors. Therefore, they must be used with caution and under the close supervision of a healthcare provider.

A muscarinic M3 receptor is a type of G protein-coupled receptor (GPCR) that binds to the neurotransmitter acetylcholine. It is a subtype of muscarinic receptors, which are named after the muscarine mushroom alkaloid that can activate them.

The M3 receptor is widely expressed in various tissues and organs, including the smooth muscle of the gastrointestinal tract, urinary bladder, respiratory system, and vasculature. When activated by acetylcholine or muscarinic agonists, it triggers a range of intracellular signaling pathways that lead to various physiological responses, such as smooth muscle contraction, glandular secretion, and modulation of neurotransmitter release.

The M3 receptor is known to couple primarily to the Gq/11 family of G proteins, which activate phospholipase C (PLC) and increase intracellular calcium levels. This leads to smooth muscle contraction and other downstream effects. The M3 receptor also interacts with other signaling pathways, such as those involving adenylyl cyclase, mitogen-activated protein kinases (MAPKs), and ion channels.

Dysregulation of muscarinic M3 receptors has been implicated in various diseases, including gastrointestinal disorders, overactive bladder syndrome, asthma, and cardiovascular diseases. Therefore, selective modulation of this receptor subtype is a potential therapeutic strategy for these conditions.

Amylases are enzymes that break down complex carbohydrates, such as starch and glycogen, into simpler sugars like maltose, glucose, and maltotriose. There are several types of amylases found in various organisms, including humans.

In humans, amylases are produced by the pancreas and salivary glands. Pancreatic amylase is released into the small intestine where it helps to digest dietary carbohydrates. Salivary amylase, also known as alpha-amylase, is secreted into the mouth and begins breaking down starches in food during chewing.

Deficiency or absence of amylases can lead to difficulties in digesting carbohydrates and may cause symptoms such as bloating, diarrhea, and abdominal pain. Elevated levels of amylase in the blood may indicate conditions such as pancreatitis, pancreatic cancer, or other disorders affecting the pancreas.

A Pharmacist is a healthcare professional who practices in the field of pharmacy, focusing on the safe and effective use of medications. They are responsible for dispensing medications prescribed by physicians and other healthcare providers, as well as providing information and counseling to patients about their medications. This includes explaining how to take the medication, potential side effects, and any drug interactions. Pharmacists may also be involved in medication therapy management, monitoring patient health and adjusting medication plans as needed. They must have a deep understanding of the properties and actions of drugs, including how they are absorbed, distributed, metabolized, and excreted by the body, as well as their potential interactions with other substances and treatments. In addition to a Doctor of Pharmacy (Pharm.D.) degree, pharmacists must also be licensed in the state where they practice.

Oral administration is a route of giving medications or other substances by mouth. This can be in the form of tablets, capsules, liquids, pastes, or other forms that can be swallowed. Once ingested, the substance is absorbed through the gastrointestinal tract and enters the bloodstream to reach its intended target site in the body. Oral administration is a common and convenient route of medication delivery, but it may not be appropriate for all substances or in certain situations, such as when rapid onset of action is required or when the patient has difficulty swallowing.

A "Drug Administration Schedule" refers to the plan for when and how a medication should be given to a patient. It includes details such as the dose, frequency (how often it should be taken), route (how it should be administered, such as orally, intravenously, etc.), and duration (how long it should be taken) of the medication. This schedule is often created and prescribed by healthcare professionals, such as doctors or pharmacists, to ensure that the medication is taken safely and effectively. It may also include instructions for missed doses or changes in the dosage.

In anatomical terms, the stomach is a muscular, J-shaped organ located in the upper left portion of the abdomen. It is part of the gastrointestinal tract and plays a crucial role in digestion. The stomach's primary functions include storing food, mixing it with digestive enzymes and hydrochloric acid to break down proteins, and slowly emptying the partially digested food into the small intestine for further absorption of nutrients.

The stomach is divided into several regions, including the cardia (the area nearest the esophagus), the fundus (the upper portion on the left side), the body (the main central part), and the pylorus (the narrowed region leading to the small intestine). The inner lining of the stomach, called the mucosa, is protected by a layer of mucus that prevents the digestive juices from damaging the stomach tissue itself.

In medical contexts, various conditions can affect the stomach, such as gastritis (inflammation of the stomach lining), peptic ulcers (sores in the stomach or duodenum), gastroesophageal reflux disease (GERD), and stomach cancer. Symptoms related to the stomach may include abdominal pain, bloating, nausea, vomiting, heartburn, and difficulty swallowing.

MedlinePlus is not a medical term, but rather a consumer health website that provides high-quality, accurate, and reliable health information, written in easy-to-understand language. It is produced by the U.S. National Library of Medicine, the world's largest medical library, and is widely recognized as a trusted source of health information.

MedlinePlus offers information on various health topics, including conditions, diseases, tests, treatments, and wellness. It also provides access to drug information, medical dictionary, and encyclopedia, as well as links to clinical trials, medical news, and patient organizations. The website is available in both English and Spanish and can be accessed for free.

Copyright is a legal concept that gives the creator of an original work exclusive rights to its use and distribution, usually for a limited period of time. In the medical field, copyright protection can apply to various works such as medical textbooks, journal articles, educational materials, software, and multimedia presentations. It is important to note that copyright law seeks to strike a balance between protecting the rights of creators and promoting the progress of science and knowledge by allowing for limited use of copyrighted material under certain circumstances, such as fair use.

It's worth mentioning that while copyright protection can apply to medical works, there are also exceptions and limitations to copyright law that may allow for the use of copyrighted material without permission from the copyright owner in certain situations. For example, in the United States, the "fair use" doctrine allows for limited use of copyrighted material without obtaining permission from the copyright owner, depending on factors such as the purpose and character of the use, the nature of the copyrighted work, the amount and substantiality of the portion used, and the effect of the use upon the potential market for or value of the copyrighted work.

When using medical works that are protected by copyright, it is important to obtain permission from the copyright owner or ensure that the use falls under an exception or limitation to copyright law, such as fair use, in order to avoid infringing on the exclusive rights of the copyright owner.

Patient medication knowledge, also known as patient medication literacy or medication adherence, refers to the ability of a patient to understand and effectively communicate about their medications, including what they are for, how and when to take them, potential side effects, and other important information. This is an essential component of medication management, as it allows patients to properly follow their treatment plans and achieve better health outcomes. Factors that can affect patient medication knowledge include age, education level, language barriers, and cognitive impairments. Healthcare providers play a key role in promoting patient medication knowledge by providing clear and concise instructions, using visual aids when necessary, and regularly assessing patients' understanding of their medications.

Drug Information Services (DIS) are specialized resources within healthcare systems, typically staffed by clinical pharmacists and pharmacy residents, that provide evidence-based information and analysis about medications to healthcare professionals and patients. The primary goal of DIS is to optimize medication use and improve patient outcomes through the provision of accurate, unbiased, and timely information on drug therapy.

DIS commonly provide a range of services, including:

1. Answering medication-related questions from healthcare providers, such as physicians, nurses, and other pharmacists, regarding drug interactions, dosing, adverse effects, and therapeutic alternatives.
2. Developing and maintaining formulary management systems to ensure the safe and cost-effective use of medications within a healthcare institution or system.
3. Providing patient education materials and resources on medication therapy, including proper administration techniques, potential side effects, and storage requirements.
4. Conducting ongoing literature evaluations and synthesizing evidence-based recommendations for medication use in various clinical scenarios.
5. Collaborating with healthcare teams to develop and implement guidelines, policies, and procedures related to medication management and safety.
6. Offering educational programs and resources for healthcare professionals and students to enhance their knowledge of pharmacotherapy and medication safety practices.
7. Participating in multidisciplinary committees focused on improving medication use processes, reducing medication errors, and promoting patient safety.

DIS are essential components of modern healthcare systems, as they help ensure the safe, effective, and efficient use of medications for improved patient outcomes.

A pharmaceutical society is a professional organization that represents and serves the interests of pharmacists and the pharmaceutical industry in a given society or country. The primary objective of these societies is to promote the advancement of the profession of pharmacy, including education, research, and practice. They also work to ensure the safe and effective use of medications, advocate for evidence-based policies and practices, and provide resources and support to their members.

Pharmaceutical societies may engage in various activities, such as:

1. Developing guidelines and standards for pharmacy education and practice.
2. Providing continuing education programs for pharmacists.
3. Conducting research and disseminating knowledge related to pharmacy and medication use.
4. Advocating for policies that promote the safe and effective use of medications.
5. Collaborating with other healthcare professionals, regulatory bodies, and industry partners to improve patient outcomes.
6. Providing resources and support to members, including career development opportunities and networking events.

Examples of pharmaceutical societies include the American Pharmacists Association (APhA), the Royal Pharmaceutical Society (RPS) in the UK, and the International Pharmaceutical Federation (FIP).

A non-medical internship is not specifically related to the field of medicine. It generally refers to an organized period of work experience, often temporary, in which a person typically a student or trainee, gains practical knowledge and skills in a particular industry or profession. The intern is supervised and mentored by experienced professionals in the field. Non-medical internships can be found in various sectors such as business, engineering, law, education, media, technology, and many others. They provide an opportunity to apply theoretical knowledge gained in the classroom to real-world situations and help interns develop professional competencies and networks.

I'm sorry for any confusion, but "Maryland" is a proper noun and does not have a medical definition. It is a state located in the Mid-Atlantic region of the United States. However, if you are referring to a specific medical term or concept that includes "Maryland," could you please provide more context? I'll do my best to help with accurate information based on the provided context.

The name bethanechol refers to its structure as the urethane of beta-methylcholine. Bethanechol alleviates dry mouth and is ... Bethanechol should be used to treat these disorders only after mechanical obstruction is ruled out as a possible cause. Its ... Use of bethanechol, as well as all other muscarinic receptor agonists, is contraindicated in patients with asthma, coronary ... Unlike acetylcholine, bethanechol is not hydrolyzed by cholinesterase and will therefore have a long duration of action. ...
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Parasympathetic stimulation, e.g. bethanechol, pilocarpine, carbachol Antihistamines e.g. chlorpheniramine, diphenhydramine, ...
Upon activation of muscarinic ACh receptors with bethanechol, margatoxin-sensitive current was suppressed. Therefore, it was ...
Now Pfizer) Phenylpiperazine Prado WA, Segalla DK (August 2004). "Antinociceptive effects of bethanechol or ...
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Pilocarpine - a similar parasympathomimetic medication for dry mouth (xerostomia) Bethanechol - a similar muscarinic ...
Choline esters Acetylcholine (all acetylcholine receptors) Bethanechol (M3 receptors) Carbachol (all muscarinic receptors and ...
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The name bethanechol refers to its structure as the urethane of beta-methylcholine. Bethanechol alleviates dry mouth and is ... Bethanechol should be used to treat these disorders only after mechanical obstruction is ruled out as a possible cause. Its ... Use of bethanechol, as well as all other muscarinic receptor agonists, is contraindicated in patients with asthma, coronary ... Unlike acetylcholine, bethanechol is not hydrolyzed by cholinesterase and will therefore have a long duration of action. ...
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BETHANECHOL, 50MG, TABLET. Common uses. This medication is typically used for urinary retention (difficulty passing urine). It ...
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BETHANECHOL CHLORIDE (bethanechol chloride 5 mg) tablet. BETHANECHOL CHLORIDE (bethanechol chloride 10 mg) tablet. BETHANECHOL ... BETHANECHOL CHLORIDE (bethanechol chloride 50 mg) tablet. NDC Code(s): 64679-965-01, 64679-966-01, 64679-967-01, 64679-968-01 * ... BETHANECHOL CHLORIDE tablet. NDC Code(s): 62135-755-90, 62135-756-12, 62135-757-12, 62135-758-12 *Packager: Chartwell RX, LLC ... BETHANECHOL CHLORIDE tablet. NDC Code(s): 60687-689-01, 60687-689-11, 60687-700-01, 60687-700-11 *Packager: American Health ...
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Cholinomimetic compounds (eg, pilocarpine, methacholine, bethanechol). *Nicotine alkaloids (eg, nicotine, coniine). *Muscarine- ...
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Cholinomimetic compounds (eg, pilocarpine, methacholine, bethanechol). *Nicotine alkaloids (eg, nicotine, coniine). *Muscarine- ...
Bethanechol, a cholinergic agonist, has limited effect on detrusor contractility. a-Adrenergic agonists such as ephedrine, ...
Bethanechol Chloride (Urecholine, Myocholine) April 14, 2021 Bethanechol chloride works to strengthen the detrusor muscles ...
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  • Bethanechol chloride tablets are indicated for the treatment of acute postoperative and postpartum nonobstructive (functional) urinary retention and for neurogenic atony of the urinary bladder with retention. (johnleepharmaceuticals.com)
  • We found 6 global bethanechol chloride Tenders from the public procurement domain worldwide. (biddetail.com)
  • Bethanechol chloride works to strengthen the detrusor muscle's contraction. (vin.com)
  • We studied whether the effects of bethanechol are mediated via a muscarinic receptor, the role of extracellular calcium on bladder contraction, and down-regulation of bladder contraction by bethanechol after activation with potassium chloride (KCl) and acetylcholine (Ach). (bvsalud.org)
  • Bethanechol is sold under the brand names Duvoid (Roberts), Myotonachol (Glenwood), Urecholine (Merck Frosst) and Urocarb (Hamilton). (wikipedia.org)
  • Low calcium levels and certain drugs (e.g., digoxin, bethanechol, physostigmine, pilocarpine) may predispose some cats to second-degree AV block-Mobitz Type 1. (petmd.com)
  • tell your doctor and pharmacist if you are allergic to bethanechol or any other drugs. (medlineplus.gov)
  • Use of bethanechol, as well as all other muscarinic receptor agonists, is contraindicated in patients with asthma, coronary insufficiency, peptic ulcers, intestinal obstruction and hyperthyroidism. (wikipedia.org)
  • Unlike acetylcholine, bethanechol is not hydrolyzed by cholinesterase and will therefore have a long duration of action. (wikipedia.org)
  • Atropine is given preoperatively to prevent voiding of the bowel/bladder during surgery, Bethanechol is then given postoperatively to revert this action. (wikipedia.org)
  • Bethanechol can help with urinating troubles associated with nerve disorders or weak bladder muscles. (gianteaglepetrx.com)
  • Bethanechol caused a dose-dependent increase in bladder contraction. (bvsalud.org)
  • supplier of Bethanechol vendor api manufacturer supplier ingredients cas# 674-38-4, It's active pharmaceutical ingredient/raw material of pharmaceutical, not finish product, Please make sure you know how to use it, formulation and side effection. (tcspharms.com)
  • 4, What's the price of Bethanechol vendor api manufacturer supplier ingredients cas# 674-38-4? (tcspharms.com)
  • 5, how to buy Bethanechol vendor api manufacturer supplier ingredients cas# 674-38-4? (tcspharms.com)
  • Bethanechol should be used to treat these disorders only after mechanical obstruction is ruled out as a possible cause. (wikipedia.org)
  • Bethanechol is used to relieve difficulties in urinating caused by surgery, drugs, or other factors. (medlineplus.gov)
  • The potency of bethanechol is higher than Ach, as shown by higher peak active isometric stress (P(max)) and lower half-maximal contraction (ED(50)) (P (bvsalud.org)
  • The contractile responses to bethanechol were diminished in the presence of atropine, nifedipine and in calcium-free medium as shown by P(max) decreased by 58%, 87% and 65% and ED(50) increased by 314-, 24- and 16-fold, respectively. (bvsalud.org)
  • Bethanechol Chloride Tablets USP are indicated for the treatment of acute postoperative and postpartum nonobstructive (functional) urinary retention and for neurogenic atony of the urinary bladder with retention. (nih.gov)
  • Bethanechol chloride, USP, a cholinergic agent, is a synthetic ester which is structurally and pharmacologically related to acetylcholine. (nih.gov)
  • Because of the selective action of bethanechol chloride, nicotinic symptoms of cholinergic stimulation are usually absent or minimal when orally or subcutaneously administered in therapeutic doses, while muscarinic effects are prominent. (nih.gov)
  • bethanechol increases and aclidinium decreases cholinergic effects/transmission. (medscape.com)
  • amifampridine and bethanechol both increase cholinergic effects/transmission. (medscape.com)
  • bethanechol increases and anticholinergic/sedative combos decreases cholinergic effects/transmission. (medscape.com)
  • bethanechol increases and cisatracurium decreases cholinergic effects/transmission. (medscape.com)
  • bethanechol increases and cyclizine decreases cholinergic effects/transmission. (medscape.com)
  • bethanechol increases and darifenacin decreases cholinergic effects/transmission. (medscape.com)
  • Bethanechol is a synthetic muscarinic stimulant. (medscape.com)
  • Bethanechol is used to relieve difficulties in urinating caused by surgery, drugs, or other factors. (medlineplus.gov)
  • tell your doctor and pharmacist if you are allergic to bethanechol or any other drugs. (medlineplus.gov)
  • Bethanechol chloride acts principally by producing the effects of stimulation of the parasympathetic nervous system. (nih.gov)
  • However, lead, like the phosphodiesterase inhibitor theophylline and unlike the calcium-influx blocker verapamil, did not inhibit bethanechol- or potassium-stimulated contractions and calcium influx into crop tissue. (nih.gov)
  • Each tablet for oral administration contains 5 mg, 10 mg, 25 mg or 50 mg bethanechol chloride, USP. (nih.gov)
  • Effects on the GI and urinary tracts sometimes appear within 30 minutes after oral administration of bethanechol chloride, but more often 60 to 90 minutes are required to reach maximum effectiveness. (nih.gov)
  • Following oral administration, the usual duration of action of bethanechol chloride is one hour, although large doses (300 to 400 mg) have been reported to produce effects for up to six hours. (nih.gov)
  • 7. A randomized phase III prospective trial of bethanechol to prevent radiotherapy-induced salivary gland damage in patients with head and neck cancer. (nih.gov)