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At least 91 records · Page 5Linked to original sources
PubMed1986

Characterization of functional beta-adrenoceptor subtypes in rabbit urinary bladder smooth muscle.

Spontaneous contractile force of muscle strips isolated from male rabbit urinary bladder dome (detrusor) and base (trigonal muscle) was significantly inhibited by isoproterenol (10(-7)-10(-5) M), a non-specific beta-adrenoceptor agonist or by terbutaline (10(-8)-10(-5) M), a selective beta 2-adrenoceptor agonist. The EC50 values for isoproterenol and terbutaline in detrusor were the same as those in trigonal muscle but the maximum relaxant response to isoproterenol or terbutaline was significantly greater in detrusor than in trigonal muscle. Dobutamine (10(-5)-10(-4) M), a relatively specific beta 1-adrenoceptor agonist caused a small but significant relaxant response in trigonal muscle but no change in detrusor. In trigonal muscle the relaxant response to dobutamine was less than that to terbutaline. The relaxant response to 10(-6) M isoproterenol in detrusor was completely blocked by butoxamine (10(-4) M), a selective beta 2-antagonist or by propranolol (10(-6) M), a non-specific beta-antagonist but not by metoprolol (10(-6)-10(-4) M), a selective beta 1-antagonist. Relaxation of trigonal muscle induced by 10(-6) M isoproterenol was inhibited by 10(-5) M metoprolol by 30%, by 10(-4) M butoxamine by 70%, or completely by 10(-6) M propranolol. These findings are consistent with the view that the density of beta-adrenoceptors is higher in the detrusor than in trigonal muscle, and that the relaxant response to beta-adrenoceptor stimulation is mediated by beta 2-subtype in the detrusor and by both of beta 1- and beta 2-subtypes in trigonal muscle of the male rabbit.

Animals↗
PubMed1978

beta-Adrenoreceptors of the posterior hypothalamus.

Cats were anaesthetized with pentobarbital sodium. A push-pull cannula was inserted into the posterior hypothalamus which was superfused through the cannula and electrically stimulated with its tip. Electrical stimulation elicited a frequency-dependent pressor response and tachycardia. Superfusion with orciprenaline, isoprenaline (beta 1- and beta 2-stimulants) or tazolol (beta 1-stimulant) led to a concentration-dependent enhancement in the pressor response. Superfusion with terbutaline caused a slight and late increase in the pressor response, while salbutamol (beta 2-stimulants) was ineffective. The tachycardia elicited by the hypothalamic stimulation was slightly increased by the hypothalamic stimulation was slightly increased by orciprenaline, tazolol and terbutaline. Superfusion with atenolol (beta 1-adrenoreceptor blocking drug) or butoxamine (beta 2-adrenoreceptor blocking drug) inhibited the pressor response and the tachycardia caused by hypothalamic stimulation. Superfusion with butoxamine prior to isoprenaline reduced the enhancing effect of isoprenaline on the pressor response, while superfusion with atenolol abolished or even reversed it. It is concluded that beta 1 and beta 2-adrenoreceptors are present in the posterior hypothalamus; apparently, beta 1- rather than beta 2-adrenoreceptors are involved in the rise of blood pressure elicited by stimulation of the hypothalamus.

Adrenergic beta-Agonists↗
PubMed1991

Beta-adrenergic receptor activity in ponies with recurrent obstructive pulmonary disease.

Pulmonary function measurements were made in control ponies and in ponies with recurrent obstructive pulmonary disease (principals) during clinical remission and during an attack of acute airway obstruction. The ponies were given beta-adrenergic antagonists and agonists to determine the role of beta receptors in recurrent obstructive pulmonary disease, and to determine the subtypes of beta receptors mediating bronchodilation in ponies. Aerosol administration of the beta antagonists, propranolol (beta 1 and beta 2), atenolol (beta 1), and butoxamine (beta 2) decreased dynamic compliance (Cdyn) and increased pulmonary resistance (RL) in the principal ponies during airway obstruction, but were without effect when the ponies were in clinical remission. Intravenous administration of atropine reversed the effect of atenolol on Cdyn and RL, but was without effect on the decrease in Cdyn and increase in RL observed after butoxamine administration. The beta antagonists did not affect airway function in the control ponies. The effect of beta blockade on Cdyn and RL suggests beta-adrenergic activation in the central and peripheral airways of principal ponies, mediated through both beta 2- and beta 1-adrenergic receptors. The aerosol beta agonists, isoproterenol (beta 1 and beta 2), and clenbuterol (beta 2) attenuated histamine-induced airway obstruction to a similar extent in control ponies that were given histamine IV. In addition, the beta 1 antagonist, atenolol, did not attenuate the bronchodilation observed with isoproterenol. We concluded that, although beta 1- and beta 2-adrenergic receptors exist in pony airways and are activated during acute airway obstruction, bronchodilation in response to beta agonists in ponies seems to be mediated primarily by beta 2-adrenergic receptors.

Aerosols↗
PubMedDate not supplied

The effect of beta-adrenoceptor antagonists alone and in combination with a GABA-elevating agent on isoniazid-induced convulsions in rats.

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. In these animals the convulsive responses were inhibited in a dose dependent manner. These compounds were found to be effective even after the induction of convulsions. The beta 1-blocker, acebutolol was able to protect rats only when injected prior to the challenge. 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). The findings indicate that the GABA-mediated anticonvulsant action of AOAA seems to be additive with that resulting from beta 1 but not beta 2-blockade.

Acebutolol↗
PubMed1988

Effects of repeated footshock stress on the chronotropic responsiveness of the isolated pacemaker of the rat: role of beta-2 adrenoceptors.

The effects of repeated footshock stress on the chronotropic responsiveness of the isolated right atria were studied. Repeated footshock stress was found to produce supersensitivity to isoproterenol and epinephrine (increase of 4.6- and 1.99-fold at pD2 level, respectively), but not to norepinephrine. Experiments using salbutamol, in the presence of an effective blocking concentration of metoprolol, showed that footshock stress increases the sensitivity (2.69-fold at pD2 level) to the selective beta-2 adrenoceptor agonist. Footshock stress had no effect on the atrial sensitivity to theophylline (1.09-fold at pD2 level). Addition of butoxamine (1 microM) suppressed footshock-induced pacemaker supersensitivity to isoproterenol and epinephrine. Footshock stress causes a small (3.23-fold) but pharmacologically unimportant increase in pacemaker pA2 value of metoprolol. However, footshock stress induces a large increase in the pacemaker beta-2 adrenoceptor affinity for butoxamine (11.48-fold, pA2 value). It is concluded that repeated footshock stress acts primarily to increase the chronotropic function of pacemaker beta-2 adrenoceptors, thus causing supersensitivity to isoproterenol, epinephrine and salbutamol.

Albuterol↗
PubMedDate not supplied

Incubated or superfused rat lung parenchymal strip: a valid preparation for direct measurement of beta-responses.

Responses to the beta-adrenoceptor agonists isoprenaline (Iso) (non selective), salbutamol (Sal) (beta 2-selective) and noradrenaline (NA) (beta 1-selective) were studied on incubated and superfused rat lung strip. In both conditions, Iso and Sal elicited dose-related relaxations of lung strip and these responses were unaffected by the presence of phentolamine (Phen) 10(-5) M. Contractile responses to NA were obtained when it was used alone whereas in the presence of Phen 10(-5) M, NA elicited relaxant responses. The relative potencies of Iso : Sal : NA (plus Phen) were 100 : 20 : 0.69. This demonstrates that beta 2-adrenoceptor is the predominant beta-subtype involved in responses. Propranolol (10(-4) M) completely abolished the relaxant responses to Iso. However, after the addition of Iso tissue responded normally to drugs acting by other mechanisms. Thus, relaxations were obtained with caffeine and contractions with acetylcholine (AcH) or NA. This shows that responses to Iso are mediated only by beta-adrenoceptors. Propranolol and the selective beta-blocking agents butoxamine (beta 2) and atenolol (beta 1) competitively antagonized the effects of Iso. The Schild plots obtained had slopes which did not differ significantly from -1 and mean pA2 values were: 7.82 for propranolol; 6.32 for butoxamine and 5.22 for atenolol. These experiments were carried out in the absence of catecholamine uptake inhibitors, since in a preliminary set of experiments no significant changes of lung strip responses to Iso were observed in the presence of cocaine (10(-5) M) or corticosterone (10(-5) M). In conclusion, it appears that incubated rat lung strip possesses intrinsic tone and, although it cannot be considered a representative preparation of peripheral airways, it provides a valid model for investigating the direct-effects of drugs which act at beta-adrenoceptors.

Albuterol↗
PubMed1984

Heterogeneity of beta adrenoceptors in right atria isolated from cold-exposed rats.

The chronotropic response of right atria isolated from 5-day-cold-exposed rats to isoproterenol and norepinephrine was studied. A large increase in the sensitivity of the pacemaker to isoproterenol and a decrease in the sensitivity to norepinephrine occurred. Determination of pA2 values of propranolol and metoprolol using isoproterenol and norepinephrine as agonists and analysis of the slopes of Schild plots suggested that in atria isolated from control rats the chronotropic effect of isoproterenol and norepinephrine resulted from the preferential interaction of the catecholamines with a homogeneous beta-1 adrenoceptor population. After cold exposure the affinity of atrial adrenoceptors for propranolol increased when the agonist was isoproterenol and decreased when norepinephrine was used. The slopes of the Schild plots of metoprolol when the agonists were isoproterenol or norepinephrine were not unitary unless the experiments were performed in the presence of butoxamine. However, butoxamine prevented the demonstration of cold-induced super-sensitivity to isoproterenol, leaving the subsensitivity to norepinephrine unaffected. It is concluded that cold-induced heterogeneity of the atrial beta adrenoceptors is responsible for the increased sensitivity to isoproterenol. Probably, subsensitivity to norepinephrine resulted from conformational alterations of the atrial beta-1 adrenoceptors.

Animals↗
PubMedDate not supplied

Vasodilator effect of terbutaline: in vivo evidence for the existence of beta 2-adrenoceptors in the microcirculation of rats, hamsters, and guinea pigs.

The characteristics of beta 2-adrenoceptors were studied in vivo in the microcirculation of cremaster muscle and mesoappendix in rats, cheek pouch in hamsters, and mesentery in guinea pigs, using a video-microscope technique. Terbutaline (beta 2-selective agonist) caused vasodilatation in all four microcirculation preparations studied, whereas butoxamine (beta 2-selective antagonist) competitively inhibited the terbutaline-induced vasodilatation. The in vivo pA2 values of butoxamine inhibition of terbutaline vasodilator effect were estimated from Schild plots. The pA2 values (6.22-6.31) were statistically identical in all four microcirculations studied and similar to in vitro values reported in other tissues. In contrast, tazolol and prenalterol (both beta 1-selective agonists) did not produce any vasodilatation in the microcirculations studied. These results supported the existence of beta 2-adrenoceptors involved in vasodilatation in the microcirculation.

Animals↗
PubMedDate not supplied

Effects of adrenolytic drugs on the antihypertensive action of beta-blocking agents in the acute neurogenic hypertensive dog.

1. The antihypertensive action of three beta-blocking agents (dl-propranolol, dl-atenolol and butoxamine) was studied before and after pretreatment with adrenolytic drugs (reserpine and guanethidine) in acute neurogenic hypertensive (sino-aortic denervated) anesthetized dogs. 2. High doses of reserpine (2 mg/kg s.c.) suppressed both the effects of sino-aortic denervation and the antihypertensive action of dl-propranolol (1 mg/kg i.v.) 3. Pretreatment with reserpine (1 mg/kg i.p.) or guanethidine (15 mg/kg i.v.) delayed the manifestation of the antihypertensive action of dl-propranolol (1 mg/kg) observed in untreated (control) animals. 4. In a similar way, both dl-atenolol (1 mg/kg i.v.) and butoxamine (1 mg/kg i.v.) lost their antihypertensive effects after reserpinization. 5. These results indicate that the antihypertensive action of the three studied beta-blocking agents seen in debuffered animals depends upon the integrity of peripheral sympathetic nervous system under our experimental conditions. These effects are compatible with the view that beta-adrenoceptor blocking agents may exert, at least partly, their antihypertensive action through blockade of peripheral beta prejunctional adrenoceptors.

Animals↗
PubMed1980

Effects of beta adrenergic agents and prostaglandin E1 on erythroid colony (CFU-E) growth and cyclic AMP formation in Friend erythroleukemic cells.

The formation of erythroid colonies from bone marrow and spleen cells infected with the polycythemic strain of the Friend virus (FV-P) was characterized in an in vitro methyl cellulose colony-forming system in response to prostaglandin E1 and the beta-2 adrenergic agonist, albuterol. Both drugs markedly inhibited the formation of CFU-E colonies of FV-P-infected bone marrow and spleen in the absence or presence of erythropoietin. The albuterol-mediated inhibition of CFU-E colonies (FV-P-infected) was selectively blocked by butoxamine, a beta-2 antagonist. Adenylate cyclase (AC) activity was also determined in FV-P spleen membrane preparations in response to albuterol and PGE1. Both agents stimulated enzyme activity, and butoxamine blocked the stimulation seen with albuterol. The ability of albuterol and PGE1 to stimulate AC activity in the FV-P-infected cells suggests that the effects of these agents on CFU-E formation may be mediated by specific beta-2 adrenergic and PG receptors through the adenylate cyclase-cyclic AMP system.

Adenylyl Cyclases↗
PubMed1986

The modulation of head-twitch behaviour by drugs acting on beta-adrenoceptors: evidence for the involvement of both beta 1- and beta 2-adrenoceptors.

Drugs selective for either the beta 1- or beta 2-adrenoceptor have been investigated for their effects on the head-twitch behaviour induced by L-5-hydroxytryptophan (L-5-HTP) in mice. All four agonists, dobutamine and prenalterol (beta 1-), and salbutamol and procaterol (beta 2-), potentiated the effect of L-5-HTP although they were ineffective in inducing the head-twitch when administered alone. The corresponding antagonists, practolol and metoprolol (beta 1-) and butoxamine and ICI 118,551 (beta 2-), were without effect on the L-5-HTP head-twitch. The antagonists each significantly reduced the effect of the corresponding agonists but, while butoxamine and ICI 118,551 were inactive against dobutamine and prenalterol potentiation, both practolol and metoprolol reduced the effect of salbutamol and procaterol. Thus it is argued that dobutamine and prenalterol potentiation is due to an action at beta 1-adrenoceptors, while at least a component of the potentiating effect of salbutamol and procaterol is exerted through beta 2-adrenoceptors. The lack of effect of the antagonists alone is discussed.

5-Hydroxytryptophan↗
PubMed1993

Involvement of alpha 2-adrenoceptors in mechanism of intragastric nicotine protection against ethanol injury in rat stomach.

To elucidate the role of alpha- and beta-adrenoceptors in the mechanism of intragastric nicotine protection against ethanol-induced gastric mucosal injury, the following studies were performed. At 0.5-hr prior to the injury study, rats were pretreated with: subcutaneous control, prazosin (0.5 mg/kg) or yohimbine (5 mg/kg) to block alpha 1- or alpha 2-adrenoceptors; or intraperitoneal control, metoprolol (2 mg/kg) or butoxamine (4 mg/kg) to block beta 1- or beta 2-adrenoceptors, respectively. At 1-hr intervals, rats received intragastric vehicle or nicotine (4 mg/kg) and 40% ethanol (10 ml/kg). Total lengths of the linear gastric corpus mucosal lesions were measured by an unbiased observer using a caliper. In a separate study, 0.5-hr after subcutaneous control or yohimbine (5 mg/kg), rats were treated with intragastric vehicle or nicotine (4 mg/kg). One hour later, gastric mucus volume, gastric juice volume and pH, and titratable acid in the gastric juice were measured. In the rat stomach, the intragastric nicotine protection against 40% ethanol-induced mucosal injury was not blocked by selective alpha 1-(prazosin), beta 1-(metoprolol), or beta 2-(butoxamine) adrenoceptor antagonists. The protection was significantly reduced although not completely abolished by selective alpha 2-(yohimbine) adrenoceptor antagonist. Yohimbine also significantly reduced basal and nicotine-stimulated increase in gastric mucus volume. These data suggest that alpha 2-adrenoceptors are involved in the protective effect of intragastric nicotine against 40% ethanol-induced gastric mucosal injury possibly by a mucus-dependent mechanism.

Adrenergic alpha-Antagonists↗
PubMed1986

Classification of beta-adrenergic subtypes in immature rabbit bone marrow erythroblasts.

The beta-adrenergic receptors of immature rabbit bone marrow erythroid cells (proerythroblasts and basophilic erythroblasts) were identified. [125I]iodocyanopindolol bound to membrane preparations derived from these erythroblasts in a rapid, reversible and saturable manner. Scatchard analysis of binding data revealed a single class of binding sites (Hill coefficient of 0.954) with an apparent equilibrium dissociation constant (Kd) of 8 pM, and a density of binding sites (Bmax) of 1.53 pM/10(6) cells, corresponding to 920 receptors per cell. The binding of [125I]iodocyanopindolol was inhibited stereospecifically by concentrations of (-)-propranolol 2 orders of magnitude lower than by the (+)-isomer. Only L-isoprenaline and L-adrenaline activated the adenylate cyclase of immature rabbit erythroblasts, while L-noradrenaline, a beta 1-adrenergic agonist, was inactive. The order of potency of different agonists for displacement of bound [125I]iodocyanopindolol was: isoprenaline greater than adrenaline greater than noradrenaline with respective EC50 (concentration required for half maximal inhibition of binding) of 7.9 X 10(-7) M, 1.5 X 10(-5) M and 7.9 X 10(-5) M. This agonist potency series did not change with differentiation of rabbit bone marrow erythroblasts. The inhibition of specific [125I]iodocyanopindolol binding to immature cells by beta 1- and beta 2-selective drugs (noradrenaline, practolol, procaterol and butoxamine) resulted in linear Hofstee plots. The inhibition curves obtained with procaterol and butoxamine, with apparent Kd values of 3.1 X 10(-9) M and 4.9 X 10(-9) M, further evidence that the high-affinity binding sites correspond to a homogeneous beta 2-receptor subtype.

Adenylyl Cyclases↗
PubMed1979

Isolated lung strips of guinea pigs: responses to beta-adrenergic agonists and antagonists.

Isolated lung strips of guinea pigs were examined as an in vitro model for assessing the direct effect of beta-adrenergic drugs at the level of peripheral airways. Changes in intrinsic tone of thin strips of lung parenchyma were measured with an isometric force transducer. Isoproterenol, a nonselective beta-adrenergic agonist, and several beta-adrenergic agonists, soterenol, salbutamol, metaproterenol and ritodrine elicited a dose-related relaxation of lung strip. Responses to isoproterenol were antagonized by propranolol and the selective beta blocking agents butoxamine (beta2) and practolol (beta1). These results were compared to data obtained with the same compounds on isolated guinea pig atria. All agonists except ritodrine were full agonists in the lung strip whereas isoproterenol and metaproterenol were the only full agonists in the atrial preparation. In the atria, practolol was a more effective blocker of isoproterenol responses than butoxamine, and the reverse was true for the lung strip.

Adrenergic beta-Agonists↗
PubMed1990

Antagonism of 8-OH-DPAT-induced behaviour in rats.

Selective activation of the 5-HT1A receptor induces lower lip retraction (LLR) in rats. 8-Hydroxy-dipropylamino tetralin (8-OH-DPAT)-induced LLR could not be antagonised by the 5-HT antagonists methysergide, metergoline or mesulergine. In fact, some 5-HT antagonists induced LLR. However, 8-OH-DPAT-induced LLR could be antagonised by pindolol, spiperone, spiroxatrine and NAN-190, but not by the beta 1-adrenoceptor antagonist metoprolol, the beta 2-adrenoceptor antagonist butoxamine or the dopamine antagonist haloperidol. This antagonism was competitive as the dose-response curve of 8-OH-DPAT was shifted to the right. Pindolol, spiperone, spiroxatrine and NAN-190 all have a high affinity for the 5-HT1A receptor. This indicates that blockade of 8-OH-DPAT-induced LLR is only possible by selective blockade of 5-HT1A receptors. A possible mechanism of action is discussed. The increased defecation induced by 8-OH-DPAT could be antagonised by pindolol and NAN-190. The effect of spiroxatrine and haloperidol on the 8-OH-DPAT-induced increase in defecation was bimodal: an increase after a low and a decrease after a high dose of 8-OH-DPAT. Metoprolol and butoxamine had no effect on the 8-OH-DPAT-induced increase in defecation, thereby excluding an influence of beta-adrenoceptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1987

Effects of sympathetic nerve stimulation in the presence of specific adrenergic antagonists on Na, K, and Cl transport in perfused rat submandibular duct.

The role of beta 1- and beta 2-adrenoceptors in the modification of Na, K, and Cl transport in submandibular main duct of rat perfused with bicarbonate saline solution was studied with direct sympathetic nerve stimulation (4 V, 5 ms, 20 Hz) in the presence of specific adrenergic antagonists. Nerve stimulation in the presence of phenoxybenzamine (3 mg/kg b. wt., i.p.) and butoxamine (3 mg/kg b. w.t., i.p.) enhanced Na (44%) and Cl (35%) absorption but inhibited K (24%) secretion. On the other hand, the nerve-evoked response in the presence of phenoxybenzamine and metoprolol (3 mg/kg b. wt., i.p.) decreased K (19%) secretion without any changes in Na and Cl absorption. Therefore, the data suggest that beta 1- and beta 2-adrenoceptors may be present in the duct cells and activation of these receptors can modify electrolyte transport. Furthermore, prior administration of phenoxybenzamine, butoxamine, and metoprolol suppressed the effects of sympathetic nerve stimulation on transductal fluxes of Na, K and Cl; this indicates that the dosages of antagonists used were sufficiently high to block a nerve-evoked response.

Animals↗
PubMed1979

Catecholamine and guanine nucleotide activation of skeletal muscle adenylate cyclase.

Activation of adenylate cyclase by guanine nucleotide and catecholamines was examined in plasma membranes prepared from rabbit skeletal muscle. The GTP analog, 5'-guanylyl imidodiphosphate caused a time and temperature-dependent activation of the enzyme which was persistent, the Ka was 0.05 microM. 5'-Guanylyl imidodiphosphate binding to the membranes was time and temperature dependent, KD 0.07 microM. Beta adrenergic amines accelerated the rate of 5'-guanylyl imidodiphosphate activation of the enzyme with an order of potency isoproterenol approximately soterenol approximately salbutamol greater than epinephrine greater than norephrine. Catecholamine activation was antagonized by propranolol and the beta2 antagonist butoxamine; the beta1 antagonist practolol was inactive. [3H]Dihydroalprenolol bound to the membranes and binding was antagonized by beta adrenergic agonists with an order of potency similar to the activation of adenylate cyclase and was antagonized by butoxamine but not by practolol. The data are consistent with the idea that adenylate cyclase in skeletal muscle plasma membranes is coupled to adrenergic receptors of the beta2 type.

Adenylyl Cyclases↗
PubMed2002

Types of adrenoreceptors mediating responses of rabbit gastric muscularis mucosae.

This study investigated adrenoreceptor-mediated responses of muscularis mucosae from the fundic and antral ends of the rabbit gastric corpus. Norepinephrine-induced fundic muscularis mucosae contractions were enhanced by propranolol and converted to relaxations by phentolamine. Methoxamine, but not clonidine, elicited large fundic contractions. Fundic muscle responded to low isoproterenol concentrations with atenolol- and butoxamine-resistant relaxations, and to high concentrations with atenolol-sensitive contractions. Norepinephrine evoked propranolol-resistant relaxations of antral muscularis mucosae that were enhanced by phentolamine. Methoxamine and clonidine elicited small antral contractions. Lower concentrations of isoproterenol caused atenolol-resistant antral relaxations that were enhanced by butoxamine; higher concentrations produced weak excitation. Fundic and antral relaxations to isoproterenol were abolished by cyanopindolol. Fundic muscularis mucosae possesses excitatory alpha1-, beta1- and inhibitory beta3-adrenoreceptors. Excitatory beta2- and inhibitory beta3-adrenoreceptors predominate in the antral region. The heterogeneous adrenoreceptor-mediated responses of the gastric muscularis mucosae suggest that adrenergic modulation of its motor activity is unlikely to be linked to acid secretion.

Adrenergic alpha-Agonists↗