An adrenergic-beta-2 antagonist that has been used for cardiac arrhythmia, angina pectoris, hypertension, glaucoma, and as an antithrombotic.
A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The beta-3 adrenergic receptors are the predominant beta-adrenergic receptor type expressed in white and brown ADIPOCYTES and are involved in modulating ENERGY METABOLISM and THERMOGENESIS.
Drugs that bind to and block the activation of ADRENERGIC BETA-3 RECEPTORS.
Drugs that bind to and block the activation of ADRENERGIC BETA-1 RECEPTORS.
Compounds that bind to and activate ADRENERGIC BETA-3 RECEPTORS.
Compounds that bind to and activate ADRENERGIC BETA-1 RECEPTORS.
Drugs that bind to but do not activate beta-adrenergic receptors thereby blocking the actions of beta-adrenergic agonists. Adrenergic beta-antagonists are used for treatment of hypertension, cardiac arrhythmias, angina pectoris, glaucoma, migraine headaches, and anxiety.
AMINO ALCOHOLS containing the propanolamine (NH2CH2CHOHCH2) group and its derivatives.
A beta-2 selective adrenergic antagonist. It is used primarily in animal and tissue experiments to characterize BETA-2 ANDRENERGIC RECEPTORS.
One of two major pharmacologically defined classes of adrenergic receptors. The beta adrenergic receptors play an important role in regulating CARDIAC MUSCLE contraction, SMOOTH MUSCLE relaxation, and GLYCOGENOLYSIS.
Drugs that selectively bind to and activate beta-adrenergic receptors.
A moderately lipophilic beta blocker (ADRENERGIC BETA-ANTAGONISTS). It is non-cardioselective and has intrinsic sympathomimetic actions, but little membrane-stabilizing activity. (From Martindale, The Extra Pharmocopoeia, 30th ed, p638)
A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The adrenergic beta-1 receptors are equally sensitive to EPINEPHRINE and NOREPINEPHRINE and bind the agonist DOBUTAMINE and the antagonist METOPROLOL with high affinity. They are found in the HEART, juxtaglomerular cells, and in the central and peripheral nervous systems.
That phase of a muscle twitch during which a muscle returns to a resting position.
The phenomenon whereby compounds whose molecules have the same number and kind of atoms and the same atomic arrangement, but differ in their spatial relationships. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 5th ed)
Contractile activity of the MYOCARDIUM.
The increase in a measurable parameter of a PHYSIOLOGICAL PROCESS, including cellular, microbial, and plant; immunological, cardiovascular, respiratory, reproductive, urinary, digestive, neural, musculoskeletal, ocular, and skin physiological processes; or METABOLIC PROCESS, including enzymatic and other pharmacological processes, by a drug or other chemical.

Beta 1-, beta 2- and atypical beta-adrenoceptor-mediated relaxation in rat isolated aorta. (1/31)

beta-adrenoceptor-mediated relaxation was investigated in ring preparations of rat isolated thoracic aorta. Rings were pre-constricted with a sub-maximal concentration of noradrenaline (1 microM) and relaxant responses to cumulative concentrations of beta-adrenoceptor agonists obtained. The concentration-response curve (CRC) to isoprenaline was shifted to the right by propranolol (0.3 microM) with a steepening of the slope. Estimation of the magnitude of the shift from EC(50) values gave a pA(2) of 7.6. Selective beta(1)- and beta(2)-adrenoceptor antagonists, CGP 20712A (0.1 microM) and ICI 118551 (0.1 microM), respectively, produced 4 and 14 fold shifts of the isoprenaline CRC. Atypical beta-adrenoceptor agonists also produced concentration-dependent relaxation of aortic rings. The order of potency of the beta-adrenoceptor agonists was (-log EC(50)): isoprenaline (6. 25)>cyanopindolol (5.59)>isoprenaline+propranolol (5.11)>CGP 12177A (4.40)>ZD 2079 (4.24)>ZM 215001 (4.07)>BRL 37344 (3.89). Relaxation to CGP 12177A and ZM 215001 was unaffected by propranolol (0.3 microM). SR 59230A (+info)

The beta3-adrenoceptor-mediated relaxation induced by epinephrine in guinea pig taenia caecum. (2/31)

The mechanisms of the beta-adrenoceptor mediated relaxation induced by epinephrine in guinea pig taenia caecum were examined. The relaxant response to epinephrine was unaffected by propranolol (approximately 10(-5) M) or phentolamine (approximately 10(-5) M). The response to epinephrine was antagonized in a concentration dependent manner by bupranolol, and Schild plot of the data revealed the pA2 value of 5.87. Epinephrine significantly increased cyclic AMP level in this preparation. Bupranolol (10(-4) M) significantly decreased the cyclic AMP level that was elicited by epinephrine, whereas propranolol (10(-5) M) produced no effect. These results suggest that the relaxant response to epinephrine in the guinea pig taenai caecum is mainly mediated by beta3-adrenoceptors.  (+info)

Partial agonistic effects of carteolol on atypical beta-adrenoceptors in the guinea pig gastric fundus. (3/31)

The properties of the beta1-/beta2-adrenoceptor partial agonist carteolol were investigated in atypical beta-adrenoceptors on the guinea pig gastric fundus. Carteolol induced concentration-dependent relaxation in this tissue (pD2 = 5.55, intrinsic activity = 0.94). However, a combination of the selective beta1-adrenoceptor antagonist atenolol (100 microM) and the selective beta2-adrenoceptor antagonist butoxamine (100 microM) produced only small rightward shifts in the concentration-response curves of carteolol in the gastric fundus (pD2 = 4.91, intrinsic activity = 0.94). In the presence of both atenolol (100 microM) and butoxamine (100 microM), the non-selective beta1-, beta2- and beta3-adrenoceptor antagonist (+/-)-bupranolol (10-100 microM) caused a concentration-dependent right-ward shift of the concentration-response curves for carteolol in the guinea pig gastric fundus. Schild plot analyses of the effects of (+/-)-bupranolol against carteolol gave the pA2 value of 5.29 and the Schild slope was not significantly different from unity. Furthermore, carteolol (10 microM) weakly but significantly antagonized the relaxant responses to catecholamines ((-)-isoprenaline, (-)-noradrenaline and (-)-adrenaline), a selective beta3-adrenoceptor agonist BRL37344 ((R*,R*)-(+/-)-4-[2-[(2-(3-chlorophenyl)-2-hydroxyethyl)amino]propyl]phenoxy-acet ic acid sodium salt) and a non-conventional partial beta3-adrenoceptor agonist (+/-)-CGP12177A ([4-[3-[(1,1dimethylethyl)amino]-2-hydroxypropoxy]-1,3-dihydro-2H-benzimidazol-2- one] hydrochloride) in the guinea pig gastric fundus. These results suggest that the partial agonistic effects of carteolol are mediated by atypical beta-adrenoceptors in the guinea pig gastric fundus.  (+info)

(+/-)-Pindolol acts as a partial agonist at atypical beta-adrenoceptors in the guinea pig duodenum. (4/31)

The agonistic and antagonistic effects of (+/-)-pindolol (1-(1H-indol-4-yloxy)-3-[(1-methylethyl)amino]-2-propanol) were estimated to clarify whether (+/-)-pindolol acts as a partial agonist on atypical beta-adrenoceptors in the guinea pig duodenum. (+/-)-Pindolol induced concentration-dependent relaxation with a pD2 value of 5.10 +/- 0.03 and an intrinsic activity of 0.83 +/- 0.03. However, the relaxations to (+/-)-pindolol were not antagonized by the non-selective beta1- and beta2-adrenoceptor antagonist (+/-)-propranolol (1 microM). In the presence of (+/-)-propranolol (1 microM), the non-selective beta1-, beta2- and beta3-adrenoceptor antagonist (+/-)-bupranolol (30 microM) induced a rightward shift of the concentration-response curves for (+/-)-pindolol (apparent pA2 = 5.41 +/- 0.06). In the presence of (+/-)-propranolol, (+/-)-pindolol (10 microM) weakly but significantly antagonized the relaxant effects to catecholamines ((-)-isoprenaline, (-)-noradrenaline and (-)-adrenaline), a selective beta3-adrenoceptor agonist BRL37344 ((R*,R*)-(+/-)-4-[2-[(2-(3-chlorophenyl)-2-hydroxyethyl) amino]propyl]phenoxyacetic acid sodium salt) and a non-conventional partial beta3-adrenoceptor agonist (+/-)-CGP12177A([4-[3-[(1,1-dimethylethyl)amino]-2-hydroxypropoxy]-1,3-dihydro-2H -benzimidazol-2-one] hydrochloride). These results demonstrate that (+/-)-pindolol possesses both agonistic and antagonistic effects on atypical beta-adrenoceptors in the guinea pig duodenum.  (+info)

Further evidence that (+/-)-carteolol-induced relaxation is mediated by beta2-adrenoceptors but not by beta3-adrenoceptors in the guinea pig taenia caecum. (5/31)

The properties of the beta1- and beta2-adrenoceptor partial agonist (+/-)-carteolol were investigated against the beta2- and beta3-adrenoceptors of the taenia caecum of the guinea pig. (--)-Isoprenaline and (+/-)-carteolol induced concentration-dependent relaxation in this tissue. The non-selective beta1- and beta2-adrenoceptor antagonist (+/-)-propranolol (10-100 nM), the selective beta2-adrenoceptor antagonist ICI 118,551 (10-100 nM) and the non-selective beta1-, beta2- and beta3-adrenoceptor antagonist (+/-)-bupranolol (10-100nM), caused a concentration-dependent rightward shift of the concentration-response curves for (--)-isoprenaline and (+/-)-carteolol. Schild regression plot analyses carried out for (+/-)-propranolol against (--)-isoprenaline and (+/-)-carteolol gave pA2 values of 8.35 and 8.24, respectively. Schild plot analyses of ICI 118,551 against (--)-isoprenaline and (+/-)-carteolol gave pA2 values of 8.47 and 8.41, respectively. Schild plot analyses of (+/-)-bupranolol against (--)-isoprenaline and (+/-)-carteolol gave pA2 values of 8.47 and 8.53, respectively. Slopes of the Schild plots were not significantly different from unity. These results suggest that the relaxant effects of (+/-)-carteolol in the guinea pig taenia caecum are mediated by beta2-adrenoceptors but not by beta3-adrenoceptors.  (+info)

Transdermal absorption of bupranolol in rabbit skin in vitro and in vivo. (6/31)

This study was designed to clarify the percutaneous penetration of bupranolol (BP), a beta-adrenoceptor antagonist, through rabbit skin and to compare the in vitro penetration with the in vivo absorption. BP penetrated across the skin slowly in the absence of enhancers in vitro. Isopropyl myristate and N-methyl-2-pyrrolidone enhanced the in vitro penetration, with a 3.6 times higher flux compared with that without enhancers. However, in the in vivo percutaneous absorption, the maximal penetration was obtained with the formulation added dlimonene, with a 3.0 times higher area under the concentration-time curve (AUC) than that for the formulation without enhancers. The plasma levels of BP determined, however, were extremely lower than the theoretical plasma steady-state concentrations predicted. The plasma levels of BP after application of these formulations were maintained in the range of 7-22 ng/ml for 30 h, of which concentrations were above the therapeutically effective concentration (1.5-4 ng/ml). Therefore, the transdermal systems will offer an efficient drug delivery system for the treatment of angina pectoris and tachycardia.  (+info)

Structure-activity relationship studies of (+/-)-terbutaline and (+/-)-fenoterol on beta3-adrenoceptors in the guinea pig gastric fundus. (7/31)

(+/-)-Terbutaline and (+/-)-fenoterol are both arylethanolamine analogs that have tertbutyl and aryliso-propyl substituents respectively at the a position on the nitrogen of the ethanolamine side chain. In the present study, we have investigated the structure-activity relationships of (+/-)-terbutaline and (+/-)-fenoterol as beta3-adrenoceptor agonists in the guinea pig gastric fundus. (+/-)-Terbutaline and (+/-)-fenoterol induced concentration-dependent relaxation of the precontracted gastric fundus with pD2 values of 4.45+/-0.10 and 5.90+/-0.09, and intrinsic activities of 1.00+/-0.03 and 0.99+/-0.01 respectively. The combination of the selective beta1-adrenoceptor antagonist (+/-)-atenolol (100 microM), and the selective beta2-adrenoceptor antagonist (+/-)-butoxamine (100 microM), produced a 2 and 6 fold rightward shift of the concentration-response curves for (+/-)-terbutaline and (+/-)-fenoterol respectively, without depressing the maximal responses. The order of potency of these agonists was (pD2 value): (+/-)-fenoterol (5.09+/-0.10) > (+/-)-terbutaline (4.13+/-0.08). In the presence of (+/-)-atenolol and (+/-)-butoxamine, however, the non-selective beta1, beta2- and beta3-adrenoceptor antagonist (+/-)-bupranolol caused a concentration-dependent rightward shift of the concentration-response curves for (+/-)-terbutaline and (+/-)-fenoterol. Schild plot analyses of the effects of (+/-)-bupranolol against these agonists gave pA2 values of 6.21+/-0.07 ((+/-)-terbutaline) and 6.37+/-0.06 ((+/-)-fenoterol) respectively, and the slopes of the Schild plot were not significantly different from unity (p>0.05). These results suggest that the relaxant responses to (+/-)-terbutaline and (+/-)-fenoterol are mainly mediated through beta3-adrenoceptors in the guinea pig gastric fundus. The beta3-adrenoceptor agonist potencies of arylethanolamine analogs depend on the size of the end of the alkylamine side chain.  (+info)

Burst-like control of lipolysis by the sympathetic nervous system in vivo. (8/31)

Rapid oscillations of visceral lipolysis have been reported. To examine the putative role of the CNS in oscillatory lipolysis, we tested the effects of beta(3)-blockade on pulsatile release of FFAs. Arterial blood samples were drawn at 1-minute intervals for 120 minutes from fasted, conscious dogs (n = 7) during the infusion of saline or bupranolol (1.5 micro g/kg/min), a high-affinity beta(3)-blocker. FFA and glycerol time series were analyzed and deconvolution analysis was applied to estimate the rate of FFA release. During saline infusion FFAs and glycerol oscillated in phase at about eight pulses/hour. Deconvolution analysis showed bursts of lipolysis (nine pulses/hour) with time-dependent variation in burst frequency. Bupranolol completely removed rapid FFA and glycerol oscillations. Despite removal of lipolytic bursts, plasma FFAs (0.31 mM) and glycerol (0.06 mM) were not totally suppressed and deconvolution analysis revealed persistent non-oscillatory lipolysis (0.064 mM/min). These results show that lipolysis in the fasting state consists of an oscillatory component, which appears to be entirely dependent upon sympathetic innervation of the adipose tissue, and a non-oscillatory, constitutive component, which persists despite beta(3)-blockade. The extinction of lipid fuel bursts by beta(3)-blockade implies a role for the CNS in the maintenance of cyclic provision of lipid fuels.  (+info)

Bupranolol is a beta-blocker medication that is primarily used to treat high blood pressure, angina (chest pain), and certain types of irregular heartbeats. It works by blocking the action of certain natural substances in your body, such as epinephrine, that affect the heart and blood vessels. This helps to reduce heart rate, lower blood pressure, and improve blood flow, which can help prevent heart attacks and strokes.

Bupranolol may also be used for other purposes, such as preventing migraines or treating anxiety disorders. It is available in immediate-release and extended-release tablets, and the dosage may vary depending on the specific condition being treated. As with any medication, bupranolol can have side effects, including dizziness, fatigue, and gastrointestinal symptoms. It is important to follow your doctor's instructions carefully when taking this medication and to report any unusual or bothersome side effects promptly.

Beta-3 adrenergic receptors (β3-AR) are a type of G protein-coupled receptor that binds catecholamines, such as norepinephrine and epinephrine. These receptors are primarily located in the adipose tissue, where they play a role in regulating lipolysis (the breakdown of fat) and thermogenesis (the production of heat).

Activation of β3-AR stimulates the enzyme hormone-sensitive lipase, which leads to the hydrolysis of triglycerides and the release of free fatty acids. This process is important for maintaining energy homeostasis and can be activated through exercise, cold exposure, or pharmacological means.

In addition to their role in metabolism, β3-AR have also been implicated in the regulation of cardiovascular function, bladder function, and inflammation. Selective β3-AR agonists are being investigated as potential therapeutic agents for the treatment of obesity, type 2 diabetes, and nonalcoholic fatty liver disease.

Adrenergic beta-3 receptor antagonists are a class of medications that block the action of adrenergic beta-3 receptors, which are found in various tissues throughout the body, including fat cells. These receptors are involved in the regulation of lipolysis (the breakdown of fats) and thermogenesis (the production of heat).

By blocking the action of these receptors, adrenergic beta-3 receptor antagonists can help to reduce the breakdown of fats and increase the amount of fat stored in the body. This may be useful in the treatment of certain medical conditions, such as obesity or diabetes, where excess weight or high blood sugar levels are contributing factors.

Examples of adrenergic beta-3 receptor antagonists include mirabegron (Myrbetriq) and SR59230A. These medications are typically taken orally and may be used in combination with other therapies to help manage weight and improve blood sugar control. As with any medication, adrenergic beta-3 receptor antagonists can have side effects and should only be used under the guidance of a healthcare professional.

Adrenergic beta-1 receptor antagonists, also known as beta blockers, are a class of medications that block the effects of adrenaline and noradrenaline (also known as epinephrine and norepinephrine) on beta-1 receptors. These receptors are found primarily in the heart and kidneys, where they mediate various physiological responses such as increased heart rate, contractility, and conduction velocity, as well as renin release from the kidneys.

By blocking the action of adrenaline and noradrenaline on these receptors, beta blockers can help to reduce heart rate, lower blood pressure, decrease the force of heart contractions, and improve symptoms of angina (chest pain). They are commonly used to treat a variety of conditions, including hypertension, heart failure, arrhythmias, and certain types of tremors. Examples of beta blockers include metoprolol, atenolol, and propranolol.

Adrenergic beta-3 receptor agonists are a type of medication that selectively binds to and activates the beta-3 adrenergic receptors. These receptors are found primarily in adipose tissue, where their activation is thought to increase lipolysis (the breakdown of fat) and thermogenesis (the production of heat).

Beta-3 adrenergic receptor agonists have been studied as a potential treatment for obesity and related conditions such as type 2 diabetes. By increasing lipolysis and thermogenesis, these drugs may help to promote weight loss and improve insulin sensitivity. However, their efficacy in humans has not been firmly established, and more research is needed to determine their safety and effectiveness.

Some examples of adrenergic beta-3 receptor agonists include mirabegron, which is approved for the treatment of overactive bladder, and solabegron, which is being studied for its potential use in treating obesity and other metabolic disorders.

Adrenergic beta-1 receptor agonists are a type of medication that binds to and activates the beta-1 adrenergic receptors, which are found primarily in the heart. When these receptors are activated, they cause an increase in heart rate, contractility, and conduction velocity, leading to an increased cardiac output.

These medications are used to treat various conditions such as heart failure, bradycardia (a slow heart rate), and cardiogenic shock. Examples of adrenergic beta-1 receptor agonists include dobutamine, dopamine, and isoproterenol. It's important to note that these medications can also have effects on other adrenergic receptors, so it's crucial to monitor for potential side effects such as hypertension, arrhythmias, and bronchodilation.

Adrenergic beta-antagonists, also known as beta blockers, are a class of medications that block the effects of adrenaline and noradrenaline (also known as epinephrine and norepinephrine) on beta-adrenergic receptors. These receptors are found in various tissues throughout the body, including the heart, lungs, and blood vessels.

Beta blockers work by binding to these receptors and preventing the activation of certain signaling pathways that lead to increased heart rate, force of heart contractions, and relaxation of blood vessels. As a result, beta blockers can lower blood pressure, reduce heart rate, and decrease the workload on the heart.

Beta blockers are used to treat a variety of medical conditions, including hypertension (high blood pressure), angina (chest pain), heart failure, irregular heart rhythms, migraines, and certain anxiety disorders. Some common examples of beta blockers include metoprolol, atenolol, propranolol, and bisoprolol.

It is important to note that while beta blockers can have many benefits, they can also cause side effects such as fatigue, dizziness, and shortness of breath. Additionally, sudden discontinuation of beta blocker therapy can lead to rebound hypertension or worsening chest pain. Therefore, it is important to follow the dosing instructions provided by a healthcare provider carefully when taking these medications.

Propanolamines are a class of pharmaceutical compounds that contain a propan-2-olamine functional group, which is a secondary amine formed by the replacement of one hydrogen atom in an ammonia molecule with a propan-2-ol group. They are commonly used as decongestants and bronchodilators in medical treatments.

Examples of propanolamines include:

* Phenylephrine: a decongestant used to relieve nasal congestion.
* Pseudoephedrine: a decongestant and stimulant used to treat nasal congestion and sinus pressure.
* Ephedrine: a bronchodilator, decongestant, and stimulant used to treat asthma, nasal congestion, and low blood pressure.

It is important to note that propanolamines can have side effects such as increased heart rate, elevated blood pressure, and insomnia, so they should be used with caution and under the supervision of a healthcare professional.

Butoxamine is a pharmaceutical drug that acts as an antagonist or blocker for β2-adrenergic receptors. These receptors are found in various tissues throughout the body and play a role in mediating the effects of catecholamines such as adrenaline and noradrenaline.

Butoxamine is primarily used in research settings to study the functions of β2-adrenergic receptors and their signaling pathways. It has been used to investigate the role of these receptors in various physiological processes, including airway smooth muscle relaxation, lipolysis, and insulin secretion.

It is important to note that Butoxamine is not approved for use in humans as a therapeutic agent, and its use is restricted to research purposes only.

Adrenergic receptors are a type of G protein-coupled receptor that binds and responds to catecholamines, such as epinephrine (adrenaline) and norepinephrine (noradrenaline). Beta adrenergic receptors (β-adrenergic receptors) are a subtype of adrenergic receptors that include three distinct subclasses: β1, β2, and β3. These receptors are widely distributed throughout the body and play important roles in various physiological functions, including cardiovascular regulation, bronchodilation, lipolysis, and glucose metabolism.

β1-adrenergic receptors are primarily located in the heart and regulate cardiac contractility, chronotropy (heart rate), and relaxation. β2-adrenergic receptors are found in various tissues, including the lungs, vascular smooth muscle, liver, and skeletal muscle. They mediate bronchodilation, vasodilation, glycogenolysis, and lipolysis. β3-adrenergic receptors are mainly expressed in adipose tissue, where they stimulate lipolysis and thermogenesis.

Agonists of β-adrenergic receptors include catecholamines like epinephrine and norepinephrine, as well as synthetic drugs such as dobutamine (a β1-selective agonist) and albuterol (a non-selective β2-agonist). Antagonists of β-adrenergic receptors are commonly used in the treatment of various conditions, including hypertension, angina pectoris, heart failure, and asthma. Examples of β-blockers include metoprolol (a β1-selective antagonist) and carvedilol (a non-selective β-blocker with additional α1-adrenergic receptor blocking activity).

Adrenergic beta-agonists are a class of medications that bind to and activate beta-adrenergic receptors, which are found in various tissues throughout the body. These receptors are part of the sympathetic nervous system and mediate the effects of the neurotransmitter norepinephrine (also called noradrenaline) and the hormone epinephrine (also called adrenaline).

When beta-agonists bind to these receptors, they stimulate a range of physiological responses, including relaxation of smooth muscle in the airways, increased heart rate and contractility, and increased metabolic rate. As a result, adrenergic beta-agonists are often used to treat conditions such as asthma, chronic obstructive pulmonary disease (COPD), and bronchitis, as they can help to dilate the airways and improve breathing.

There are several different types of beta-agonists, including short-acting and long-acting formulations. Short-acting beta-agonists (SABAs) are typically used for quick relief of symptoms, while long-acting beta-agonists (LABAs) are used for more sustained symptom control. Examples of adrenergic beta-agonists include albuterol (also known as salbutamol), terbutaline, formoterol, and salmeterol.

It's worth noting that while adrenergic beta-agonists can be very effective in treating respiratory conditions, they can also have side effects, particularly if used in high doses or for prolonged periods of time. These may include tremors, anxiety, palpitations, and increased blood pressure. As with any medication, it's important to use adrenergic beta-agonists only as directed by a healthcare professional.

Pindolol is a non-selective beta blocker that is used in the treatment of hypertension (high blood pressure) and certain types of arrhythmias (irregular heart rhythms). It works by blocking the action of certain hormones such as adrenaline and noradrenaline on the heart, which helps to reduce the heart rate, contractility, and conduction velocity, leading to a decrease in blood pressure.

Pindolol is also a partial agonist at beta-2 receptors, which means that it can stimulate these receptors to some extent, reducing the likelihood of bronchospasm (a side effect seen with other non-selective beta blockers). However, pindolol may still cause bronchospasm in patients with a history of asthma or chronic obstructive pulmonary disease (COPD), so it should be used with caution in these populations.

Pindolol is available in immediate-release and extended-release formulations, and the dosage is typically individualized based on the patient's response to therapy. Common side effects of pindolol include dizziness, fatigue, and gastrointestinal symptoms such as nausea and diarrhea.

Beta-1 adrenergic receptors (also known as β1-adrenergic receptors) are a type of G protein-coupled receptor found in the cell membrane. They are activated by the catecholamines, particularly noradrenaline (norepinephrine) and adrenaline (epinephrine), which are released by the sympathetic nervous system as part of the "fight or flight" response.

When a catecholamine binds to a β1-adrenergic receptor, it triggers a series of intracellular signaling events that ultimately lead to an increase in the rate and force of heart contractions, as well as an increase in renin secretion from the kidneys. These effects help to prepare the body for physical activity by increasing blood flow to the muscles and improving the efficiency of the cardiovascular system.

In addition to their role in the regulation of cardiovascular function, β1-adrenergic receptors have been implicated in a variety of physiological processes, including lipolysis (the breakdown of fat), glucose metabolism, and the regulation of mood and cognition.

Dysregulation of β1-adrenergic receptor signaling has been linked to several pathological conditions, including heart failure, hypertension, and anxiety disorders. As a result, β1-adrenergic receptors are an important target for the development of therapeutics used in the treatment of these conditions.

Muscle relaxation, in a medical context, refers to the process of reducing tension and promoting relaxation in the skeletal muscles. This can be achieved through various techniques, including progressive muscle relaxation (PMR), where individuals consciously tense and then release specific muscle groups in a systematic manner.

PMR has been shown to help reduce anxiety, stress, and muscle tightness, and improve overall well-being. It is often used as a complementary therapy in conjunction with other treatments for conditions such as chronic pain, headaches, and insomnia.

Additionally, muscle relaxation can also be facilitated through pharmacological interventions, such as the use of muscle relaxant medications. These drugs work by inhibiting the transmission of signals between nerves and muscles, leading to a reduction in muscle tone and spasticity. They are commonly used to treat conditions such as multiple sclerosis, cerebral palsy, and spinal cord injuries.

Stereoisomerism is a type of isomerism (structural arrangement of atoms) in which molecules have the same molecular formula and sequence of bonded atoms, but differ in the three-dimensional orientation of their atoms in space. This occurs when the molecule contains asymmetric carbon atoms or other rigid structures that prevent free rotation, leading to distinct spatial arrangements of groups of atoms around a central point. Stereoisomers can have different chemical and physical properties, such as optical activity, boiling points, and reactivities, due to differences in their shape and the way they interact with other molecules.

There are two main types of stereoisomerism: enantiomers (mirror-image isomers) and diastereomers (non-mirror-image isomers). Enantiomers are pairs of stereoisomers that are mirror images of each other, but cannot be superimposed on one another. Diastereomers, on the other hand, are non-mirror-image stereoisomers that have different physical and chemical properties.

Stereoisomerism is an important concept in chemistry and biology, as it can affect the biological activity of molecules, such as drugs and natural products. For example, some enantiomers of a drug may be active, while others are inactive or even toxic. Therefore, understanding stereoisomerism is crucial for designing and synthesizing effective and safe drugs.

Myocardial contraction refers to the rhythmic and forceful shortening of heart muscle cells (myocytes) in the myocardium, which is the muscular wall of the heart. This process is initiated by electrical signals generated by the sinoatrial node, causing a wave of depolarization that spreads throughout the heart.

During myocardial contraction, calcium ions flow into the myocytes, triggering the interaction between actin and myosin filaments, which are the contractile proteins in the muscle cells. This interaction causes the myofilaments to slide past each other, resulting in the shortening of the sarcomeres (the functional units of muscle contraction) and ultimately leading to the contraction of the heart muscle.

Myocardial contraction is essential for pumping blood throughout the body and maintaining adequate circulation to vital organs. Any impairment in myocardial contractility can lead to various cardiac disorders, such as heart failure, cardiomyopathy, and arrhythmias.

A chemical stimulation in a medical context refers to the process of activating or enhancing physiological or psychological responses in the body using chemical substances. These chemicals can interact with receptors on cells to trigger specific reactions, such as neurotransmitters and hormones that transmit signals within the nervous system and endocrine system.

Examples of chemical stimulation include the use of medications, drugs, or supplements that affect mood, alertness, pain perception, or other bodily functions. For instance, caffeine can chemically stimulate the central nervous system to increase alertness and decrease feelings of fatigue. Similarly, certain painkillers can chemically stimulate opioid receptors in the brain to reduce the perception of pain.

It's important to note that while chemical stimulation can have therapeutic benefits, it can also have adverse effects if used improperly or in excessive amounts. Therefore, it's essential to follow proper dosing instructions and consult with a healthcare provider before using any chemical substances for stimulation purposes.

... eye drops (0.05%-0.5%) are used against glaucoma.[citation needed] Bupranolol is quickly and completely absorbed ... Bupranolol has a plasma half life of about two to four hours, with levels never reaching 1 µg/L in therapeutic doses. The main ... Bupranolol is a non-selective beta blocker without intrinsic sympathomimetic activity (ISA), but with strong membrane ... Like other beta blockers, oral bupranolol can be used to treat hypertension and tachycardia.[citation needed] The initial dose ...
Propranolol, Atenolol, Bupranolol, Timolol, are some examples of clinically available beta-blockers. "High blood pressure ( ...
... bupranolol: 0.11 μM; CGP-20,712A (β1 antagonist): 6.09 μM; ICI-118,551 (β2 antagonist): 3.58 μM; SR-5923A (β3 antagonist): 17 ...
... amine Bromocresol green Bupranolol, a non-selective beta blocker Chloro-m-cresol which is used as a household disinfectant ...
Bevantolol Bisoprolol Bopindolol Bornaprolol Brefonalol Bucindolol Bucumolol Bufetolol Bufuralol Bunitrolol Bunolol Bupranolol ...
... bupranolol MeSH D02.033.100.624.210 - carteolol MeSH D02.033.100.624.240 - celiprolol MeSH D02.033.100.624.302 - ephedrine MeSH ... bupranolol MeSH D02.033.755.624.210 - carteolol MeSH D02.033.755.624.240 - celiprolol MeSH D02.033.755.624.302 - ephedrine MeSH ... bupranolol MeSH D02.092.063.624.698.207 - carteolol MeSH D02.092.063.624.698.268 - celiprolol MeSH D02.092.063.624.698.512 - ...
... bupranolol (INN) Buprenex buprenorphine (INN) bupropion (INN) buquineran (INN) buquinolate (INN) buquiterine (INN) buramate ( ...
This lipolysis was inhibited completely by bupranolol (considered to be a non-selective β-blocker), CGP 20712A (considered to ...
C07AA07 Sotalol C07AA12 Nadolol C07AA14 Mepindolol C07AA15 Carteolol C07AA16 Tertatolol C07AA17 Bopindolol C07AA19 Bupranolol ...
Bupranolol eye drops (0.05%-0.5%) are used against glaucoma.[citation needed] Bupranolol is quickly and completely absorbed ... Bupranolol has a plasma half life of about two to four hours, with levels never reaching 1 µg/L in therapeutic doses. The main ... Bupranolol is a non-selective beta blocker without intrinsic sympathomimetic activity (ISA), but with strong membrane ... Like other beta blockers, oral bupranolol can be used to treat hypertension and tachycardia.[citation needed] The initial dose ...
Pertenso information about active ingredients, pharmaceutical forms and doses by Schwarz Pharma, Pertenso indications, usages and related health products lists
Literature References: b-Adrenergic blocker. Prepn: Kunz et al., DE 1236523 (1967 to Sanol-Arzneimittel Dr. Schwarz), C.A. 67, 64046k (1967) and US 3309406 (1967). Pharmacology: Waterloh et al., Arzneim.-Forsch. 19, 153, 330, 1710 (1969); Pendleton et al., Arch. Int. Pharmacodyn. Ther. 187, 75 (1970); P. Montastruc et al., Arch. Farmacol. Toxicol. 3, 93 (1977). ...
Zelaszczyk et al., 2009, Four close bupranolol analogues are antagonists at the low-affinity state of beta1-adrenoceptors., J. ...
Bupranolol-d9. CAS Number: 2468771-00-6 Chemical Name: Bupranolol-d9 Molecular Formula: C14H13D9ClNO2 Molecular Weight: 280.84 ...
Cirazoline is a full agonist at the α1A adrenergic receptor, a partial agonist at both the α1B and α1D adrenergic receptors,[1] and a nonselective antagonist to the α2 adrenergic receptor.[2] It is believed that this combination of properties could make cirazoline an effective vasoconstricting agent.[2] Cirazoline has also been shown to decrease food intake in rats, purportedly through activation of α1 adrenoceptors in the paraventricular nucleus in the hypothalamus of the brain.[3] Administration of cirazoline also seemed to present impairment in the spatial memory of monkeys through the activation of the same receptors that showed decreased food intake in rats.[4][5] However, in preliminary studies, through stimulation of α2 adrenoceptors, working memory is comparatively improved.[4] ...
Bupranolol • Burocrolol • Butaxamine • Butidrine • Butofilolol • Capsinolol • Carazolol • Carpindolol • Carteolol • Carvedilol ...
Beta blockers are a class of drugs that block the action of β-adrenergic receptors. This class includes drugs that block all β-adrenergic receptors in a - pharmacyguide.biz
... bupranolol, metipranolol, nadolol, mepindolol, carazolol, sotalol, metoprolol, betaxolol, celiprolol, bisoprolol, carteolol, ...
8.3.2. CYP2D6 CYP2D6 metabolizes about 25% of all drug substances, including drugs relevant to the treatment of ADHD Elvanse (AMP) Atomoxetine Nortrypti...
Morfolini: Fenbutrazat • Morazon • Fendimetrazin • Fenmetrazin; Oksazolini: 4-Metilaminoreks (4-MAR, 4-MAX) • Aminoreks • Klominoreks • Ciklazodon • Fenozolon • Fluminoreks • Pemolin • Tozalinon; Fenetilamini (takođe amfetamini, katinoni, fentermini, itd): 2-Hidroksifenetilamin (2-OH-PEA) • 4-CAB • 4-Metilamfetamin (4-MA) • 4-Metilmetamfetamin (4-MMA) • Alfetamin • Amfekloral • Amfepentoreks • Amfepramon • Amfetamin (Dekstroamfetamin • Levoamfetamin) • Amfetaminil • β-Metilfenetilamin (β-Me-PEA) • Benzodioksolilbutanamin (BDB) • Benzodioksolilhidroksibutanamin (BOH) • Benzfetamin • Bufedron • Butilon • Katin • Katinon • Klobenzoreks • Klortermin • D-deprenil • Dimetoksiamfetamin (DMA) • Dimetoksimetamfetamin (DMMA) • Dimetilamfetamin • Dimetilkatinon (Dimetilpropion, metamfepramon) • Etkatinon (Etilpropion) • Etilamfetamin • Etilbenzodioksolilbutanamin (EBDB) • Etilon • Famprofazon • Fenetilin • Fenproporeks ...
Bupranolol • Burocrolol • Butaksamin • Butidrin • Butofilolol • Kapsinolol • Karazolol • Karpindolol • Karteolol • Karvedilol ...
Propranolol, bupranolol and butoxamine produced shifts of the concentration-response curve for fenoterol. Schild regression ... The response to dopamine was antagonized in a concentration-dependent manner by bupranolol (3 x 10(-6)-3 x 10(-5) M), and ... Schild plot analyses of the effects of (+/-)-bupranolol against these agonists gave pA2 values of 6.21+/-0.07 ((+/-)- ... Bisoprolol Bopindolol Bornaprolol Brefonalol Bucindolol Bucumolol Bufetolol Bufuralol Bunitrolol Bunolol Bupranolol Butaxamine ...
Bupranolol, tertatolol, IPS339, spirendolol, ICI118551 were selected from an article comparing the electronic structure of β- ...
InChI=1S/C15H25NO3/c1-12(2)16-10-14(17)11-19-15-6-4-13(5-7-15)8-9-18-3/h4-7,12,14,16-17H,8-11H2,1-3H3 ...
Bupranolol D2.33.100.624.160 D2.33.755.624.160 Butylscopolammonium Bromide D2.145.74.722.900.700.200 D2.145.74.722.822.200 ...
D4.345.349.100 Bupranolol D2.33.100.624.698.146 D2.33.755.624.698.146 C-Peptide D6.472.699.587.740.250 D6.472.699.587.200.500. ...
D4.345.349.100 Bupranolol D2.33.100.624.698.146 D2.33.755.624.698.146 C-Peptide D6.472.699.587.740.250 D6.472.699.587.200.500. ...
Bupranolol D2.33.100.624.160 D2.33.755.624.160 Butylscopolammonium Bromide D2.145.74.722.900.700.200 D2.145.74.722.822.200 ...
D4.345.349.100 Bupranolol D2.33.100.624.698.146 D2.33.755.624.698.146 C-Peptide D6.472.699.587.740.250 D6.472.699.587.200.500. ...
D4.345.349.100 Bupranolol D2.33.100.624.698.146 D2.33.755.624.698.146 C-Peptide D6.472.699.587.740.250 D6.472.699.587.200.500. ...
Bupranolol D2.33.100.624.160 D2.33.755.624.160 Butylscopolammonium Bromide D2.145.74.722.900.700.200 D2.145.74.722.822.200 ...
D4.345.349.100 Bupranolol D2.33.100.624.698.146 D2.33.755.624.698.146 C-Peptide D6.472.699.587.740.250 D6.472.699.587.200.500. ...
Bupranolol D2.33.100.624.160 D2.33.755.624.160 Butylscopolammonium Bromide D2.145.74.722.900.700.200 D2.145.74.722.822.200 ...
Bupranolol Action Pathway;Nebivolol Action Pathway;Amlodipine Action Pathway;Verapamil Action Pathway;Nitrendipine Action ...
Bupranolol [D02.033.100.624.698.146] Bupranolol * Carteolol [D02.033.100.624.698.207] Carteolol * Celiprolol [D02.033.100.624. ...
This graph shows the total number of publications written about "Bunolol" by people in this website by year, and whether "Bunolol" was a major or minor topic of these publications ...
Wiki-wiki: a wiki resource centered on human protein-protein interactions
This graph shows the total number of publications written about "Bisoprolol" by people in this website by year, and whether "Bisoprolol" was a major or minor topic of these publications ...
Wiki-wiki: a wiki resource centered on human protein-protein interactions
  • Bupranolol has a plasma half life of about two to four hours, with levels never reaching 1 µg/L in therapeutic doses. (wikipedia.org)
  • Effect of the beta-adrenergic blocking agent bupranolol on the plasma renin activity in normotensive rats]. (nih.gov)
  • Babu, r.j. and pandit, j.k., effect of penetration enhancers on the transdermal delivery of bupranolol through rat skin, drug deliv. (safetoseas.com)