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At least 73 records · Page 4Linked to original sources
PubMed1996

Differentiation of binding sites of CGP12177, a beta 3-adrenoceptor partial agonist, and carteolol, a beta 1/beta 2-adrenoceptor partial agonist, to the beta-adrenoceptors in guinea-pig taenia caecum.

Differentiation of binding sites of CGP12177 and carteolol to the beta-adrenoceptors in the guinea-pig taenia caecum was investigated. Carteolol and CGP12177 competitively antagonized the relaxation responses to isoprenaline, and the pA2 values were 9.87 and 9.33, respectively. Butoxamine, a beta 2-selective antagonist, caused competitive antagonism of the relaxant responses to carteolol, and the pA2 value for butoxamine was 6.22. However, butoxamine (10(-4) M) did not significantly affect the relaxant responses to CGP12177. CGP12177 caused competitive antagonism of the relaxant responses to carteolol, and the pA2 value for CGP12177 was 9.32. However, carteolol (10(-6) M) did not significantly affect the relaxant responses to CGP12177. The competitive inhibition curve for specific binding of 50 nM [3H]befunolol by carteolol showed a biphasic shape, although the curve by CGP12177 was monophasic. Moreover, the competitive inhibition curve for specific binding of 100 nM [3H]CGP12177 by CGP12177 showed a biphasic shape, although the curve by carteolol indicated partial inhibition. These results suggest that the low affinity site of beta-adrenoceptor and beta 3-adrenoceptors are different from each other.

Adrenergic beta-Agonists↗
PubMed1979

Long-term haloperidol-treatment of mice: a change in beta-adrenergic receptor responsiveness.

Mice administered haloperidol 3 mg/kg/day in their drinking water for 21 days were tested for their locomotor responsiveness to saline or acid vehicle, dl-, l- or d-propranolol, metoprolol, butoxamine or practolol. Haloperidol-treated animals administered saline or acid-vehicle were, in five of six experiments, more active than animals withdrawn from vehicle-treatment. Haloperidol- and vehicle-treated animals responded differently to the non-selective beta-adrenoreceptor antagonists (dl-propranolol and l-propranolol) and selective beta1-adrenoreceptor antagonists (practolol and metoprolol), but not to a selective beta2-adrenoreceptor antagonist (butoxamine). With dl-propranolol (4 mg/kg) the locomotor activity of haloperidol-treated animals was significantly (0.01 less than P less than 0.02) greater than that of the vehicle-treated animals. Similar effects in the same direction were seen with l-propranolol (1 mg/kg, 0.005 less than P less than 0.01), practolol (10 and 100 mg/kg, 0.025 less than P less than 0.05 and 0.01 less than P less than 0.025 respectively) and metoprolol 8 mg/kg, 0.005 less than P less than 0.01). The d-isomer of propranolol which is about 50 times less active as a beta-adrenoreceptor antagonist than the l-isomer, although having equal membrane stabilizing effects, did not differentially affect haloperidol- or vehicle-treated groups. The results suggest that there has been a change in beta 1-adrenoreceptor responsiveness in animals withdrawn from long-term haloperidol treatment.

Adrenergic beta-Antagonists↗
PubMed1976

Adrenergic inhibition of cell proliferation in the buccal epithelium of rat.

Mitotic rates in the basal layer of cells in the buccal epithelium of rat were measured using a stathmokinetic technique. Adrenaline was found to inhibit cell proliferation in this tissue and the effect of adrenaline could be blocked by the beta-adrenergic antagonist propranolol but not by the alpha-adrenergic antagonist phentolamine nor by the specific beta2-adrenergic antagonist butoxamine. Cell proliferation in the buccal mucosa was also inhibited by terbutaline, a synthetic beta2-adrenergic agonist. The effect of terbutaline was not blocked by either butoxamine or by the specific beta1-adrenergic antagonist practolol.

Animals↗
PubMed1994

Cardiovascular teratogenicity of terbutaline and ritodrine in the chick embryo.

OBJECTIVE: We determined the teratogenic effects of terbutaline and ritodrine, both beta 2-sympathomimetic agonists, on the stage 24 (4-day) chick embryo. STUDY DESIGN: We used a topical method of application of terbutaline or ritodrine to the stage 24 chick embryo in ovo. Doses of terbutaline ranged from 5.5 x 10(-10) to 6.5 x 10(-9) mol per embryo, and ritodrine doses ranged from 4.6 x 10(-11) to 4.6 x 10(-8) mol per embryo. To further determine the pharmacologic nature of the teratogenic potential of terbutaline or ritodrine, the experiments were repeated after pretreatment with butoxamine hydrochloride, a preferential beta 2-antagonist, or metoprolol tartrate, a preferential beta 1-antagonist, 4 hours before application of terbutaline or ritodrine. RESULTS: Terbutaline treatment was associated with significantly higher rates of anomalies than in controls at all dosages used, whereas ritodrine induced significantly more anomalies at or above doses of 4.6 x 10(-9) mol per embryo. At an equimolar dose pretreatment with butoxamine hydrochloride significantly reduced the cardiovascular teratogenic effects of terbutaline and ritodrine. Pretreatment with metoprolol tartrate at any dose did not significantly reduce terbutaline's potential. Metoprolol, at doses tenfold or 100-fold higher than ritodrine, was able to significantly reduce the teratogenic effects of ritodrine. CONCLUSIONS: Our data suggest that terbutaline and ritodrine are teratogenic in the chick and that these agents exert their teratogenic effects primarily through stimulation of the beta 2-adrenergic receptor.

Animals↗
PubMed1991

Alpha- and beta-adrenoceptors in the sheep urinary bladder.

A study was undertaken to determine the presence and distribution of alpha- and beta-adrenoceptors in the sheep bladder body and base. In the bladder body, noradrenaline and isoproterenol induced relaxation which was significantly inhibited by propranolol, pafenolol and butoxamine. In the presence of propranolol (10(-5) M), noradrenaline induced a small contraction, as well as phenylephrine, but B-HT 920 failed to cause any effect on the bladder body. In the bladder base, noradrenaline caused a contraction that was significantly inhibited by prazosin but not by yohimbine. Phenylephrine also induced a contractile response in this structure which was inhibited by prazosin. Isoproterenol caused a relaxation that was significantly inhibited by propranolol and pafenolol but not by butoxamine. Relaxation was mediated by both beta 1 and beta 2-adrenoceptors in the detrusor muscle and by beta 1-adrenoceptors in the bladder base. Alpha 1-adrenoceptors contributed to maintain the detrusor tone and contract the bladder base.

Adrenergic beta-Antagonists↗
PubMed1998

Activation by Phoneutria nigriventer spider venom of autonomic nerve fibers in the isolated rat heart.

In the isolated rat heart, Phoneutria nigriventer spider venom (10-100 microg) produced a dose-dependent and reversible rise in left ventricular developed pressure. A low dose (10 microg) of venom induced a short-lasting, positive inotropic effect (P < 0.05) with no change in heart rate or coronary flow. At a dose of 50 microg, the venom caused significant positive inotropic and chronotropic responses associated with occasional ventricular arrhythmia, whereas coronary flow was not significantly affected within 10 min after venom administration. The highest dose of venom (100 microg) caused bradycardia, transient cardiac arrest, rhythm disturbances and an increase in end diastolic pressure followed by a reduction in coronary flow. Hearts treated with the non-selective beta-adrenoceptor antagonist propranolol (3 microM) and the selective beta1-adrenoceptor antagonist CGP-20712A (10 microM) were protected against all the cardiac actions of the venom. The selective beta2-adrenoceptor antagonist butoxamine (10 microM) slightly reduced the cardiac response to 50 microg, but not to 100 microg of venom. Butoxamine also prevented the reduction in coronary flow induced by 100 microg of venom. Hearts from reserpine-treated rats (5 mg kg(-1) day(-1), i.p., for 2 days) showed a marked decrease in all venom (< or = 100 microg)-induced cardiac responses. The muscarinic receptor antagonist atropine (1 microM) slightly potentiated the response to 50 microg of venom but had little or no effect on the responses to 100 microg of venom. The cardiac responses to venom (50-100 microg) were unaltered in hearts from rats treated with 8-methyl N-vanillyl-6-nonenamide (capsaicin; 50 mg/kg, s.c.). These findings indicate that P. nigriventer venom releases norepinephrine from cardiac sympathetic nerve endings and this may explain the observed increase in contractile force and heart rate.

Adrenergic Uptake Inhibitors↗
PubMed1997

Characteristics of [3H]CGP12177 binding sites at beta 2- and beta 3-adrenoceptors in the guinea pig taenia caecum.

1. Experiments were carried out to characterize the [3H]CGP12177 binding sites in the microsomal fraction from the guinea pig taenia caecum. 2. The Scatchard plot in the absence of butoxamine (10(-4) M) or bupranolol (10(-4) M) was concave, suggesting two affinity sites: high and low affinity binding sites. 3. The Scatchard plot in the presence of butoxamine gave a straight line, indicating only the low affinity site. 4. The Scatchard plot in the presence of bupranolol was undetectable. 5. These results suggest that the high affinity binding sites for [3H]CGP12177 correspond to beta 2-adrenoceptors in the microsomal fraction from the guinea pig taenia caecum, whereas the low affinity binding sites represent beta 3-adrenoceptors.

Adrenergic beta-Agonists↗
PubMed1986

Intraocular pressure and aqueous humor dynamics in rabbit and primate with d- and 1-adrenergic compounds.

The effects of the d- and 1-isomers of epinephrine and norepinephrine have been determined on intraocular pressure (IOP) in conscious rabbits and rhesus monkeys, and on aqueous humor turnover rate (AHTR) in rabbits. Relatively specific beta-adrenergic antagonists (butoxamine and metoprolol) were used to attempt to modify the responses. The effects on IOP in both species are similar to those of racemic mixtures. The d- and 1-isomers of norepinephrine and epinephrine reduced IOP, and reduced AHTR in rabbits. The d- and 1-isomers of norepinephrine had little effect on IOP in monkeys while d- and 1-epinephrine increased IOP. Metoprolol, a beta 1-antagonist was more effective than butoxamine (beta 2-antagonist) at modifying the effect of the norepinephrine isomers in rabbits.

Animals↗
PubMed1979

alpha And beta-adrenoceptors in the detrusor muscle and bladder base of the pig and beta-adrenoceptors in the detrusor muscle of man.

1 The presence and type of adrenoceptors in the smooth muscle of the pig and human urinary bladder was assessed on the basis of the relative potency of alpha- and beta-adrenoceptor agonists and antagonists.2 In isolated, carbachol-contracted bladder strips from the pig detrusor muscle the relaxing potency of isoprenaline was four times that of salbutamol and ritodrine and thirty times that of noradrenaline.3 Propranolol caused a parallel shift to the right of the noradrenaline dose-response curve which was not changed by phentolamine.4 Propranolol and butoxamine showed, in contrast to practolol, a dose-dependent antagonism of the response to isoprenaline. A pA(2) value of 9.2 +/- 0.2 and 6.8 +/- 0.2 (mean +/- s.e. mean) for the first two antagonists was calculated.5 In the bladder base of the pig, propranolol caused a parallel shift to the right and phentolamine a shift to the left of the dose-response curve to noradrenaline.6 In the human detrusor muscle the potency and maximum effect of isoprenaline and salbutamol were less than those in the pig detrusor muscle. The potency of isoprenaline was sixty times that of salbutamol.7 Whereas a parallel shift to the right of the dose-response curve to isoprenaline was obtained with propranolol, no antagonism was obtained with butoxamine or practolol.8 The results are interpreted as indicating the presence of beta(2)-adrenoceptors in the detrusor muscle of the pig and beta-adrenoceptors with neither beta(1)- nor beta(2)-characteristics in the detrusor muscle of man. An indication of the presence of alpha-adrenoceptors in the bladder base but not in the detrusor muscle of the pig was obtained.

Adult↗
PubMed1979

Beta-adrenoceptors in the pregnant and non-pregnant myometrium of the goat and cow.

The muscle relaxing effect of beta-adrenoceptor agonists was examined without and with the presence of beta-adrenoceptor antagonists in strips from the pregnant and non-pregnant myometrium of the goat and from the pregnant myometrium of the cow. Isoprenaline, salbutamol and ritodrine caused a dose-dependent reduction of the spontaneous contractions of the pregnant myometrium and a dose-related and parallel shift to the right of the isoprenaline dose-response curve was obtained with butoxamine but not with practolol. Isoprenaline but neither salbutamol nor ritodrine caused a dose-related reduction of the spontaneous contractions in the non-pregnant myometrium and a dose-related and parallel shift to the right of the dose-response curve of isoprenaline was brought about with propranolol but not with either butoxamine or practolol. The muscle relaxing effect of ritodrine on the pregnant myometrium of the goat and cow shown in vitro was also demonstrated in vivo in the same species within eight hours of delivery. It is concluded that the beta-adrenoceptors in the pregnant myometrium of the goat and cow belong to the beta2-group whereas those in the non-pregnant myometrium cannot be classified as either beta1- or beta2-adrenoceptors.

Albuterol↗
PubMed1989

A study of beta-adrenoceptors in rat lung parenchymal strip.

The aim of the present study was to characterize the beta-adrenoceptor population in rat lung strip. For this purpose, Schild plots were obtained for the beta-adrenoceptor antagonists atenolol (beta 1-selective), butoxamine (beta 2-selective) and propranolol (non-selective), using three different agonists:isoprenaline (non-selective), salbutamol (beta 2-selective) and noradrenaline (beta 1-selective). The slopes of these Schild plots were close to the theoretical value of unity, and pA2 values determined with isoprenaline, salbutamol and noradrenaline as agonists were: for propranolol, 7.86 +/- 0.22, 7.72 +/- 0.15 and 7.89 +/- 0.23; for atenolol, 5.19 +/- 0.05, 5.33 +/- 0.07 and 5.47 +/- 0.22 and for butoxamine, 6.31 +/- 0.11, 6.34 +/- 0.03 and 5.99 +/- 0.23, respectively. These data suggest that pharmacological responses of rat isolated lung strip to beta-adrenoceptor agents are mediated by a homogeneous population of beta 2-adrenoceptors, although the presence of a minor population of beta 1-adrenoceptors undetected by the agonists used cannot be excluded.

Albuterol↗
PubMed1988

Slow to fast alterations in skeletal muscle fibers caused by clenbuterol, a beta 2-receptor agonist.

Chronic treatment of rats with clenbuterol, a beta 2-receptor agonist (8-12 wk), caused hypertrophy of histochemically identified fast- but not slow-twitch fibers within the soleus, while the mean areas of both fiber types were increased in the extensor digitorum longus (EDL). In contrast, treatment with the beta 2-receptor antagonist, butoxamine, reduced fast-twitch fiber size in both muscles. In the solei and to a lesser extent in the EDLs, the ratio of the number of fast- to slow-twitch fibers was increased by clenbuterol, while the opposite was observed with butoxamine. The muscle fiber hypertrophy observed in the EDL was accompanied by parallel increases in maximal tetanic tension and muscle cross-sectional area, while in the solei, progressive increases in rates of force development and relaxation toward values typical of fast-twitch muscles were also observed. Our results suggest a role of beta 2-receptors in regulating muscle fiber type composition as well as growth.

Animals↗
PubMed1979

Influence of albuterol on erythropoietin production and erythroid progenitor cell activation.

The effect of albuterol, a potent beta2-adrenergic agonist, on kidney production of erythropoietin (Ep) was studied. Its effects on erythroid colony (CFU-E) formation in vitro in rabbit bone marrow cultures were also assessed. Albuterol produced a significant increase in plasma Ep levels in conscious rabbits following 7 h intravenous infusion (50 (microgram/kg)/min). This effect was blocked by pretreatment of the rabbits with butoxamine (5 mg/kg ip), a potent beta2-adrenergic blocker. Albuterol in doses of 10(-10) to 10(-8) M in combination with Ep was also found to produce a significant increase in the numbers of CFU-E in the plasma clot culture system of rabbit bone marrow. This effect was blocked completely by DL-propranolol (10(-8) M) and by butoxamine (10(-8) M). The data presented suggest that albuterol, a potent activator of beta2-adrenergic receptors, increases kidney production of Ep in vivo and also produces a direct effect in combination with Ep on the proliferation of the erythroid progenitor cell compartment.

Albuterol↗
PubMed1993

Mechanisms underlying cardiovascular defense reaction evoked by dorsal periaqueductal gray stimulation.

Hemodynamic and autonomic mechanisms underlying the cardiovascular defense reaction elicited by electrical stimulation of the dorsolateral periaqueductal gray region were evaluated in pentobarbital sodium-anesthetized Sprague-Dawley rats. Stimulation of this area produced transient increases in mean arterial pressure and more sustained increases in heart rate, hindlimb blood flow, and plasma catecholamine levels. The pressor component of the defense reaction was due entirely to increased total peripheral vascular resistance; elevations in cardiac output occurred only at the end of the stimulation period when blood pressure had returned to resting values. The hindlimb vasodilatory response included distinct early and late components. The late component was produced by epinephrine-mediated activation of beta 2-receptors because it was abolished by bilateral adrenalectomy or treatment with butoxamine, a beta 2-receptor selective antagonist. In contrast, the early component was only partially reduced by adrenalectomy or butoxamine treatment. During conditions of constant flow provided by a pump-perfused hindlimb preparation, the early hindlimb vasodilatory response was eliminated and a neurogenic vasoconstrictor response revealed. This finding suggests that the early hindlimb blood flow response may result from shunting of blood from highly vasoconstricted vascular beds to relatively less constricted hindlimb vasculature.

Adrenalectomy↗
PubMed1996

Relaxant responses by optical isomers of ephedrine and methylephedrine in guinea pig tracheal smooth muscle.

The effects of optical isomers of ephedrine and methylephedrine on the guinea pig tracheal smooth muscle were studied. l-Ephedrine markedly caused a graded relaxation of the guinea pig trachea where the tone had been raised spontaneously. A rightward shift of the l-ephedrine concentration-response curve was observed for propranolol and butoxamine, and the pA2 values for propranolol and butoxamine were 8.55 and 6.38, respectively. d-Methylephedrine markedly caused a graded relaxation of the guinea pig trachea contracted with histamine. Propranolol and bupranolol did not affect the relaxant response to d-methylephedrine. d-Methylephedrine competitively antagonized the contractile responses to histamine, and the pA2 value for d-methylephedrine was 5.12. These results suggest that l-ephedrine-induced relaxation of the guinea pig trachea is mediated through beta 2-adrenoceptors, whereas d-methylephedrine relaxes the guinea pig trachea by blocking histamine receptors.

Animals↗
PubMedDate not supplied

beta2-adrenergic receptor stimulation-induced immunosuppressive effects possibly through down-regulation of co-stimulatory molecules, ICAM-1, CD40 and CD14 on monocytes.

We examined the effects of beta2-adrenergic receptor (beta2-AR) agonists on the expression of co-stimulatory molecules on lipopolysaccharide (LPS)-stimulated human peripheral blood mononuclear cells. The study found that beta2-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 beta2-AR antagonist, butoxamine. The selective beta2-AR agonists salbutamol and terbutaline induced a similar co-stimulatory molecule expression pattern. The LPS-induced production of tumour necrosis factor-alpha was inhibited by AR agonists, and this was also antagonized by butoxamine, and mimicked by salbutamol and terbutaline. The AR agonists also inhibited T-cell proliferation through beta2-AR stimulation. This study clearly demonstrated that endogenous catecholamines elicited immunosuppressive effects through beta2-AR stimulation, possibly due to down-regulation of the expression of ICAM-1, CD40 and CD14 on monocytes. These results suggested that the sympathetic nervous system might regulate the T-helper cell balance via the peripheral end-effectors of the stress system.

Adrenergic beta-2 Receptor Agonists↗
PubMed2004

Effect of orthovanadate on platelet aggregation induced by platelet-activating factor.

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.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2001

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

(+/-)-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.

Adrenergic beta-Agonists↗