A beta-2 selective adrenergic antagonist. It is used primarily in animal and tissue experiments to characterize BETA-2 ANDRENERGIC RECEPTORS.
Drugs that bind to and block the activation of ADRENERGIC BETA-2 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.
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.
A subclass of beta-adrenergic receptors (RECEPTORS, ADRENERGIC, BETA). The adrenergic beta-2 receptors are more sensitive to EPINEPHRINE than to NOREPINEPHRINE and have a high affinity for the agonist TERBUTALINE. They are widespread, with clinically important roles in SKELETAL MUSCLE; LIVER; and vascular, bronchial, gastrointestinal, and genitourinary SMOOTH MUSCLE.
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.
Isopropyl analog of EPINEPHRINE; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant.
A widely used non-cardioselective beta-adrenergic antagonist. Propranolol has been used for MYOCARDIAL INFARCTION; ARRHYTHMIA; ANGINA PECTORIS; HYPERTENSION; HYPERTHYROIDISM; MIGRAINE; PHEOCHROMOCYTOMA; and ANXIETY but adverse effects instigate replacement by newer drugs.
The active sympathomimetic hormone from the ADRENAL MEDULLA. It stimulates both the alpha- and beta- adrenergic systems, causes systemic VASOCONSTRICTION and gastrointestinal relaxation, stimulates the HEART, and dilates BRONCHI and cerebral vessels. It is used in ASTHMA and CARDIAC FAILURE and to delay absorption of local ANESTHETICS.
Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)
The sounds heard over the cardiac region produced by the functioning of the heart. There are four distinct sounds: the first occurs at the beginning of SYSTOLE and is heard as a "lubb" sound; the second is produced by the closing of the AORTIC VALVE and PULMONARY VALVE and is heard as a "dupp" sound; the third is produced by vibrations of the ventricular walls when suddenly distended by the rush of blood from the HEART ATRIA; and the fourth is produced by atrial contraction and ventricular filling.
A subclass of alpha-adrenergic receptors found on both presynaptic and postsynaptic membranes where they signal through Gi-Go G-PROTEINS. While postsynaptic alpha-2 receptors play a traditional role in mediating the effects of ADRENERGIC AGONISTS, the subset of alpha-2 receptors found on presynaptic membranes signal the feedback inhibition of NEUROTRANSMITTER release.
A general class of ortho-dihydroxyphenylalkylamines derived from tyrosine.
Severe or complete loss of motor function in all four limbs which may result from BRAIN DISEASES; SPINAL CORD DISEASES; PERIPHERAL NERVOUS SYSTEM DISEASES; NEUROMUSCULAR DISEASES; or rarely MUSCULAR DISEASES. The locked-in syndrome is characterized by quadriplegia in combination with cranial muscle paralysis. Consciousness is spared and the only retained voluntary motor activity may be limited eye movements. This condition is usually caused by a lesion in the upper BRAIN STEM which injures the descending cortico-spinal and cortico-bulbar tracts.
Severe or complete loss of motor function in the lower extremities and lower portions of the trunk. This condition is most often associated with SPINAL CORD DISEASES, although BRAIN DISEASES; PERIPHERAL NERVOUS SYSTEM DISEASES; NEUROMUSCULAR DISEASES; and MUSCULAR DISEASES may also cause bilateral leg weakness.
A usually benign, well-encapsulated, lobular, vascular tumor of chromaffin tissue of the ADRENAL MEDULLA or sympathetic paraganglia. The cardinal symptom, reflecting the increased secretion of EPINEPHRINE and NOREPINEPHRINE, is HYPERTENSION, which may be persistent or intermittent. During severe attacks, there may be HEADACHE; SWEATING, palpitation, apprehension, TREMOR; PALLOR or FLUSHING of the face, NAUSEA and VOMITING, pain in the CHEST and ABDOMEN, and paresthesias of the extremities. The incidence of malignancy is as low as 5% but the pathologic distinction between benign and malignant pheochromocytomas is not clear. (Dorland, 27th ed; DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1298)
Penetrating and non-penetrating injuries to the spinal cord resulting from traumatic external forces (e.g., WOUNDS, GUNSHOT; WHIPLASH INJURIES; etc.).
Cardiac arrhythmias that are characterized by excessively slow HEART RATE, usually below 50 beats per minute in human adults. They can be classified broadly into SINOATRIAL NODE dysfunction and ATRIOVENTRICULAR BLOCK.
Transmission of the readings of instruments to a remote location by means of wires, radio waves, or other means. (McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed)
Chairs mounted on wheels and designed to be propelled by the occupant.
Alkyl compounds containing a hydroxyl group. They are classified according to relation of the carbon atom: primary alcohols, R-CH2OH; secondary alcohols, R2-CHOH; tertiary alcohols, R3-COH. (From Grant & Hackh's Chemical Dictionary, 5th ed)
Behaviors associated with the ingesting of alcoholic beverages, including social drinking.
A zinc-containing enzyme which oxidizes primary and secondary alcohols or hemiacetals in the presence of NAD. In alcoholic fermentation, it catalyzes the final step of reducing an aldehyde to an alcohol in the presence of NADH and hydrogen.
A subclass of enzymes which includes all dehydrogenases acting on primary and secondary alcohols as well as hemiacetals. They are further classified according to the acceptor which can be NAD+ or NADP+ (subclass 1.1.1), cytochrome (1.1.2), oxygen (1.1.3), quinone (1.1.5), or another acceptor (1.1.99).
Isomeric forms and derivatives of butanol (C4H9OH).
Drugs that mimic the effects of stimulating postganglionic adrenergic sympathetic nerves. Included here are drugs that directly stimulate adrenergic receptors and drugs that act indirectly by provoking the release of adrenergic transmitters.
The fluid containing digestive enzymes secreted by the pancreas in response to food in the duodenum.
A nodular organ in the ABDOMEN that contains a mixture of ENDOCRINE GLANDS and EXOCRINE GLANDS. The small endocrine portion consists of the ISLETS OF LANGERHANS secreting a number of hormones into the blood stream. The large exocrine portion (EXOCRINE PANCREAS) is a compound acinar gland that secretes several digestive enzymes into the pancreatic ductal system that empties into the DUODENUM.
An indirect sympathomimetic. Tyramine does not directly activate adrenergic receptors, but it can serve as a substrate for adrenergic uptake systems and monoamine oxidase so it prolongs the actions of adrenergic transmitters. It also provokes transmitter release from adrenergic terminals. Tyramine may be a neurotransmitter in some invertebrate nervous systems.
A sympathomimetic that acts mainly by causing release of NOREPINEPHRINE but also has direct agonist activity at some adrenergic receptors. It is most commonly used as a nasal vasoconstrictor and an appetite depressant.
Secondary headache disorders attributed to a variety of cranial or cervical vascular disorders, such as BRAIN ISCHEMIA; INTRACRANIAL HEMORRHAGES; and CENTRAL NERVOUS SYSTEM VASCULAR MALFORMATIONS.
Tests based on the biochemistry and physiology of the exocrine pancreas and involving analysis of blood, duodenal contents, feces, or urine for products of pancreatic secretion.
The branch of pharmacology that deals directly with the effectiveness and safety of drugs in humans.
An amino acid that occurs in vertebrate tissues and in urine. In muscle tissue, creatine generally occurs as phosphocreatine. Creatine is excreted as CREATININE in the urine.
Injections made into a vein for therapeutic or experimental purposes.
A sustained and usually painful contraction of muscle fibers. This may occur as an isolated phenomenon or as a manifestation of an underlying disease process (e.g., UREMIA; HYPOTHYROIDISM; MOTOR NEURON DISEASE; etc.). (From Adams et al., Principles of Neurology, 6th ed, p1398)
Products in capsule, tablet or liquid form that provide dietary ingredients, and that are intended to be taken by mouth to increase the intake of nutrients. Dietary supplements can include macronutrients, such as proteins, carbohydrates, and fats; and/or MICRONUTRIENTS, such as VITAMINS; MINERALS; and PHYTOCHEMICALS.
The time it takes for a substance (drug, radioactive nuclide, or other) to lose half of its pharmacologic, physiologic, or radiologic activity.
Acquired, familial, and congenital disorders of SKELETAL MUSCLE and SMOOTH MUSCLE.
A selective adrenergic beta-1 blocking agent that is commonly used to treat ANGINA PECTORIS; HYPERTENSION; and CARDIAC ARRHYTHMIAS.
A cardioselective beta-1 adrenergic blocker. It is effective in the management of HYPERTENSION and ANGINA PECTORIS.
A class of drugs that act by selective inhibition of calcium influx through cellular membranes.
A cardioselective beta-1 adrenergic antagonist that has intrinsic symopathomimetic activity. It is used in the management of ANGINA PECTORIS and HYPERTENSION.
A methyl xanthine derivative from tea with diuretic, smooth muscle relaxant, bronchial dilation, cardiac and central nervous system stimulant activities. Theophylline inhibits the 3',5'-CYCLIC NUCLEOTIDE PHOSPHODIESTERASE that degrades CYCLIC AMP thus potentiates the actions of agents that act through ADENYLYL CYCLASES and cyclic AMP.
The metabolic process of breaking down LIPIDS to release FREE FATTY ACIDS, the major oxidative fuel for the body. Lipolysis may involve dietary lipids in the DIGESTIVE TRACT, circulating lipids in the BLOOD, and stored lipids in the ADIPOSE TISSUE or the LIVER. A number of enzymes are involved in such lipid hydrolysis, such as LIPASE and LIPOPROTEIN LIPASE from various tissues.
A beta-1 adrenergic antagonist that has been used in the emergency treatment of CARDIAC ARRYTHMIAS.
Specialized connective tissue composed of fat cells (ADIPOCYTES). It is the site of stored FATS, usually in the form of TRIGLYCERIDES. In mammals, there are two types of adipose tissue, the WHITE FAT and the BROWN FAT. Their relative distributions vary in different species with most adipose tissue being white.
One of the ADRENERGIC BETA-ANTAGONISTS used as an antihypertensive, anti-anginal, and anti-arrhythmic agent.
A trihydroxy sugar alcohol that is an intermediate in carbohydrate and lipid metabolism. It is used as a solvent, emollient, pharmaceutical agent, and sweetening agent.

Impaired isoproterenol-induced hyperpolarization in isolated mesenteric arteries of aged rats. (1/38)

Stimulation of vascular beta-adrenoceptors leads to membrane hyperpolarization, presumably via the beta-adrenoceptor/G(s) protein/adenylate cyclase signaling cascade; the ionic mechanisms of this phenomenon remain unclear. beta-Adrenoceptor-mediated vascular relaxation is impaired with aging; however, little is known concerning whether beta-adrenoceptor-mediated hyperpolarization is altered with aging. We sought to determine the ionic mechanisms of isoproterenol-induced hyperpolarization in the rat mesenteric resistance artery, as well as the age-related changes in isoproterenol-induced hyperpolarization and their underlying mechanisms. Isoproterenol-induced hyperpolarization was inhibited by high-K(+) solution and glibenclamide (10(-6) mol/L), an inhibitor of ATP-sensitive K(+) channels (K(ATP)), but not by apamin, iberiotoxin, or charybdotoxin, inhibitors of Ca(2+)-activated K(+) channels. Isoproterenol-induced hyperpolarization was markedly less in aged rats (>/=24 months) than in adults rats (12 to 20 weeks) (3x10(-6) mol/L; -3.1 versus -9.9 mV; P<0.001; n=8 to 9). Cholera toxin (10(-9) g/mL), an activator of G(s), evoked hyperpolarization only in adult rats. Hyperpolarization to forskolin, a direct activator of adenylate cyclase, was also reduced to some extent in aged rats (10(-5) mol/L; -8.8 versus -13 mV; P<0.05; n=6), whereas hyperpolarization to levcromakalim, a K(ATP) opener, was comparable in both groups. These findings suggest that isoproterenol elicits hyperpolarization via an opening of K(ATP) in the rat resistance artery and that isoproterenol-induced hyperpolarization is attenuated in aged rats mainly because of a defective coupling of beta-adrenoceptors to adenylate cyclase and partly because of a defect at the level of adenylate cyclase, but not because of an alteration of K(ATP) per se.  (+info)

Presynaptic beta(2)-adrenoceptors mediate nicotine-induced NOergic neurogenic dilation in porcine basilar arteries. (2/38)

We previously reported that nicotine-induced nitric oxide (NO)-mediated cerebral neurogenic vasodilation was dependent on intact sympathetic innervation. We hypothesized that nicotine acted on sympathetic nerve terminals to release norepinephrine (NE), which then acted on adrenoceptors located on the neighboring nitric oxidergic (NOergic) nerve terminals to release NO, resulting in vasodilation. The adrenoceptor subtype in mediating nicotine-induced vasodilation in isolated porcine basilar arterial rings denuded of endothelium was therefore examined pharmacologically and immunohistochemically. Results from using an in vitro tissue bath technique indicated that propranolol and preferential beta(2)-adrenoceptor antagonists (ICI-118,551 and butoxamine), in a concentration-dependent manner, blocked the relaxation induced by nicotine (100 microM) without affecting the relaxation elicited by transmural nerve stimulation (TNS, 8 Hz). In contrast, preferential beta(1)-adrenoceptor antagonists (atenolol and CGP-20712A) did not affect either nicotine- or TNS-induced relaxation. Results of double-labeling studies indicated that beta(2)-adrenoceptor immunoreactivities and NADPH diaphorase reactivities were colocalized in the same nerve fibers in basilar and middle cerebral arteries. These findings suggest that NE, which is released from sympathetic nerves upon application of nicotine, acts on presynaptic beta(2)-adrenoceptors located on the NOergic nerve terminals to release NO, resulting in vasodilation. In addition, nicotine-induced relaxation was enhanced by yohimbine, an alpha(2)-adrenoceptor antagonist, which, however, did not affect the relaxation elicited by TNS. Prazosin, an alpha(1)-adrenoceptor antagonist, on the other hand, did not have any effect on relaxation induced by either nicotine or TNS. The predominant facilitatory effect of beta(2)-adrenoceptors in releasing NO may be compromised by presynaptic alpha(2)-adrenoceptors.  (+info)

Structure-activity relationship studies of (+/-)-terbutaline and (+/-)-fenoterol on beta3-adrenoceptors in the guinea pig gastric fundus. (3/38)

(+/-)-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)

The beta2- and beta3-adrenoceptor-mediated relaxation induced by fenoterol in guinea pig taenia caecum. (4/38)

Fenoterol, a beta2-adrenoceptor selective agonist, belongs to the arylethanolamine class. To understand the receptor subtypes responsible for beta-adrenoceptor-mediated relaxation of guinea pig taenia caecum, we investigated the effect of fenoterol. Fenoterol caused concentration-dependent relaxation of the guinea pig taenia caecum. Propranolol, bupranolol and butoxamine produced shifts of the concentration-response curve for fenoterol. Schild regression analyses carried out for propranolol, butoxamine and bupranolol against fenoterol gave pA2 values of 8.41, 6.33 and 8.44, respectively. However, in the presence of 3 x 10(-4) M atenolol, 10(-4) M butoxamine and 10(-6) M phentolamine to block the beta1-, beta2- and a-adrenoceptor effects, respectively, Schild regression analysis carried out for bupranolol against fenoterol gave pA2 values of 5.80. These results suggest that the relaxant response to fenoterol in the guinea pig taenia caecum is mediated by both the beta2- and the beta3-adrenoceptors.  (+info)

Interaction between noradrenaline or adrenaline and the beta 1-adrenergic receptor in the nervous system triggers early metamorphosis of larvae in the ascidian, Ciona savignyi. (5/38)

Molecular mechanisms underlying the metamorphosis of larvae, e.g., ligand and receptor interaction, have to be determined and roles for the nervous system in marine invertebrates are not well understood. We report here that treatment of swimming larvae of the ascidian Ciona savignyi with noradrenaline or adrenaline promoted morphological changes in early metamorphosis, e.g., tail resorption. Antagonists of the beta-adrenergic receptor, propranolol, and the beta(1)-adrenergic receptor, metoprolol, inhibited the noradrenaline-induced tail resorption, while an antagonist of the alpha-adrenergic receptor, phentolamine, and of the beta(2)- adrenergic receptor, butoxamine, had no inhibitory effects. In addition, a selective agonist of the beta-adrenergic receptor, isoproterenol, the concentration of which was lower than the effective concentration of the neurotransmitters, facilitated tail resorption. Immunohistochemical studies, using an anti-dopamine-hydroxylase antibody, showed that neurotransmitters such as noradrenaline and adrenaline localized around the brain vesicle of the larvae during metamorphosis. The beta(1)-adrenergic receptor stained with antibodies was localized on the nervous system. Temporal expression of the beta(1)-adrenergic receptor was intense in the nervous system in the larvae competent for metamorphosis. We propose that interactions between noradrenaline or adrenaline and the beta(1)-adrenergic receptor in the nervous system mediate the process of metamorphosis of Ciona larvae.  (+info)

The beta3-adrenoceptor-mediated relaxation induced by dopamine in guinea pig taenia caecum. (6/38)

The mechanisms of the beta-adrenoceptor-mediated relaxation induced by dopamine in guinea pig taenia caecum were examined. The relaxant response to dopamine was unaffected by propranolol (10(-8)-10(-5) M) or phentolamine (10(-8)-10(-5) M). Atenolol (3 x 10(-7)-3 x 10(-4) M), butoxamine (10(-7)-10(-4) M), prazosin (10(-8)-10(-5) M), yohimbine (10(-8)-10(-5) M), SCH 23390 (10(-8)-10(-5) M) and haloperidol (10(-8)-10(-5) M) had no effect on the potency of dopamine. 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 of the data revealed the pA2 value of 5.55 and the slope of the regression line was 1.13. These results suggest that the relaxant response to dopamine in the guinea pig taenia caecum is mainly mediated by the beta3-adrenoceptors.  (+info)

Nebivolol increases arterial distensibility in vivo. (7/38)

Arterial stiffness is a key determinant of cardiovascular risk in hypertensive patients. beta-Blockers appear to be less effective than other drugs in improving outcome in hypertensive patients, and a potential explanation may be that beta-blockers are less effective in reducing arterial stiffness. The aim of this study was to assess the direct effect of beta-blockade on pulse wave velocity (PWV), a robust measure of arterial distensibility, using a local, ovine, hind-limb model. In addition, we hypothesized that the vasodilating beta-blocker nebivolol, but not atenolol, would increase arterial distensibility in vivo. All studies were conducted in anesthetized sheep. PWV was recorded in vivo using a dual pressure-sensing catheter placed in the common iliac artery. Intraarterial infusion of nebivolol reduced PWV by 6+/-3% at the higher dose (P<0.001), but did not alter mean arterial pressure (change of -1+/-3 mm Hg, P=0.1). In contrast, atenolol had no effect on PWV (P=0.11) despite a small drop in mean pressure (change of -5+/-3 mm Hg, P<0.01). Infusion of glyceryl trinitrate led to a dose-dependent fall in PWV, and 2 nmol/min produced a similar reduction in PWV to the higher dose of nebivolol (500 nmol/min). The effect of nebivolol on PWV was significantly attenuated during coinfusion of N(G)-monomethyl-L-arginine (P=0.003) and also during coinfusion of butoxamine (P=0.02). These results demonstrate that nebivolol, but not atenolol, increases arterial distensibility. This effect of nebivolol is mediated through the release of NO via a beta2 adrenoceptor-dependent mechanism. Thus, nebivolol may be of benefit in conditions of increased large artery stiffness, such as isolated systolic hypertension.  (+info)

Effect of orthovanadate on platelet aggregation induced by platelet-activating factor. (8/38)

Orthovanadate (vanadate) inhibited the platelet aggregation induced by platelet-activating factor (PAF) in a dose-dependent manner. Propranolol, a nonspecific beta-adrenergic receptor antagonist, and H-8, a selective inhibitor of cAMP-dependent protein kinase (PKA), suppressed the inhibition of the PAF-induced platelet aggregation by vanadate. Vanadate increased the cAMP content in platelets accompanied by the activation of PKA. The beta-adrenergic receptors of platelets have been reported to be abundant in the beta(2) isoform, coupled to adenylyl cyclases (R. Kerry and M. C. Scrutton, Br. J. Pharmacol., 79, 681-691 (1983)). When the washed platelets were preincubated with vanadate, salbutamol, a selective beta(2)-adrenergic receptor agonist, or 8-Br-cAMP, the latter two mimicked the vanadate-induced anti-platelet aggregation and prolongation of clotting time of plasma, suggesting involvement of the increased intracellular cAMP content in both actions of vanadate. Butoxamine, a selective beta(2)-adrenergic receptor antagonist, suppressed both actions of vanadate. The vanadate-induced increase in cAMP content was inhibited in part by butoxamine or genistein. These results suggest that vanadate inhibits the PAF-induced platelet aggregation by the stimulation of a cAMP/PKA-dependent process via the beta(2)-adrenergic receptor and receptor tyrosine kinases, and that the anti-platelet aggregation is involved in part in mechanisms of the anticoagulant action of vanadate.  (+info)

Prior biochemical studies have suggested that beta adrenergic receptors in the ciliary process are mostly of the beta-2 subtype. The present experiments evaluate a number of beta adrenergic antagonists, including several recently developed drugs, for their ability to block rabbit and human ciliary process and heart beta adrenergic receptors activating adenylate cyclase. Three of these agents (alpha-methylpropranolol, IPS 339 and ICI 118,551) demonstrated a high degree of oculoselectivity in both rabbit and human. The other agents (S 37-429, S 32-468, ICI 78,462,H35/25, butoxamine, propranolol, timolol, atenolol and practolol) showed either modest or no oculoselectivity. Structure-activity studies suggested that, among antagonists of the aryloxymethyl type, methylation of the side-chain alpha-carbon or the aromatic ring may enhance oculoselectivity primarily by decreasing potency at cardiac beta adrenergic receptors. Additional physiological studies of cardiac chronotropic response revealed that, ...
The effects of various adrenergic beta receptor agonists and antagonists on lipolysis (measured as glycerol release) in human adipose tissue in vitro were studied. Of the agonists investigated, the potency rank order was isoproteronol greater than norepinephrine greater than salbutamol. Adrenergic beta receptor blocking drugs inhibited catecholamineinduced lipolysis competitively. Propranolol was the overall most effective compound, followed by metoprolol, alprenolol and practolol, whereas butoxamine and H35/25 were weak inhibitors. The results indicate that the adrenergic reciptor mediating lipolysis in human adipose tissue is of type beta-1. Basal and theophylline-induced lipolysis was reduced when higher concentrations of these drug were used. ...
Detection of pregnancy specific beta1-glycoprotein in formalin-fixed tissues.: Using an enzyme-bridge immunoperoxidase method, pregnancy specific beta1-glycopro
View Notes - ps_8_answers from BIO 115 at UCSC. Bio 115 Problem set #8 March 11, 2005 1. You are studying Slater syndrome, which is associated with a progressive loss of balance, social withdrawal
BioAssay record AID 47971 submitted by ChEMBL: In vivo beta adrenergic receptor blocking potency was determined by inhibition of tachycardia produced by isoproterenol (0.2 mg/kg iv) in cat preparation.
It is now well established that any given ligand for a G-protein-couple receptor (GPCR) does not simply possess a single defined efficacy. Rather, a ligand possesses multiple efficacies, depending on the specific down-stream signal transduction pathway analyzed. This diversity may be based on ligand-specific GPCR conformations and is often referred to as functional selectivity. It has been known for a century that stereoisomers of catecholamines differ in their potency and, in some systems, also in their efficacy. However, the molecular basis for efficacy differences of GPCR ligand stereoisomers has remained poorly defined. In an elegant study published in this issue of Molecular Pharmacology, Woo et al. (p. 158) show that stereoisomers of the β2-adrenoceptor selective agonist fenoterol differentially activates Gs- and Gi-proteins in native rat cardiomyocytes. This study is so important because it is the first report to show that even the subtle structural differences within a ligand ...
Beta adrenergic receptor kinase carboxyl-terminus (also βARKct) is a peptide composed of the last 194 amino acid residues of the carboxyl-terminus of beta adrenergic receptor kinase 1 (βARK1). It binds the βγ subunits of G proteins located in the plasma membrane of cells. It is currently an experimental gene therapy for the treatment of heart failure. During heart failure, the heart is not able to pump enough blood to the rest of the body and will begin to undergo processes in order to compensate for its decreased function. These processes will attempt to increase the hearts output; however, the heart may become overstressed and eventually dysfunctional as a result. The sympathetic nervous system increases norepinephrine release to stimulate β-adrenergic receptors (βARs) located on heart cell (cardiomyocyte) membranes to increase the hearts rate and force of contraction. If the heart is already stressed or damaged, this will cause the heart to work above its capacity. Continuous ...
Single assays of Schwangerschaftsprotein 1 (SP1) and serum human placental lactogen (HPL) were performed in 500 consecutive patients attending a routine ante-natal clinic for their first visit. All samples were taken before 112 days gestation. Of the
The optimum pH of salivary amylase is approximately 6.7 to 7, according to Worthington Biochemical Corporation, meaning very slightly acidic. If the pH is significantly out of this range, the enzyme...
Terbutaline is a medicine available in a number of countries worldwide. A list of US medications equivalent to Terbutaline is available on the Drugs.com website.
"Butaxamine". pubchem.ncbi.nlm.nih.gov. U.S. National Library of Medicine. Archived from the original on October 18, 2017. ... Metoprolol Nebivolol Esmolol Butaxamine ICI-118,551 SR 59230A Nebivolol Agents with intrinsic sympathomimetic action (ISA) ...
ICI-118,551 Butaxamine Propranolol Betablocker Beta-2 adrenergic receptor Beta2-adrenergic agonist Bilski, AJ; Halliday, SE; ... like Butaxamine and ICI-118,551, or non-specifically (an antagonist for β2 and for β1 or β3 adrenoceptors) like the non- ...
It is an intermediate in synthesis of organic compounds, including pharmaceuticals such as methoxamine and butaxamine.[citation ...
... is an α1-adrenergic receptor agonist, somewhat similar in structure to butaxamine and 2,5-DMA. It is no longer ...
... butoxamine* First generation (non-selective) β-blockers ICI-118,551* Propranolol * denotes selective antagonist to the receptor ...
Bisoprolol Bopindolol Bornaprolol Brefonalol Bucindolol Bucumolol Bufetolol Bufuralol Bunitrolol Bunolol Bupranolol Butaxamine ...
Atenolol Betaxolol Bisoprolol Celiprolol Esmolol Metoprolol Nebivolol β2-selective agents Butaxamine (weak α-adrenergic agonist ...
... butaxamine (INN) Butazolidin butedronic acid (INN) butenafine (INN) buterizine (INN) butetamate (INN) Butex Forte buthalital ...
The molecular formula C15H25NO3 (molar mass : 267.36 g/mol, exact mass : 267.183444) may refer to: Butaxamine ...
... (INN, also known as butoxamine) is a β2-selective beta blocker. Its primary use is in experimental situations in ... Bupropion Methoxamine "Definition: butoxamine from Online Medical Dictionary". Hillman KL, Doze VA, Porter JE (August 2005). " ...
... (INN) (brand name Nopron) is a sedative-hypnotic drug of the phenylpiperazine group.[1][2] It has been used in the treatment of sleep disturbances since the early 1970s in several European countries including France, Italy, and Luxembourg.[3][4] It is commonly used with children and adolescents on account of its favorable safety and tolerability profile and lack of abuse potential.[5][6][7][8][9][10] Originally believed to act as an antihistamine and anticholinergic,[11] niaprazine was later discovered to have low or no binding affinity for the H1 and mACh receptors (Ki = , 1 μM), and was instead found to act as a potent and selective 5-HT2A and α1-adrenergic receptor antagonist (Ki = 75 nM and 86 nM, respectively).[12] It possesses low or no affinity for the 5-HT1A, 5-HT2B, D2, and β-adrenergic, as well as at SERT and VMAT (Ki = all , 1 μM), but it does have some affinity for the α2-adrenergic receptor (Ki = 730 nM),[12] likely acting as an antagonist there as well. Niaprazine ...
... is a selective β2 adrenergic receptor (adrenoreceptor) antagonist or beta blocker[1][2] . ICI binds to the β2 subtype with at least 100 times greater affinity than β1 or β3, the two other known subtypes of the beta adrenoceptor.[3][4] The compound was developed by Imperial Chemical Industries, which was acquired by AkzoNobel in 2008. ICI-118,551 has no known therapeutic use in humans although it has been used widely in research to understand the action of the β2 adrenergic receptor, as few other specific antagonists for this receptor are known.[5] ICI-118,551 has been used in pre-clinical studies using murine models.[6][7][8] When dissolved in saline, the compound crosses the blood-brain barrier. Common systemic doses used in rodent research are 0.5 or 1 mg/kg although efficacy has been demonstrated at doses as low as 0.0001 mg/kg in rhesus monkeys.[9] Doses up to 20 mg/kg have been used without toxicity. At room temperature in saline, the ICI 118,551 hydrochloride is soluble to ...
There are a variety of clinically useful ergoline derivatives for the purpose of vasoconstriction, the treatment of migraines, and treatment of Parkinson's disease. Ergoline alkaloids found their place in pharmacology long before modern medicine as preparations of ergot were often used by midwives in the 12th century to stimulate childbirth.[10] Following Arthur Stoll's isolation of ergometrine, the therapeutic use of ergoline derivatives became well explored. The induction of uterine contractions via the preparation of ergot was attributed to ergonovine, an ergoline derivative found in ergot, which is a powerful oxytocic. From this, methergine, a synthetic derivative, was elucidated.[7] While used to facilitate child birth, ergoline derivatives can pass into breast milk and should not be used during breastfeeding.[11] They are uterine contractors that can increase the risk of miscarriage during pregnancy.[3] Another example of medically relevant ergoline alkaloids is ergotamine, an alkaloid ...
The most common side effect is eye irritation felt as stinging or burning, which occurs in up to a third of patients. Blepharoconjunctivitis occurs in up to 5% of patients. Rarer adverse effects include keratitis, edema and increased lacrimation.[2][3] Allergies are rare, but seem to be more common than under the related drug timolol.[1] If the substance reaches the nasal mucosa via the tear duct, it can be absorbed into the bloodstream and cause systemic side effects. These include orthostatic hypotension (low blood pressure) and other effects on the heart and circulatory system, breathing problems in people with asthma, and skin symptoms such as itching and aggravation of psoriasis.[1] ...
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... (INN) is a drug which is used in scientific research. It acts as both a selective α2 adrenergic receptor antagonist, and an antagonist for the imidazoline receptor.[1][2] Idazoxan has been under investigation as an antidepressant, but it did not reach the market as such. More recently, it is under investigation as an adjunctive treatment in schizophrenia. Due to its alpha-2 receptor antagonism it is capable of enhancing therapeutic effects of antipsychotics, possibly by enhancing dopamine neurotransmission in the prefrontal cortex of the brain, a brain area thought to be involved in the pathogenesis of schizophrenia. ...
... , also known as eformoterol, is a long-acting β2 agonist (LABA) used as a bronchodilator in the management of asthma and chronic obstructive pulmonary disease (COPD). Formoterol has an extended duration of action (up to 12 h) compared to short-acting β2 agonists such as salbutamol (albuterol), which are effective for 4 h to 6 h. LABAs such as formoterol are used as "symptom controllers" to supplement prophylactic corticosteroid therapy. A "reliever" short-acting β2 agonist (e.g., salbutamol) is still required, since LABAs are not recommended for the treatment of acute asthma. It was patented in 1972 and came into medical use in 1998.[2] It is also marketed in the combination formulations budesonide/formoterol and mometasone/formoterol. ...
Since silodosin has high affinity for the α1A adrenergic receptor, it causes practically no orthostatic hypotension (in contrast to other α1 blockers). On the other side, the high selectivity seems to be the cause of silodosin's typical side effect of loss of seminal emission.[3] As α1A adrenoceptor antagonists are being investigated as a means to male birth control due to their ability to inhibit ejaculation but not orgasm, a trial with 15 male volunteers was conducted. While silodosin was completely efficacious in preventing the release of semen in all subjects, 12 out of the 15 patients reported mild discomfort upon orgasm. The men also reported the psychosexual side effect of being strongly dissatisfied by their lack of ejaculation.[4] ...
Brand names include Eskazinyl, Eskazine, Jatroneural, Modalina, Stelazine, Terfluzine, Trifluoperaz, Triftazin. In the United Kingdom and some other countries, trifluoperazine is sold and marketed under the brand 'Stelazine'. The drug is sold as tablet, liquid and 'Trifluoperazine-injectable USP' for deep intramuscular short-term use. GP studying pharmacological data has indicated cases of neck vertebrae irreversible fusing leading to NHS preparations being predominantly of the liquid form trifluoperazine as opposed to the tablet form as in Stela zine etc. In the past, trifluoperazine was used in fixed combinations with the MAO inhibitor (antidepressant) tranylcypromine (tranylcypromine/trifluoperazine) to attenuate the strong stimulating effects of this antidepressant. This combination was sold under the brand name Jatrosom N. Likewise a combination with amobarbital (potent sedative/hypnotic agent) for the amelioration of psychoneurosis and insomnia existed under the brand name Jalonac. In ...
... eye drops may cause blurred vision, eye irritation and dilated pupils.[6] Tetryzoline is not suitable for prolonged use as its vasoconstrictive effects within the eye eventually decrease or stop. When body is accustomed to tetryzoline, ceasing its use may cause redness of the eyes.[7] Intranasal use of tetryzoline may cause transient burning, stinging, or dryness of the mucosa and sneezing. Prolonged intranasal use often causes opposite effects in the form of rebound congestion with effects such as chronic redness, swelling and rhinitis. Prolonged use thus may result in overuse of the drug.[6] Overdose most often causes slow heart rate. Respiratory depression, low blood pressure, constricted pupils, hypothermia, brief episodes of high blood pressure,[8] drowsiness, headaches and vomiting may also occur.[9] In serious cases some of these effects may result in circulatory shock.[6] Most often overdoses occur in children who have ingested the drug.[8] There is no antidote for ...
The drug works by stimulating adrenergic receptors on the lamina propria of blood vessels in the nose. The decongestant effect is due to constriction of large veins in the nose which swell up during the inflammation of any infection or allergy of the nose. The smaller arteries are also constricted and this causes the colour of the nasal epithelium to be visibly paler after dosage. Xylometazoline is an imidazole derivative which is designed to mimic the molecular shape of adrenaline. It binds to α1 and α2 adrenergic receptors[8] in the nasal mucosa. Due to its sympathomimetic effects, it should not be used by people with high blood pressure, or other heart problems. Extended usage of xylometazoline can result in decreased effectiveness or a buildup of tolerance against the drug.[9] The number of receptors decreases, and when the administration of the drug is ceased, chronic congestion can occur; this is called rhinitis medicamentosa, commonly referred to as rebound congestion. Moreover, ...
Ipratropium/salbutamol, sold under the brand name Combivent among others, is a combination medication used to treat chronic obstructive pulmonary disease (COPD).[2][3] It contains ipratropium (an anticholinergic) and salbutamol (albuterol, a β2-adrenergic agonist).[2] It is taken by inhalation.[4] Common side effects include sore throat, muscle cramps, and nausea.[2] Other side effects may include bronchospasm, allergic reactions, and upper respiratory tract infections.[2] Safety in pregnancy is unclear.[1] Each medication typically decreases bronchospasm and does so via different mechanisms.[2] The combination was approved for medical use in the United States in 1996.[4] It is available as a generic medication.[3] Sixty doses in the United Kingdom costs the NHS about 18 £ as of 2019.[3] In the United States the wholesale cost of this amount is about US$9.50.[5] In 2016 it was the 166th most prescribed medication in the United States with more than 3 million prescriptions.[6] ...
Haddad, S; Poulin, P; Funk, C (2010). "Extrapolating in vitro metabolic interactions to isolated perfused liver: Predictions of metabolic interactions between R-bufuralol, bunitrolol, and debrisoquine". Journal of Pharmaceutical Sciences. 99 (10): 4406-26. doi:10.1002/jps.22136. PMID 20310018 ...
... is an intermediate-acting[citation needed] β2 adrenoreceptor agonist used for the treatment of asthma. It has never been filed for FDA evaluation in the United States, where it is not marketed. The drug is readily oxidized in the presence of moisture and air, making it unsuitable for therapeutic use by inhalation.[1] Pharmaceutical company Parke-Davis/Warner-Lambert researched a stabilizer to prevent oxidation, but an effective one was never developed.[1] It was patented in 1974 and came into medical use in 1980.[2] ...
... , sold under the brand name Azafen or Azaphen, is an antidepressant approved in Russia for the treatment of depression.[1][2][3][4] It was introduced in the late 1960s and is still used today.[5][6] Pipofezine has been shown to act as a potent inhibitor of the reuptake of serotonin.[7][8] In addition to its antidepressant action, pipofezine has sedative effects as well, suggesting antihistamine activity.[4] Other properties such as anticholinergic or antiadrenergic actions are less clear but are likely.[citation needed] ...
... , also known as thymoxamine, is a drug used in urology for the treatment of erectile dysfunction.[1] It is an α1-adrenergic antagonist.[2] In the United Kingdom, Moxisylte is marketed as Opilon (Archimedes Pharma UK Ltd) and is used for the short-term treatment of primary Reynaud's syndrome. This is a condition where the fingers and toes become discoloured and is triggered by responses to cold, or emotional distress. Opilon tablets help by improving blood circulation to the extremities.[3][4] ...
... , also known as α-ethylphenethylamine, Butanphenamine, B or AEPEA,[1] is a stimulant drug of the phenethylamine class. It is a higher homologue of amphetamine, differing from amphetamine's molecular structure only by the substitution of the methyl group at the alpha position of the side chain with an ethyl group. Compared to amphetamine, phenylisobutylamine has strongly reduced dopaminergic effects, and instead acts as a selective norepinephrine releasing agent.[citation needed] The dextroisomer of phenylisobutylamine partially substitutes for dextroamphetamine in rats.[1] A number of derivatives of phenylisobutylamine are known, including BDB, MBDB, EBDB, butylone (bk-MBDB), eutylone (bk-EBDB), Ariadne (α-Et-DOM), 4-CAB, and 4-MAB. "Phenylisobutylamine" is in fact a chemical misnomer because isobutylamine itself contains a branched chain. The correct name after this style for this class of compound would be "phenylsecbutylamine". ...
InChI=1S/C23H40N2O4/c1-5-6-7-8-9-10-11-23(27)25-15-19-12-13-21(22(14-19)28-4)29-17-20(26)16-24-18(2)3/h12-14,18,20,24,26H,5-11,15-17H2,1-4H3,(H,25,27 ...
... was discovered by scientists at Angelini, who also discovered trazodone.[15] Its development names have included ST-1191 and McN-A-2673-11.[16][1] The INN etoperidone was proposed in 1976 and recommended in 1977.[17][18] The drug was given brand names in Spain (Centren (Esteve) and Depraser (Lepori)) and Italy (Staff (Sigma Tau))[1] and was also given the brand names Axiomin and Etonin,[16] but it is not entirely clear if it was actually marketed; the Pharmaceutical Manufacturing Encyclopedia provides no dates for commercial introduction.[19] According to Micromedex's Index Nominum: International Drug Directory, etoperidone was indeed previously marketed in Spain and Italy.[1] ...
Butaxamine (INN, also known as butoxamine) is a β2-selective beta blocker. Its primary use is in experimental situations in ... Bupropion Methoxamine "Definition: butoxamine from Online Medical Dictionary". Hillman KL, Doze VA, Porter JE (August 2005). " ...
... butoxamine manufacturers and suppliers in China, we warmly welcome you to wholesale chiral compounds at low price from our ... Hot tags: (+/-)-butoxamine, China, manufacturers, suppliers, factory, wholesale, low price, high quality ...
"Butaxamine". pubchem.ncbi.nlm.nih.gov. U.S. National Library of Medicine. Archived from the original on October 18, 2017. ...
3. Beta blockers • Beta1, beta2: propranolol • Beta 1: metoprolol and atenolol • Beta 2: butoxamine ...
Suitable anti-diabetic therapeutic agents include, but are not limited to, Acetohexamide; Buformin; Butoxamine Hydrochloride; ...
Butoxamine (5 mg/kg, i.p., in PBS) and RU486 (5 mg/kg, i.p., in ethanol/sesame oil 1:10) were administrated immediately before ... Butoxamine (Butox; a selective β2AR antagonist; 5 mg/kg) and RU486 (a glucocorticoid receptor antagonist; 5 mg/kg) were ... To test this hypothesis, selective β2AR (butoxamine; 5 mg/kg) and GR antagonists (RU486; 5 mg/kg) were injected ... repeat injections of butoxamine and RU486 significantly reduced splenic atrophy (Fig. 9A) and restored immune function to ...
alcohol secundario (es); 第2級アルコール (ja); Alcool secondaire (fr); alkohol drugorzędowy (pl); вторичный спирт (ru); 仲醇 (lzh); 이차 알코올 (ko); secondary alcohol (en); sekundara alkoholo (eo); sekundární alkohol (cs); 仲醇 (zh) każdy alkohol, w którym grupa hydroksylowa przyłączona jest do drugorzędowego atomu węgla (pl) вторичные спирты (ru); Alcool Secondaire (fr); 2차 알코올 (ko); secondary alcohols (en); alkohole drugorzędowe (pl ...
Inability of either atenolol or butoxamine to inhibit the male sexual behavior, and inhibition of the same by the mixture of ... To investigate the role of specific adrenoreceptors subtypes on sexual behavior, atenolol, butoxamine, a mixture of atenolol ... On the other hand, application of either atenolol or butoxamine alone did not inhibit copulatory activity. But it produced ... Stimulation of some components of sexual behavior on application of atenolol or butoxamine could be attributed to an unbalanced ...
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RESULTS: Although propranolol improved early and late erythroblasts, only butoxamine and selective 3-antagonist administrations ... butoxamine (selective 2 antagonist), or SR59230A (selective 3 antagonist) for 6 days after burn. Total bone marrow cells were ...
Study autonomic nervous system stuff flashcards from Carl Dernell
Butaxamine • Butidrine • Butofilolol • Capsinolol • Carazolol • Carpindolol • Carteolol • Carvedilol • Celiprolol • Cetamolol ...
B The β2 receptor antagonist butoxamine (BUTO, 5 mg/kg) also reversed the visceral hyperalgesia induced by NMD + AMS in a time- ... In the behavioral experiments, 5 mg/kg butoxamine (BUTO, a β2 antagonist; Sigma, St. Louis, MO), 3 mg/kg propranolol (PROP, a ... Inhibition of β2 adrenergic receptors with propranolol or butoxamine enhanced the colorectal distention threshold and ... application of butoxamine also reversed the enhanced hypersensitivity of DRG neurons. Overall, our data demonstrate that AMS ...
The effect of practolol and butoxamine on aortic arch malformations in beta receptor stimulated chick embryos. Teratology.1977; ...
Study 76 Pharm Final flashcards from Kate B. on StudyBlue.
... and butoxamine were from Sigma-Aldrich (St Louis, MO). Unless otherwise indicated, reagents were reconstituted and diluted in ... or the β2-specific AR antagonist butoxamine (160 μM for 30 minutes (P , .05, n = 5), (C) a PKA inhibitor (PKAI) (36 nM for 1 ... whereas the β2-specific antagonist butoxamine inhibited adhesion by 62% (P , .001) (Figure 5B). These data are consistent with ...
Using the selective beta2-AR antagonist butoxamine, the authors observed a dose-dependent reversal of OIH. Furthermore, ...
The enzyme secretion was inhibited by different adrenolytic drugs (phenoxybenzamine, practolol, butoxamine), by tetracain, ...
Butaxamine (weak α-adrenergic agonist activity). Comparative information. Pharmacological differences. *Agents with intrinsic ...
... butoxamine, and propranolol) caused a slight reduction (,10%) in tCr content. ...
Butaxamine Butidrine Butofilolol Capsinolol Carazolol Carpindolol Carteolol Carvedilol Celiprolol Cetamolol Cicloprolol ... Butaxamine (weak α-adrenergic agonist activity): No common clinical applications, but used in experiments ...
Butaxamine • Butidrine • Butofilolol • Capsinolol • Carazolol • Carpindolol • Carteolol • Carvedilol • Celiprolol • Cetamolol ...
Propranolol was the overall most effective compound, followed by metoprolol, alprenolol and practolol, whereas butoxamine and ...
Os agentes que são altamente selectivos para o beta receptor 2 incluem o butaxamine e as diversas outras terapias actualmente ...
... metaprolol and butoxamine), angiotensin-II receptor antagonists (e.g., losartan, valsartan, irbesartan, candesartan, eprosartan ...
The other agents (S 37-429, S 32-468, ICI 78,462,H35/25, butoxamine, propranolol, timolol, atenolol and practolol) showed ...
... butoxamine), angiotensin-II receptor antagonists (such as losartan, valsartan, irbesartan, candesartan and telmisartan), and ...
Effect of Butoxamine Pretreatment on Salbutamol and BRL 37344 Activity. Salbutamol, administered further to butaxamine, did not ... The influence of butoxamine (But; 10-4 M), a selective antagonist of β2-adrenoceptors on changes in the tension (A), frequency ... The antagonists: butoxamine (a selective β2-adrenoceptor antagonist; Sigma), propranolol (a nonselective β1- and β2- ... BRL 37344, administered further to butaxamine, caused a reduction of the tension (Fig. 4A) and frequency (Fig. 4B) at ...
Selective β2-adrenergic antagonist butoxamine reduces orthodontic tooth movement. J Dent Res. 93:807-812. 2014. View Article : ...
  • METHODS: Burn mice were randomized to receive daily injections of propranolol (nonselective 1/ 2 antagonist), nadolol (long-acting 1/ 2 antagonist), butoxamine (selective 2 antagonist), or SR59230A (selective 3 antagonist) for 6 days after burn. (bireme.br)
  • RESULTS: Although propranolol improved early and late erythroblasts, only butoxamine and selective 3-antagonist administrations were positively reflected in the peripheral blood hemoglobin and red blood cells count. (bireme.br)
  • Inhibition of β 2 adrenergic receptors with propranolol or butoxamine enhanced the colorectal distention threshold and application of butoxamine also reversed the enhanced hypersensitivity of DRG neurons. (springer.com)
  • Propranolol was the overall most effective compound, followed by metoprolol, alprenolol and practolol, whereas butoxamine and H35/25 were weak inhibitors. (aspetjournals.org)
  • Changes in the contractility of myometrial strips were assessed further to the administration of increasing concentrations of the agonists (10 -9 to 10 -5 M ) with and without β-adrenergic receptor antagonists: butoxamine, propranolol, and bupranolol at 10 -4 M . Moreover, the -log EC 50 (pD 2 ) of the agonists were compared. (animalsciencepublications.org)
  • A delay in the onset of isoniazid-induced convulsions was found in rats pretreated with the beta 2-adrenoceptor blocker, butoxamine and the nonspecific beta-blocker, propranolol. (bvsalud.org)
  • The anticonvulsant effect of acebutolol and propranolol but not that of butoxamine was found to be enhanced in animals pretreated with a gamma-aminobutyric acid (GABA) elevating agent, aminooxyacetic acid (AOAA). (bvsalud.org)
  • The acetylcholine-dependent metabolic alterations were not inhibited by the beta 2-antagonist butoxamine (10 microM), although the overflow of noradrenaline was nearly completely blocked and the output of adrenaline was slightly decreased. (biochemj.org)
  • These effects were attenuated or completely abolished by the ganglionic blocker chlorisondamine (3 mg/kg i.p.), by adrenal demedullation, by a selective β-adrenergic antagonist (nadolol, 0.4 mg/kg), and additively by a selective β 1 - (atenolol, 1-6 mg/kg) and a selective β 2 -antagonist (either butoxamine 4-32 mg/kg or ICI-118,551 0.3-8 mg/kg). (elsevier.com)
  • The study found that β2-AR agonists inhibited the expression of intercellular adhesion molecule-1 (ICAM-1), CD40 and CD14 on monocytes, and that AR agonist activity was antagonized by the selective β2-AR antagonist, butoxamine. (elsevier.com)
  • In the first experiment rats were intravenously pretreated with vehicle (V), atenolol 30 mg/kg (ATE, β1-adrenergic antagonist), or butoxamine 25 mg/kg (BUT, β2-adrenergic antagonist). (bvsalud.org)
  • Butoxamine, a specific β 2 -adrenergic antagonist, significantly blocked changes induced by procaterol. (pulmonarycellnews.com)
  • Cotreatment with a b2-adrenergic receptor antagonist, butoxamine, suggests that the effect of terbutaline is mediated by activation of b2-adrenergic receptors. (korea.ac.kr)
  • The problem of the characterization of butoxamine as a specific antagonist of the metabolic effects of sympathomimetics Traditionally, binding proteins are known to regulate the activity of ligands by prolonging their half-life, and insulin-like growth factor (IGF)-binding proteins (IGFBPs) are no exception to this. (storysteel.cf)
  • Butaxamine (INN, also known as butoxamine) is a β2-selective beta blocker. (wikipedia.org)
  • Atenolol or butoxamine injection at the lateral septum doesn't inhibit male sexual behavior in rats. (bvsalud.org)
  • To investigate the role of specific adrenoreceptors subtypes on sexual behavior , atenolol , butoxamine , a mixture of atenolol and butoxamine , and saline (vehicle) were injected into the lateral septum in four different groups of sexually active male rats . (bvsalud.org)
  • Application of a mixture of atenolol and butoxamine produced inhibition of copulatory activity. (bvsalud.org)
  • On the other hand , application of either atenolol or butoxamine alone did not inhibit copulatory activity. (bvsalud.org)
  • Inability of either atenolol or butoxamine to inhibit the male sexual behavior , and inhibition of the same by the mixture of atenolol and butoxamine , indicate that both beta-adrenoreceptors at the lateral septum are involved in the elaboration of male sexual behavior . (bvsalud.org)
  • Stimulation of some components of sexual behavior on application of atenolol or butoxamine could be attributed to an unbalanced activity of beta-adrenoreceptors. (bvsalud.org)
  • was inhibited by AR agonists, and this was also antagonized by butoxamine, and mimicked by salbutamol and terbutaline. (elsevier.com)
  • In parotid gland, [Na] of sympathetically evoked saliva in the presence of phentolamine (3 mg/kg, i.p.) was not different from that of nerve-evoked saliva in the presence of phentolamine and butoxamine (3 mg/kg, i.p.), except for the last 20 min of stimulation when [Na] of nerve-elicited saliva was higher. (mysciencework.com)
  • K] of saliva with sympathetically evoked stimulation was the same in the presence of phentolamine alone as it was or in the presence of phentolamine and butoxamine. (mysciencework.com)
  • In particular, salbutamol prevented non-NMDA-induced motor neuron loss and this effect was abolished by the concomitant administration of butoxamine. (onlinebeats.tk)
  • In addition, to characterize the molecular mechanism involved in the effect exerted by ASA on left ventricular pressure, some drugs such as estrone (0.001-100 nM), tamoxifen (1 nM), butoxamine (1 nM) and ZM-241385 (1 nM) were used. (openpharmacologyjournal.com)