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.

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)

... (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, an example of beta 2 blocker, has no clinical use but is used in research. Due to the relatively limited study on ... "Butaxamine". pubchem.ncbi.nlm.nih.gov. Retrieved 2021-03-15. (CS1: long volume value, Drugs, Sympathetic nervous system, ... Phenoxybenzamine Phentolamine Prazosin Tamsulosin Yohimbine Propranolol Timolol Atenolol Metoprolol Butaxamine Still under ...
"Butaxamine". pubchem.ncbi.nlm.nih.gov. U.S. National Library of Medicine. Archived from the original on October 18, 2017. ... Butaxamine ICI-118,551 SR 59230A Nebivolol Agents with intrinsic sympathomimetic action (ISA) Acebutolol, pindolol, labetalol, ...
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 ...
... butoxamine MeSH D02.092.471.683.338 - dexfenfluramine MeSH D02.092.471.683.386 - dimethoxyphenylethylamine MeSH D02.092.471.683 ...
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 ...
Butoxamine - Preferred Concept UI. M0003096. Scope note. A beta-2 selective adrenergic antagonist. It is used primarily in ... Butaxamine Entry term(s):. Butaxamine. Butoxamine Hydrochloride. Hydrochloride, Butoxamine. Tree number(s):. D02.092.471.683. ...
In the first study, mice were butoxamine, as ß2AR blocker, with vehicle or 10mg/kg FL orally. We found that pretreatment with ... butoxamine prevented the increases of EE, the mRNA expression of UCP-3, and phosphorylated AMPKα that were induced in the ...
Atenolol or butoxamine injection at the lateral septum doesnt inhibit male sexual behavior in rats.. Gulia, K K; Mallick, H N ...
Butoxamine (MeSH Term). *cerivastatin (Supplementary Concept). *cetilistat (Supplementary Concept). *Chitosan (MeSH Term) ...
Butoxamine Hydrochloride Narrower Concept UI. M0003097. Registry Number. 2O68ZJ8BLQ. Terms. Butoxamine Hydrochloride Preferred ... Butaxamine Butoxamine Hydrochloride Pharm Action. Hypolipidemic Agents. Hypoglycemic Agents. Sympatholytics. Adrenergic beta-2 ... Butoxamine Preferred Term Term UI T005885. Date01/01/1999. LexicalTag NON. ThesaurusID ... Butoxamine Preferred Concept UI. M0003096. Registry Number. 0NM31M53PW. Related Numbers. 2922-20-5. 2O68ZJ8BLQ. 5696-15-1. ...
Butoxamine Hydrochloride Narrower Concept UI. M0003097. Registry Number. 2O68ZJ8BLQ. Terms. Butoxamine Hydrochloride Preferred ... Butaxamine Butoxamine Hydrochloride Pharm Action. Hypolipidemic Agents. Hypoglycemic Agents. Sympatholytics. Adrenergic beta-2 ... Butoxamine Preferred Term Term UI T005885. Date01/01/1999. LexicalTag NON. ThesaurusID ... Butoxamine Preferred Concept UI. M0003096. Registry Number. 0NM31M53PW. Related Numbers. 2922-20-5. 2O68ZJ8BLQ. 5696-15-1. ...
... friend bioparox explanatum retrievers pentahydroxycycloartane conchaphila blastic colistimethate butoxamine antioco ...
4I5PG5VZ0V BUTOPYRONOXYL C76864 QV897JC36D BUTORPHANOL C61659 2L7I72RUHN BUTORPHANOL TARTRATE C61658 2O68ZJ8BLQ BUTOXAMINE ...
We found metoprolol not butoxamine attenuated the reactivation-induced strengthening of fear retention and restored the ... Intra-amygdala infusion of metoprolol not butoxamine attenuated reactivation-induced enhancement of fear retention. Our results ... ß2-adrenergic receptor antagonist-butoxamine on the retention of conditioned fear memory and synaptic adaptation in the lateral ...
ADRENERGIC AGENTS BUTOXAMINE ADRENERGIC AGENTS CARTEOLOL ADRENERGIC AGENTS CELIPROLOL ADRENERGIC AGENTS CLENBUTEROL ADRENERGIC ... ADRENERGIC BETA-ANTAGONISTS BUTOXAMINE ADRENERGIC BETA-ANTAGONISTS CARTEOLOL ADRENERGIC BETA-ANTAGONISTS CELIPROLOL ADRENERGIC ... AUTONOMIC AGENTS BUTOXAMINE AUTONOMIC AGENTS BUTYLSCOPOLAMMONIUM BROMIDE AUTONOMIC AGENTS CARBACHOL AUTONOMIC AGENTS CARTEOLOL ... ANTILIPEMIC AGENTS BUTOXAMINE ANTILIPEMIC AGENTS CHOLESTYRAMINE ANTILIPEMIC AGENTS CLOFENAPATE ANTILIPEMIC AGENTS CLOFIBRATE ...
Butoxamine [D02.092.471.683.221] Butoxamine * Dexfenfluramine [D02.092.471.683.338] Dexfenfluramine * Dimethoxyphenylethylamine ...

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