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.
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 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.
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.
A general class of ortho-dihydroxyphenylalkylamines derived from tyrosine.
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.

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, ...
Extracellular ATP is a broad-spectrum cytotoxic agent that produces effects via cell surface P2 purinoceptors. The ligand-gated P2X purinoceptor subtype has very high sequence homology with theRP-2 gene, which encodes for apoptosis. The P2X RNA found in rat vas deferens is expressed preferentially by apoptotic thymocytes. P2X purinoceptor-mediated phasic (twitch) motor responses of the isolated rat vas deferens to neurogenic or exogenous ATP were rapidly, specifically and irreversibly potentiated by bis(2-chloroethyl)sulfide (HD 10-100 μM). Both untreated and HD-potentiated neurogenic responses were Ca++ dependent, blocked in the absence of Ca++ plus 0.1 mM EGTA, by the neuronal Ca++channel blocker ω-conotoxin-MVIIC (3 μM), by the P2 purinoceptor antagonist suramin (100 μM) and by tetrodotoxin (100 nM). HD also potentiated the effects of ATP on isolated guinea pig taenia caecum, where the nucleotide acts at G protein-coupled P2Y purinoceptor subtypes to cause relaxation. HD failed to inhibit ...
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 (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). " ...
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- ...
"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 ...
Free flashcards to help memorize facts about intro. Other activities to help include hangman, crossword, word scramble, games, matching, quizes, and tests.
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 ...
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 ...
Rabbits treated with dl-propranolol (4 or 8 mg/kg i.p.) or butoxamine (15 or 30 mg/kg i.p.) produced significantly less ESF in ... The effects of dl-propranolol, d-propranolol, butoxamine or practolol on erythropoietin (ESF) production in rabbits exposed to ... Based on the proposed selectivity of butoxamine for beta2 adrenergic receptors and of practolol for beta1 adrenergic receptors ...
... 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 ...
butoxamine beta-2 receptor antagonist. note: tool only, there are no drugs on the market that block only beta-2 ...
... butoxamine), angiotensin-II receptor antagonists (such as losartan, valsartan, irbesartan, candesartan and telmisartan), and ...
... metaprolol and butoxamine), angiotensin-II receptor antagonists (e.g., losartan, valsartan, irbesartan, candesartan, eprosartan ...
  • 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)
  • The effects of dl-propranolol, d-propranolol, butoxamine or practolol on erythropoietin (ESF) production in rabbits exposed to hypoxia (0.42 atmosphere) for 18 hours were investigated. (aspetjournals.org)
  • Rabbits treated with dl-propranolol (4 or 8 mg/kg i.p.) or butoxamine (15 or 30 mg/kg i.p.) produced significantly less ESF in response to hypoxia than did saline-treated control animals. (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)
  • 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)
  • Based on the proposed selectivity of butoxamine for beta2 adrenergic receptors and of practolol for beta1 adrenergic receptors, it is suggested that ESF production in rabbits exposed to hypoxia may involve the activation of beta2 adrenergic receptors. (aspetjournals.org)
  • was inhibited by AR agonists, and this was also antagonized by butoxamine, and mimicked by salbutamol and terbutaline. (elsevier.com)
  • Butaxamine (INN, also known as butoxamine) is a β2-selective beta blocker. (wikipedia.org)
  • 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)

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